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This study investigated the druggability, pharmacokinetics and ethyl acetate extract of Teucrium polium (EA T. polium) and the protective effect against carbon tetrachloride (CCl4) induced liver cirrhosis in rats. The total antioxidant capacity (TAC) and scavenging activity of the extract were examined. The in vivo protective study was based on the use of an animal model of CCl4-induced liver cirrhosis. Four groups of rats have been used: Group I: control rats; Group II: received CCl4 in olive oil (0.5 mL/kg); Group III: received the EA T. polium (25 mg/kg) of pretreatment for seven days by gavage then CCl4 in olive oil by gavage for 15 days. Group IV: received the EA of T. polium for seven days (25 mg/kg). EA T. polium was found to possess significant antioxidant capacity. CCl4 caused a hepatotoxicity associated increase in both levels of AST and ALT, which were reduced back to normal values following EA T. polium pretreatment. Hepatotoxicity associated structural modifications of liver tissues and increase in thiobarbituric acid reactive substances (TBARS), conjugated dienes (CD) and carbonyl proteins (CP), associated decreases in several assessed antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT). The in vivo findings on the protective effect of T. polium were supported by its druggability, its pharmacokinetic properties and molecular docking assays. These results confirm the modulatory antioxidant and hepatoprotective potential of T. polium in this experimental liver cirrhosis model. T. polium phytochemicals are good candidates for further pharmaceutical explorations and drug design. [ABSTRACT FROM AUTHOR]

Several theories regarding acute kidney injury (AKI)-related mortality have been entertained, although mounting evidence supports the paradigm that impaired kidney function directly and adversely affects the function of several remote organs. The kidneys and liver are fundamental to human metabolism and detoxification, and it is therefore hardly surprising that critical illness complicated by hepatorenal dysfunction portends a poor prognosis. Several diseases can simultaneously impact the proper functioning of the liver and kidneys, although this review will address the impact of AKI on liver function. While evidence for this relationship in humans remains sparse, we present supportive studies and then discuss the most likely mechanisms by which AKI can cause liver dysfunction. These include 'traditional' complications of AKI (uremia, volume overload and acute metabolic acidosis, among others) as well as systemic inflammation, hepatic leukocyte infiltration, cytokine-mediated liver injury and hepatic oxidative stress. We conclude by addressing the therapeutic implications of these findings to clinical medicine. [ABSTRACT FROM AUTHOR]

Background: Some researches reveal that pharmacologic and phytotherapeutic agents have benefits on neurological disorders associated with the effects of reactive oxygen species. Aim: The purpose of this research was to evaluate the protective effects of curcumin and memantine in a cerebral ischemia/reperfusion model in rats. Materials and Methods: This experimental study was conducted at the Bagcilar Training and Research Hospital, Istanbul, Turkey. Rats were separated into five experimental groups ( n=8) as follows: Curcumin (Group I), Memantine (Group II), Curcumin+Memantine (Group III), ischemia (Group IV), and sham (Group V). Cerebral ischemia was performed surgically with bilateral common carotid artery occlusion for 30 min, followed by reperfusion for 72 hr. Tissue and serum samples were collected and assessed for tumor necrosis factor-α, interleukin-6, lactate dehydrogenase, catalase, glutathione peroxidase, xanthine dehydrogenase, superoxide dismutase, and malondialdehyde levels. Further, in tissue samples, both neuronal loss and caspase-3 levels were determined. Results: Serum and tissue levels of interleukin-6, tumor necrosis factor-α, malondialdehyde, and lactate dehydrogenase were found significantly lower in the Group I, II, and III compared to Group IV ( p<0.001). Glutathione peroxidase, superoxide dismutase, and catalase levels in Group I, II, and III were significantly higher than those of Group IV ( p<0.001). Conclusion: Curcumin, Memantine, and Curcumin+Memantine treatment were found to be efficacious in decreasing oxidative damage in cerebral ischemia but failed to prevent tissue damage. [ABSTRACT FROM AUTHOR]

Aims: We aimed to resolve the uncertainty as to whether betulin exerted neuroprotection on early brain injury (EBI) caused by subarachnoid hemorrhage (SAH), and to investigate the related molecular mechanisms., Methods: Bioinformatic analysis was performed to pre-study the differently expressed genes (DEGs) and the possible signaling pathways. Rat and cellular model of SAH were introduced in this study, and betulin, an activator of DJ-1 protein, was administered to reveal the effect. Gross assessment regarding mortality, neurofunctions, SAH grade, brain water content (BWC) along with multiple cellular and molecular studies in vivo or/and in vitro such as immunofluorescence (IF) staining, western blot (WB), reactive oxygen species (ROS) assay, and flow cytometry (FCM) were all conducted after SAH induction to verify the protective effect and the relevant mechanisms of DJ-1 in diverse levels. In addition, MK2206 (selective inhibitor of Akt) and iRNADj-1 (interfering RNA to Dj-1) were utilized to confirm the mechanisms of the effect., Results: The data from our study showed that DJ-1 protein was moderately expressed in neurons, microglia, and astrocytes; its level in brain tissue elevated and peaked at 24-72 h after SAH induction. Betulin could efficaciously induce the expression of DJ-1 which in turn activated Akt and Bcl-2, and anti-oxidative enzymes SOD2 and HO-1, functioning to reduce the activation of cleaved caspase-3 (c-Casp-3) and reactive oxygen species (ROS). The induced DJ-1 could upregulate the expression of Nrf2. However, Akt seemed no direct effect on elevating the expression of Nrf2. DJ-1 alone could as well activate Akt-independent antiapoptotic pathway via suppressing the activation of caspase-8 (Casp-8)., Conclusions: Betulin which was a potent agonist of DJ-1 had the ability to induce its expression in brain tissue. DJ-1 had neuroprotective effect on EBI through comprehensive mechanisms, including facilitating intrinsic and extrinsic antiapoptotic pathway, and reducing oxidative injury by upregulating the expression of redox proteins. Betulin as an inexpensive drug showed the potential for SAH treatment., (© 2024 The Author(s). CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.)

Iron (Fe) starvation in Strategy II plants is a major nutritional problem causing severe visual symptoms and yield reductions. This prompted us to investigate the physiological and molecular consequences of Fe deficiency responses at an early stage in sorghum plants. The Fe-starved sorghum did not show shoot biomass reduction, but the root length, biomass, and chlorophyll synthesis were severely affected. The chlorophyll a fluorescence analysis showed that the quantum yield efficiency of PSII (Fv/Fm) and photosynthesis performance index (Pi_ABS) in young leaves significantly reduced in response to low Fe. Besides, Fe concentration in root and shoot significantly declined in Fe-starved plants relative to Fe-sufficient plants. Accordingly, this Fe reduction in tissues was accompanied by a marked decrease in PS-release in roots. The qPCR experiment showed the downregulation of SbDMAS2 (deoxymugineic acid synthase 2), SbNAS3 (nicotianamine synthase 3), and SbYSL1 (Fe-phytosiderophore transporter yellow stripe 1) in Fe-deprived roots, suggesting that decreased rhizosphere mobilization of Fe(III)-PS contributes to reduced uptake and long-distance transport of Fe. The cis-acting elements of these gene promoters are commonly responsive to abscisic acid and methyl jasmonate, while SbYSL1 additionally responsive to salicylic acid. Further, antioxidant defense either through metabolites or antioxidant enzymes is not efficient in counteracting oxidative damage in Fe-deprived sorghum. These findings may be beneficial for the improvement of sorghum genotypes sensitive to Fe-deficiency through breeding or transgenic approaches.

AIM:To investigate the protective effects of naringin(Nar)phospholipid complex(NPC)on oxidative injury in retinal pigment epithelium cells(ARPE-19 cells)induced by tert-butyl hydroperoxide(t-BHP)and elucidate the underlying mechanism.METHODS:The NPC was prepared by solvent method. Experimental cells are divided into seven groups: control group [cultured with dimethylsulfoxide(DMSO)], model group(intervention with 200μmol/L t-BHP), nuclear factor erythroid 2-related factor 2(Nrf2)-siRNA group(cell transfection for Nrf2 gene), naringin group(add 200μmol/L t-BHP after pretreatment with 200μmol/L naringin medium), NPC group(add 200μmol/L t-BHP after pretreatment with 200μmol/L NPC medium), Nrf2-siRNA+ naringin group(after 200μmol/L naringin pretreatment, Nrf2 gene interference, then add 200μmol/L t-BHP)and Nrf2-siRNA+ NPC group(after 200μmol/L NPC pretreatment, Nrf2 gene interference, then add 200μmol/L t-BHP). The intracellular levels of superoxide dismutase(SOD), malondialdehyde(MDA)and total antioxidant capacity(T-AOC)were detected, intracellular level of reactive oxygen species(ROS)was detected by DCFH-DA staining method. The mRNA and protein expressions of HO-1, NQO-1, GCL and Nrf2 were detected by real-time PCR and western blot, respectively. RESULTS:NPC more significantly increased the levels of SOD and T-AOC, reduced the contents of ROS and MDA than naringin in t-BHP-treated ARPE-19 cells. After naringin and NPC pre-protected ARPE-19 cells, the relative expression and protein expression of Nrf2, HO-1, NQO-1 and GCL mRNA were higher than those of the model group and Nrf2-siRNA group. There were statistically significant differences in the relative expression of 4 genes and the expression levels of 4 proteins in the naringin group and the NPC group, the Nrf2-siRNA+naringin group and the Nrf2-siRNA+NPC group. The expression of Nrf2, HO-1 and NQO-1 protein in the Nrf2-siRNA+naringin group was not significantly different than that in the Nrf2-siRNA group. Compared with the Nrf2-siRNA group, the expression of 4 proteins in the Nrf2-siRNA+NPC group was statistically significant, and the effect of NPC was significantly stronger than that of naringin.CONCLUSION: After naringin forms a phospholipid complex, it can significantly increase the antioxidant capacity in cells and reduce the oxidation level. It up-regulates the expression of Nrf2 and its downstream antioxidant enzymes and phase Ⅱ detoxification enzymes by activating the Nrf2/ARE antioxidative stress pathway to better protect ARPE-19 cells from oxidative damage.

Age-related cataract (ARC) is one of the leading blinding eye diseases worldwide. Chronic oxidative stress and the apoptosis of human lens epithelial cells (HLECs) have been suggested to be the mechanism underlying cataract formation. Acetyl-11-keto-β-boswellic acid (AKBA) is a pentacyclic triterpene with antioxidative and antiapoptotic effects. In this study, we investigated the potential effects of AKBA on oxidative-induced HLECs injury and cataract formation. H2O2 was used to simulate HLECs oxidative injury in vitro, and Na2SeO3 was applied to establish an in vivo cataract model. In our current study, a cell counting kit-8 (CCK-8) assay was performed to evaluate the effects of H2O2 and AKBA on cell viability in vitro. Intracellular reactive oxygen species (ROS) levels were measured with the ROS assay to verify the antioxidant capacity of AKBA. Apoptotic cells were detected and measured by TUNEL staining and flow cytometry, and quantitative real-time (qRT)-PCR and Western blotting were applied to examine the transcription and expression of apoptosis-related proteins. Furthermore, immunofluorescence staining was performed to locate factor-erythroid 2-related factor 2 (Nrf2), and the protein levels of Nrf2, kelch-like ECH-associated protein 1 (Keap1) and heme oxygenase-1 (HO-1) were determined by Western blotting. Finally, we observed the degree of lens opacity and performed hematoxylin-eosin (H&E) staining to assess the protective effect of AKBA on cataract formation in vivo. AKBA increased HLECs viability under H2O2 stimulation, decreased intracellular ROS levels and alleviated the cell apoptosis rate in vitro. AKBA significantly decreased the expression of caspase-3 and Bax and increased the content of Bcl-2. The results of immunofluorescence and immunohistochemical staining proved that the expression and nuclear translocation of Nrf2 were activated with AKBA treatment in vivo and in vitro. Moreover, computational docking results showed that AKBA could bind specifically to the predicted Keap1/Nrf2 binding sites. After AKBA activation, Nrf2 dissociates from the Nrf2/Keap1 complex, translocates into the nucleus, and subsequently promotes HO-1 expression. In addition, AKBA attenuated lens opacity in selenite-induced cataracts. Overall, these findings indicated that AKBA alleviated oxidative injury and cataract formation by activating the Keap1/Nrf2/HO-1 cascade. Therefore, our current study highlights that AKBA may serve as a promising treatment for ARC progression.

The present study was undertaken to appraise the efficacy of exogenous taurine in alleviating boron (B) and chromium (Cr) toxicity. Taurine protects cell membranes from lipid peroxidation due to its function as a ROS scavenger. However, there exists no report in the literature on the role of taurine in plants under abiotic stresses. The present investigation indicated the involvement of exogenous taurine in mediating plant defense responses under B and Cr toxicity. Wheat plants manifested a significant drop in growth, chlorophyll molecules, SPAD values, relative water content, nitrate reductase activity, and uptake of essential nutrients under B, Cr, and combined B-Cr toxicity. Plants showed significant oxidative damage due to enhanced cellular levels of superoxide radicals (O2•−), hydrogen peroxide (H2O2), malondialdehyde (MDA), relative membrane permeability, and activity of lipoxygenase (LOX). Additionally, a significant negative correlation existed in B and Cr levels with the uptake of essential nutrients. Taurine substantially improved growth, photosynthetic pigments, and nutrient uptake by regulating ROS scavenging, secondary metabolism, and ions homeostasis under stress. Taurine protected plants from the detrimental effects of B and Cr by upregulating the production of nitric oxide, hydrogen sulfide, glutathione, and phenolic compounds. [ABSTRACT FROM AUTHOR]

Objective: The aim is to examine the possible protective effect of Cuscuta sp. extract against liver damage induced by biliary obstruction in rats. Materials and Methods: To induce biliary obstruction, the bile duct ligation (BDL) method was used. Sprague Dawley rats were allocated to 4 groups: Control (C), Cuscuta (CUS), bile duct ligation (BDL), and bile duct ligation + Cuscuta (BDL+CUS). Control and BDL rats were given physiological saline (SF), while CUS and BDL+CUS groups were administered 250 mg/kg of Cuscuta extract by oral gavage. At the end of 28th day, the rats were decapitated, serum and tissue samples were collected, and aspartate aminotransferase (AST), alanine transaminase (ALT), and direct and total bilirubin (DB and TB) levels were determined in blood samples. In liver tissues, transforming growth factor-ß (TGF-ß), 8-hydroxyguanosine (8-OHdG), hydroxyproline, and sodium-potassium ATPase (Na+/K+-ATPase) levels were determined. Results: Serum samples of rats with cholestasis had high ALT, AST, DB, and TB levels, while TGF-ß, 8-OHdG, and hydroxyproline concentrations were found to be significantly high in tissues. Hepatic Na+/K+-ATPase levels were decreased through biliary obstruction. Biochemical parameters were drastically reversed by Cuscuta care; also, this was supported histologically. Conclusion: Results showed that Cuscuta extract, through its antioxidant and anti-inflammatory properties, provided protection against oxidative injury by biliary obstruction. Also, these results confirm the traditional use of Cuscuta sp. as hepatoprotective. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to investigate the effects of pomegranate (Punica granatum L.) seed hydro-ethanolic extract (PSE) on cholinergic dysfunction, neuroinflammation, and oxidative stress in the scopolamine-induced amnesic rats. Methods: The rats were given PSE (200, 400, and 800 mg/kg, gavage) for 3 weeks. In the third week, scopolamine was administered 30 min before the Morris water maze (MWM) and passive avoidance (PA) tests. Oxidative stress indicators, acetylcholinesterase (AChE) activity, and mRNA expression of necrosis factor (TNF)-α, interleukin (IL)-1β, AChE, and M1 acetylcholine receptor (CHRM1) in the brain, were measured. Results: PSE reduced the time (maximum 173%) and distance (maximum 332%) required to reach the platform during MWM learning (P < 0.001). In the prob test (P < 0.001), it increased the target area time (maximum 44%) and distance (maximum 30%). PSE also increased delay and light time (maximums of 86 and 48%, respectively) (P < 0.001), while decreasing the time in dark region of PA (maximums 727%) (P < 0.001). PSE also reduced malondialdehyde and AChE in the cortex (maximum 168 and 171%, respectively) and hippocampus (maximum 151 and 182%, respectively) (P < 0.001). In the PSE-treated groups, the levels of thiol and superoxide dismutase were increased in the cortex (maximum 54 and 65%, respectively) and hippocampus (maximum 90 and 51%, respectively) (P < 0.001). TNF-α, IL-1β, and AChE expressions in the hippocampus were reduced by PSE (maximum 114, 137, and 106%, respectively, P < 0.01). Meanwhile, CHMR expression was increased (66%). Conclusion: PSE successfully alleviated scopolamine-induced memory and learning deficits in rats which is probably via modulating cholinergic system function, oxidative stress, and inflammatory cytokines. [ABSTRACT FROM AUTHOR]

Spinal injury is a complicated disease and is reported to be associated with damages on spinal astrocytes induced by oxidative injury. Astragali Radi, a famous traditional Chinese medicine, is reported to have promising efficacy in protecting injuries in the central nervous system. This study aims to investigate the effect of calycosin, an isoflavone phytoestrogens isolated from Astragali Radi, on oxidative injury in spinal astrocytes induced by H2O2 and the underlying mechanism. Primary rat spinal astrocytes were pretreated with 5, 10, and 20 μM calycosin and subjected to H2O2 treatment for 24 h to establish an oxidative injury model. Cell viability was detected using the CCK-8 assay to screen the optimized concentration of calycosin. Flow cytometry was used to evaluate the apoptotic rate and cell cycle. The expression level of Brdu was visualized using the immunofluorescence assay. Western blotting was used to measure the expression levels of p-JAK2, p-STAT3, p-AKT, GP130, and IL-6 in spinal astrocytes. We found that proliferation was inhibited and that apoptosis was induced by the stimulation of H2O2. The expression levels of p-JAK2, p-STAT3, p-AKT, GP130, and IL-6 were significantly elevated in H2O2-treated astrocytes. After the treatment of calycosin, proliferation was facilitated, and apoptosis was suppressed. These phenomena were accompanied by the downregulation of p-JAK2, p-STAT3, p-AKT, GP130, and IL-6, which were abolished by the co-administration of PI3K (ly294002) or STAT3 (stattic) inhibitor. Overall, calycosin alleviated oxidative injury in spinal astrocytes by mediating the GP130/JAK/STAT pathway. [ABSTRACT FROM AUTHOR]

Background: Oxidative stress has been shown to be an important factor, which plays a significant role in the pathogenesis of neurodegenerative disorders. Heat Shock Protein-27 (HSP-27) has been implicated in antioxidant responses against oxidative stress. Trehalose is a natural disaccharide widely used in a variety of food products with demonstrated protective effects against several neurodegenerative diseases. This study investigated the effects of trehalose on antioxidant responses, and the gene expressions for HSP-27 and caspase-3 against hydrogen peroxide (H2O2 ) induced oxidative injury in PC-12 cell line. Methods: The PC-12 cells were treated with various concentrations of H2O2 and trehalose for 24hr. The cell viability was assessed, using MTT and Lactate Dehydrogenase (LDH) release assays. Moreover, the activity of Catalase (CAT) and Glutathione Peroxidase (GPx) enzymes, and the Malondialdehyde (MDA) levels were determined. In addition, the levels of HSP-27 and caspase-3 gene expressions were measured. Results: The results indicated that the pretreatment with trehalose increased cell survival against the H2O2-induced oxidative injury. Furthermore, trehalose elevated the CAT and GPx activities and reduced MDA levels compared to that of control group (P˂0.05). Moreover, trehalose upregulated the HSP-27 gene expression, while reducing the expression of caspase-3 gene compared to that of the untreated cells (P˂0.05). All of these biochemical changes were found to be dose-dependent for trehalose. Conclusion: Based on the study findings, trehalose had the capacity to attenuate the oxidative stress and cell injury. Therefore, trehalose may be suggested as a therapeutic agent to treat neurodegenerative disorders caused by oxidative stress damages. [ABSTRACT FROM AUTHOR]

Most degenerative diseases are caused by free radicals. Antioxidin-RL peptide is a free radical scavenger found in the skin of plateau frog Odorrana livida, which is more stable than vitamin C as it resists light-induced degradation. However, whether and how antioxidin-RL protects cells from oxidative stress was not clear. Here we addressed this issue, and in addition, we designed a series of antioxidin cognates by adding tyrosine residues to enhance free radical-binding capability. We performed free radical-clearing assays in solution to screen the mutants, and found a mutant antioxidin-2 that was as stable as antioxidin-RL and cleared free radical faster. By using PC-12 cells as a model, we demonstrated that both antioxidin-2 and antioxidin-RL inhibited the accumulation of intracellular free radicals triggered by H2O2, reduced mitochondria membrane potential dissipation, maintained mitochondrial morphology, and decreased the expression of dynamin-related protein-1 in mitochondria, with antioxidin-RL more effective. Antioxidin-RL also attenuated the changes in SOD1 and GPx1 expression induced by H2O2. These findings provide insight into the anti-oxidative mechanisms of antioxidin-RL and its derivatives, which will provide rational basis for the development of more effective antioxidants to cure diseases.

Salinity is persistently a decisive feature confining agricultural sustainability and food security in arid and semi-arid regions. Biochar (Bi) has been advocated as a means of lessening climate changes by sequestering carbon, concurrently supplying energy and rising crop productivity under normal or stressful conditions. Melatonin (Mt) has been shown to mediate numerous biochemical pathways and play important roles in mitigating multi-stress factors. However, their integrated roles in mitigating salt toxicity remain largely inexpressible. A completely randomized design was conducted to realize the remediation potential of Bi and/or Mt in attenuation salinity injury on borage plants by evaluating its effects on growth, water status, osmotic adjustment, antioxidant capacity, ions, and finally the yield. Salinity stress significantly decreased the plant growth and attributed yield when compared with non-salinized control plants. The depression effect of salinity on borage productivity was associated with the reduction in photosynthetic pigment and ascorbic acid (AsA) concentrations, potassium (K+) percentage, K+-translocation, and potassium/sodium ratio as well as catalase (CAT) activity. Additionally, borage plants' water status was disrupted by salinity through decreasing water content (WC), relative water content (RWC), and water retention capacity (WTC), as well as water potential (Ψw), osmotic potential (Ψs), and turgor potential (Ψp). Moreover, salinity stress evoked oxidative bursts via hyper-accumulation of hydrogen peroxide (H2O2) and malondialdehyde (MDA), as well as protein carbonyl, which is associated with membrane dysfunction. The oxidative burst was connected with the hyper-accumulation of sodium (Na+) and chloride (Cl−) in plant tissues, coupled with osmolytes' accumulation and accelerating plants' osmotic adjustment (OA) capacity. The addition of Bi and/or Mt had a positive effect in mitigating salinity on borage plants by reducing Cl−, Na+, and Na+-translocation, and oxidative biomarkers as well as Ψw, Ψs, and Ψp. Moreover, Bi and/or Mt addition to salt-affected plants increased plant growth and yield by improving plant water status and OA capacity associated with the activation of antioxidant capacity and osmolytes accumulation as well as increased photosynthetic pigments, K+, and K+/Na+ ratio. Considering these observations, Bi and/or Mt can be used as a promising approach for enhancing the productivity of salt-affected borage plants due to their roles in sustaining water relations, rising solutes synthesis, progressing OA, improving redox homeostasis, and antioxidant aptitude. [ABSTRACT FROM AUTHOR]

Sanguisorba minor (S. minor) has neuroprotective and antioxidant activities. However, its potential benefits in ameliorating learning and memory functions have been explored in no studies up to now. So, in the current study, rats were treated with S. minor hydro-ethanolic extract (50, 100, and 200 mg/kg, intraperitoneal (i.p.)) as well as rivastigmine (0.5 mg/kg, i.p.) for 21 consecutive days. Thereafter, their behavioral performance was assessed using Morris water maze (MWM) and passive avoidance (PA) tasks. Notably, 30 min before conducting the tasks, scopolamine was injected. Finally, the biochemical assessments were done using the brain tissue. The extract characterization was performed by liquid chromatography-mass spectrometry, which confirmed the presence of quercetin, myricetin, kaempferol, catechin, ellagic acid, and gallic acid derivatives. In the MWM test, the extract reduced both escape latency and the travelled distance, compared to the scopolamine group. Moreover, in the PA test, the latency to enter the dark chamber significantly increased by the extract, compared to the scopolamine group (p < 0.05-p < 0.001). Notably, the beneficial effects of S. minor on cognitive performance of the scopolamine-treated rats appeared to be similar or even better than rivastigmine in behavior performance. Similar to rivastigmine, it was observed that the extract attenuated both AChE activity and oxidative injury in the brain as evidenced by the increased antioxidant enzymes and total thiol content; however, it decreased malondialdehyde level (p < 0.05-p < 0.001). In conclusion, the results suggested the effectiveness of S. minor in preventing cognitive dysfunction induced by scopolamine. Accordingly, these protective effects might be produced by the regulation of cholinergic activity and oxidative stress. S. minor could be considered as a potential alternative therapy in cognition disorders. [ABSTRACT FROM AUTHOR]

Although the low temperature is a critical growth constraint on plants, the physiological mechanism remains unclear, especially in mangrove plants. Hence, the morphological characteristics of five mangrove plants (Bruguiera gymnorrhiza, Rhizophora stylosa, Aegiceras corniculatum, Avicennia marina, and Kandelia obovata) were compared under chilling stress. The contents of hydrogen peroxide (H2O2), malondialdehyde (MDA), and proline were tested. Activities of reactive oxygen species (ROS)-scavenging enzyme [superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT)] were also measured after chilling stress. It was concluded that K. obovata can well tolerate chilling stress, and B. gymnorrhiza suffered the most severe chilling damage. Leaf-morphology observation exhibited that K. obovata and A. corniculatum can sustain chilling stress, while B. gymnorrhiza wilted and A. marina turned brown. The content of H2O2 increased at first and subsequently decreased in all plants. MDA increased instantaneously in B. gymnorrhiza and R. stylosa but changed slowly in K. obovata and A. corniculatum. The high content of proline accumulated in B. gymnorrhiza and K. obovata. The activities of the SOD, POD, and CAT increased at first and then decreased in all mangrove species. The antioxidants maintained high activity in K. obovata while decreasing earliest in A. marina exposed to the long-term chilling stress. Principal component analysis (PCA) indicated that high antioxidant enzyme activities play key roles in chilling tolerance for mangrove plants. The longer-term chilling tolerance of K. obovata may be related to the high antioxidant enzyme activities and proline accumulation. Lower H2O2 and MDA contents strengthen the anti-chilling ability of A. corniculatum. Further investigation on the molecular mechanisms will facilitate the understanding of the anti-chilling ability of mangrove plants.

Asthma is characterized by airway inflammation, hyper-responsiveness, symptoms of dyspnea, wheezing and coughing. In most patients, asthma is well controlled using inhaled corticosteroids and bronchodilators. A minority of patients with asthma develop severe disease, which is frequently only partially responsive or even resistant to treatment with corticosteroids. Severe refractory asthma is associated with structural changes in the airways, termed "airway remodeling", and/or with neutrophilic rather than eosinophilic airway inflammation. While oxidative stress plays an important role in the pathophysiology of asthma, cyclic nitroxide stable radicals, which are unique and efficient catalytic antioxidants, effectively protect against oxidative injury. We have demonstrated that the nitroxide 3-carbamoyl proxyl (3-CP) attenuates airway inflammation and hyperresponsiveness in allergic asthma as well as bleomycin-induced fibrosis both using murine models, most probably through modulation of oxidative stress. The present study evaluates the effect of 3-CP on airway inflammation and remodeling using two murine models of severe asthma where mice are sensitized and challenged either by ovalbumin (OVA) or by house dust mite (HDM). 3-CP was orally administered during the entire period of the experiment or during the challenge period alone where its effect was compared to that of dexamethasone. The induced increase by OVA and by HDM of BALf cell counts, airway hyperresponsiveness, fibrosis, transforming growth factor-beta (TGF-β) levels in BALf and protein nitration levels of the lung tissue was significantly reduced by 3-CP. The effect of 3-CP, using two different murine models of severe asthma, is associated at least partially with attenuation of oxidative stress and with TGF-β expression in the lungs. The results of this study suggest a potential use of 3-CP as a novel therapeutic agent in different forms of severe asthma. [Display omitted] • Severe asthma is related to airway remodeling and/or neutrophilic airway inflammation. • Nitroxides, such as 3-carbamoyl-proxyl (3-CP), are powerful catalytic antioxidants. • 3-CP was delivered orally to mice using two models of severe asthma. • 3-CP reduces airway inflammation, airway remodeling, AHR, TGF-β and protein nitration levels. • The protective effect of 3-CP is associated at least partially with attenuation of oxidative injury. [ABSTRACT FROM AUTHOR]

Objective: By inhibiting the synthesis of thymidine and purine, and thereby DNA synthesis, Methotrexate (MTX), suppresses the proliferation of cancer cells. It is thought that the side-effect mechanism is related to oxidant molecules derived from MTX metabolism. In this study, we examined whether the Petroselinum crispum extracts (PCr; parsley) of which the antioxidant properties have been previously shown, was protective against MTX induced liver damage. Materials and Methods: Sprague Dawley rats (female/male; 200-250 g) were used. MTX was injected intraperitoneally and PCr extract was given orally. A single dose of 20mg/kg MTX was administered to the groups that were to experience hepatotoxicity. Then, a physiological saline (MTX group) or PCr (2 g/kg, MTX + PCr group) treatment was applied for 5 days. The same treatments were applied to the other groups (control group, PCr group) for 5 days after a single dose saline injection. At the end of the study, the biochemical parameters were examined in the blood and liver tissues taken from animals sacrificed by decapitation. Results: MTX caused a significant increase in malondialdehyde and collagen levels and myeloperoxidase and caspase-3 activities, while glutathione levels were found to have decreased. PCr treatment showed protective efficacy by preventing these increases. Conclusion: It appears that the administration of PCr to MTX treated rats prevented the accumulation of lipid peroxides, inflamatory reactions and depletion of antioxidant glutathione, and thus protected liver tissues against oxidative stress. [ABSTRACT FROM AUTHOR]

Hypothyroidism has been reported to be associated with cognitive decline. Considering the role of folic acid (FA) in cognitive performance, the present study was designed to investigate the effects of FA on hypothyroidism-induced cognitive impairment, oxidative damage, and alterations in acetylcholinesterase (AChE) activity in rat model of propylthiouracil (PTU)-induced hypothyroidism. In this study, PTU (0.05% in drinking water) and FA (5, 10, and 15 mg/kg, oral gavage) were administered for the rats during 7 weeks. Then, behavioral performance was tested using Morris water maze (MWM) and passive avoidance (PA) tasks. Finally, oxidative stress indicators and AChE activity were assayed in the brain tissues. The impairing effect of hypothyroidism on cognitive performance was markedly alleviated by FA especially at higher doses. In the MWM test, FA reduced escape latency and travelled distance, compared to the non-treated hypothyroid group. In the PA test, latency to enter dark chamber was significantly enhanced by FA compared to the non-treated hypothyroid group (p < 0.05–p < 0.001). Besides, FA attenuated AChE activity and malondialdehyde level but it increased activity of superoxide dismutase enzyme and total thiol content (p < 0.05–p < 0.001). In conclusion, our findings revealed that FA could improve learning and memory ability in hypothyroid rats. The observed protective effects may have been mediated through regulation of oxidative stress and AChE activity. [ABSTRACT FROM AUTHOR]

Nuclear factor E2-related factor 2 (Nrf2) activation could efficiently protect myocardial cells from oxygen glucose deprivation/re-oxygenation (OGDR). An ultra-large structure-based virtual screening has discovered iKeap1 as a novel, direct and potent Keap1 inhibitor. Here we found that iKeap1 efficiently activated Nrf2 signaling in H9c2 myocardial cells and primary murine myocardiocytes. iKeap1 induced Keap1-Nrf2 disassociation, cytosol Nrf2 protein stabilization and nuclear translocation. The antioxidant response element (ARE) activity and expression of Nrf2 cascade genes (HO1 , NQO1 and GCLC) were increased in iKeap1-treated myocardial cells. In H9c2 cells and murine myocardiocytes, iKeap1 potently inhibited OGDR-induced oxidative injury by inhibiting reactive oxygen species (ROS) production, mitochondrial depolarization, lipid peroxidation and DNA damage. In addition, OGDR-induced myocardial cell death and apoptosis were largely ameliorated after pretreatment with the novel Keap1 inhibitor. Significantly, in H9c2 cells iKeap1-induced myocardial cytoprotection against OGDR was abolished with Nrf2 silencing or knockout (using CRISPR/Cas9 method). Moreover, CRISPR/Cas9-induced Keap1 knockout led to constitutive activation of Nrf2 cascade and inhibited OGDR-induced oxidative injury. Importantly, iKeap1 was unable to further protect Keap1-knockout H9c2 cells from OGDR. Together, iKeap1 activated Nrf2 signaling to protect myocardial cells from OGDR-induced oxidative injury and cell death. • iKeap1 activates Nrf2 signaling cascade in myocardial cells. • iKeap1 ameliorates OGDR-induced oxidative injury in myocardial cells. • iKeap1 ameliorates OGDR-induced myocardial cell death. • iKeap1-induced myocardial cytoprotection against OGDR requires Nrf2 activation. [ABSTRACT FROM AUTHOR]

Melatonin is a crucial biological hormone associated with many physiological and biochemical processes in plants and also enhances resistance against various abiotic stresses. However, the mechanisms underlying the melatonin-assisted mitigation of salt stress in tomato (Solanum lycopersicum L.) plant are still poorly understood. A hydroponic experiment was conducted to investigate the protective role of melatonin in two tomato cultivars (Roma and FM9) under a highly saline growth medium (160 mM NaCl). The one level of melatonin (1.0 µmol L−1) was applied exogenously, sole, or in combination with the salinity stress. NaCl-induced phytotoxicity significantly (P < 0.05) reduced shoot and root dry matter accumulation, chlorophyll contents, relative water contents (RWC), membrane stability index (MSI), and antioxidant enzymatic activities in both cultivars as compared to the control treatment. Moreover, salt treatment alone increased soluble sugar contents (sucrose and fructose), sodium (Na+) uptake, as well as oxidative damage in the leaves of tomato seedlings. However, exogenous supply of melatonin alleviated salt toxicity in tomato seedlings which were more obvious in Roma cultivar as compared to FM 9 cultivar, as demonstrated by a higher increment in the values of growth indicators, RWC, MSI, gaseous exchange attributes, activities of superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), and ascorbate peroxidase (APX). In addition, melatonin also alleviated salt-induced oxidative stress by suppressing malondialdehyde (MDA) and hydrogen peroxide (H2O2) contents as well as significantly reduced Na+ uptake at the root surface of tomato plants. It can be concluded that melatonin-induced salt tolerance in tomato is due to enhancement of plant water relations, and improved photosynthetic and antioxidant capacity along with ion homeostasis. [ABSTRACT FROM AUTHOR]

Objective To explore the effect of ginsenoside Rb1 (gRb1) on oxidative damage of human umbilical vein endothelial cells (HUVECs) resulted from hydrogen peroxide (H2O2). Methods HUVECs were divided into control group, H2O2 group and gRb1 group. MTT assay was used to determine cell survival; annexin V-FITC/PI double staining was used to detect cell apoptosis; SOD1 activity was measured with xanthine oxidase method; MDA concentration was detected by thibatituric acid assay; protein expression of ICAM-1 and VCAM-1 was analysed by Western blot. Results Compared with control group, the apoptosis rate, MDA production and the protein level of ICAM-1 and VCAM-1 significantly increased, but the cell viability and SOD1 activity decreased. Compared with H2O2 group, gRb1 reversed the parameters mentioned above. Conclusions gRb1 can alleviate oxidative damage of HUVECs by reducing cell apoptosis, oxidative stress and protein expression of ICAM-1 and VCAM-1.

Seyfi Kartal,1 Gülay Kip,2 Ayşegül Küçük,3 Seyhan Sümeyra Aşçı,1 Özlem Erdem,4 Mustafa Arslan,2 Mustafa Kavutçu5 1Health Science University, Kanuni Training and Research Hospital, Department of Anaesthesiology and Reanimation, Trabzon, Turkey; 2Gazi University, School of Medicine, Department of Anaesthesiology and Reanimation, Ankara, Turkey; 3Kütahya Health Science University, School of Medicine, Department of Physiology, Kütahya, Turkey; 4Gazi University, School of Medicine, Department of Medical Pathology, Ankara, Turkey; 5Gazi University, School of Medicine, Department of Medical Biochemistry, Ankara, TurkeyCorrespondence: Mustafa ArslanGazi University, School of Medicine, Department of Anaesthesiology and Reanimation, Ankara 06510, TurkeyTel +90 312 202 53 13Fax +90 312 202 4166Email mustarslan@gmail.comBackground: The objective of this research was to evaluate the oxidative and histopathological effects of dexmedetomidine and ketamine on the pulmonary contusion model resulting from blunt chest trauma.Methods: Rats were randomly assigned to 5 equal groups (n=6): control group (Group C), pulmonary contusion group (Group PC), PC-dexmedetomidine group (Group PC-D), PC-ketamine group (Group PC-K), and PC-dexmedetomidine + ketamine (Group PC-D+K). The PC was performed by dropping a weight of 500 g (2.45 Joules) from a height of 50 cm. In Group PC-D, after chest trauma, dexmedetomidine (100 μg/kg) was administered intraperitoneally. In Group PC-K, after chest trauma, ketamine (100 mg/kg) was administered intraperitoneally. In Group PC-D+K, dexmedetomidine and ketamine were administered together. At the end of the 6th hour, rats were sacrificed. Malondialdehyde (MDA) level, superoxide dismutase (SOD) enzyme activities, neutrophil infiltration/aggregation, and thickness of the alveolar wall were evaluated.Results: MDA levels were significantly higher in Group PC than Groups C, PC-D, and PC-D+K. SOD enzyme activity was significantly higher in Group PC than Groups C, PC-D, and PC-D+K. In addition, neutrophil infiltration/aggregation and total pulmonary injury scores were significantly higher in Group PC than in other groups, and the thickness of the alveolar wall was significantly higher in Group PC compared to Groups C, PC-D, and PC-D+K. MDA level, SOD enzyme activities, neutrophil infiltration/aggregation, and thickness of alveolar wall were similar in PC-D and PC-D+K groups.Conclusion: Dexmedetomidine and dexmedetomidine+ketamine have protective effects on blunt chest trauma but no protective effect was observed when ketamine was administered alone. We concluded that the administration of dexmedetomidine and ketamine after contusion is beneficial against pulmonary injury in rats.Keywords: dexmedetomidine, ketamine, pulmonary contusion, oxidative injury, neutrophil infiltration/aggregation

Objective To investigate the effect of melatonin on oxidative injury of rat carotid arteries after balloon injury. Methods Twenty male sprague-dawley rats were randomized into control, melatonin, smoking, and smoking plus melatonin. An established protocol of smoking was carried out. The carotid arteries were collected 7 days later. The average content of ROS was measured. And Western blot was used to detected the expression of NF-κB, MCP-1, VCAM-1 and ICAM-1. Results Smoking significantly induced the increase of ROS and the expression of NF-κB, MCP-1, VCAM-1 and ICAM-1 in rat carotid arteries. Moreover, cigarette smoke exposure inhibited the expression of eNOS. Melatonin minimized the effect resulted from smoking. Conclusions Melatonin may attenuate the the oxidative injury and the expression of inflammatory mediators in rat carotid arteries resulted from smoking.

Abstract Background In herpes simplex epithelial keratitis, excessive TLR3-induced cellular responses after virus infection evoke inflammatory cascades that might be destructive to the host cornea. Nerve growth factor (NGF), a pluripotent neurotrophic factor with immune regulatory effect, was proved to be effective in Herpes simplex keratitis (HSK) treatment, although the detailed mechanisms remain unclear. This study aims to investigate the effects of NGF on modulating inflammatory responses triggered by TLR3 activation in human corneal epithelial cells (HCECs) in vitro. Methods HCECs were stimulated with TLR3 agonist, poly(I:C), in the absence or presence of NGF. Cell viability and cytotoxicity were measured by a CCK-8 assay and LDH release assay, respectively. The activation of NF-κB signaling pathway was examined using immunofluorescence staining and western blotting. Levels of proinflammatory cytokines were determined by ELISA or RT-qPCR. ROS generation and 8-OHdG positive cells were examined by a fluorometric analysis. Results It was shown that NGF significantly inhibited the generation of proinflammatory cytokines in HCECs triggered by TLR3 activation (P

Objectives: The adverse deleterious influences of Ipomoea carnea on brain tissue and Taurine's relative ability to prevent this neurotoxicity have been examined. Methods: We utilized sixty Wistar male rats weighing 1752 g. The rats were allotted into 4 groups of fifteen each: The control group got saline i.p. daily for eight weeks; the Ipomoea carnea extract (ICE) group received ICE (15 mg/kg b.w./day) orally for eight weeks. Taurine-treated rats, in which rats were administered Taurine (200 mg·kg−1, i.p./Day) for 2 months. Taurine + ICE group in which rats were supplemented with (200 mg·kg−1, i.p. Taurine + ICE 15 mg/kg b.w./day orally) for 2 months. Result: The findings indicated that Ipomoea persuaded an increase in lipid peroxidation markers as well as a disruption in antioxidant homeostasis, along with brain and serum cholinesterase (AChE) elevated levels, tumor necrosis factor (TNF), total creatine phosphokinase (CPK), creatine phosphokinase isoenzymes BB (CPK-BB), and lactate dehydrogenase (LDH). A considerable drop (P

More research is required to understand how melatonin protects neurons. The study aimed to find out if and how long non-coding RNA (lncRNA) contributes to melatonin’s ability to defend the hippocampus from H2O2-induced oxidative injury. LncRNAs related to oxidative injury were predicted by bioinformatics methods. Mouse hippocampus-derived neuronal HT22 cells were treated with H2O2 with or without melatonin. Viability and apoptosis were detected by Cell Counting Kit-8 and Hoechst33258. RNA and protein levels were measured by quantitative real-time PCR, Western blot, and immunofluorescence. Bioinformatics predicted that 38 lncRNAs were associated with oxidative injury in mouse neurons. LncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) was related to H2O2-induced oxidative injury and up-regulated by melatonin in HT22 cells. The knockdown of NEAT1 exacerbated H2O2-induced oxidative injury, weakened the moderating effect of melatonin, and abolished the increasing effect of melatonin on the mRNA and protein level of Slc38a2. Taken together, melatonin attenuates H2O2-induced oxidative injury by upregulating lncRNA NEAT1, which is essential for melatonin stabilizing the mRNA and protein level of Slc38a2 for the survival of HT22 cells. The research may assist in the treatment of oxidative injury-induced hippocampal degeneration associated with aging using melatonin and its target lncRNA NEAT1.

Iron (Fe) starvation in Strategy II plants is a major nutritional problem causing severe visual symptoms and yield reductions. This prompted us to investigate the physiological and molecular consequences of Fe deficiency responses at an early stage in sorghum plants. The Fe-starved sorghum did not show shoot biomass reduction, but the root length, biomass, and chlorophyll synthesis were severely affected. The chlorophyll a fluorescence analysis showed that the quantum yield efficiency of PSII (Fv/Fm) and photosynthesis performance index (Pi_ABS) in young leaves significantly reduced in response to low Fe. Besides, Fe concentration in root and shoot significantly declined in Fe-starved plants relative to Fe-sufficient plants. Accordingly, this Fe reduction in tissues was accompanied by a marked decrease in PS-release in roots. The qPCR experiment showed the downregulation of SbDMAS2 (deoxymugineic acid synthase 2), SbNAS3 (nicotianamine synthase 3), and SbYSL1 (Fe-phytosiderophore transporter yellow stripe 1) in Fe-deprived roots, suggesting that decreased rhizosphere mobilization of Fe(III)-PS contributes to reduced uptake and long-distance transport of Fe. The cis -acting elements of these gene promoters are commonly responsive to abscisic acid and methyl jasmonate, while SbYSL1 additionally responsive to salicylic acid. Further, antioxidant defense either through metabolites or antioxidant enzymes is not efficient in counteracting oxidative damage in Fe-deprived sorghum. These findings may be beneficial for the improvement of sorghum genotypes sensitive to Fe-deficiency through breeding or transgenic approaches. [ABSTRACT FROM AUTHOR]

The biological activity of neohesperidin (NH, a flavanone glycoside) is limited due to instability in the physiological environment. Thus, the current study aimed to explore the protective effect of NH-loaded pectin-chitosan decorated liposomes (P-CH-NH-NL) against palmitic acid (PA)-induced hepatic oxidative injury in L02 cells. The particles were characterized using DLS, TEM, HPLC, DSC, and cellular uptake study. Then, the protective effect of NH-loaded liposomal systems (NH-NLs) against PA-induced oxidative injury was evaluated in terms of cell viability study, intracellular ROS, superoxide ions (O 2 −), MMP, and cellular GSH determination. Our results exhibited that NH-NLs significantly lessened the PA-induced hepatic oxidative injury in L02 cells via decreasing ROS and O 2 − generation, reducing MMP collapse, and attenuating GSH reduction, whereas the free NH samples were ineffective. Furthermore, the coated NH-NLs were more effective than that of uncoated nanoliposome. Overall, our study confirmed that P-CH-NH-NL was capable of reducing PA-induced hepatic oxidative injury. Therefore, the pectin-chitosan decorated nanoliposome can be considered as an efficient delivery system for enhancing cellular uptake of lipophilic compound with controlled release and greater biological activity. • Neohesperidin (NH) is a flavanone glycoside rich in citrus fruits. • Free NH exerted the limited biological activity. • NH was encapsulated in pectin-chitosan decorated nanoliposome. • NH-loaded decorated nanoliposome (P-CH-NH-NL) showed higher L02 cells uptake. • P-CH-NH-NL ameliorated the palmitic acid-induced hepatic oxidative injury. [ABSTRACT FROM AUTHOR]

Oxidative injury or cellular damage arising from free radicals or reactive oxygen species (ROS) has been implicated in the pathogenesis of many human diseases. These ROS are generated through normal metabolism of drugs, environmental chemicals and other xenobiotics as well as endogenous chemicals. Accumulated evidence suggests that ROS can be scavenged through chemoprevention utilizing natural antioxidant compounds present in foods and medicinal plants. The aim of this study is to evaluate antioxidant activities of aqueous extract of Bryophyllum pinnatum using carbon tetrachloride-induced albino rats as model. An in-vivo antioxidant activity was carried out on the CCl4 induced rats by administration of aqueous extract of Bryophyllum pinnatum at doses of 50, 100 and 200mg/Kg bw for 14 consecutive days, and one group was treated with Silymarin at a dose of 50 mg/Kg as a standard drug. The antioxidant activities were estimated by evaluating its effects on antioxidant parameters in the tissues of albino rats (Serum, Liver and Heart). The activity of catalase (CAT), Superoxide dismutase (SOD), Glutathione peroxidase (GPx) and the levels of MDA and GSH were evaluated in tissue homogenates. Results showed that the rats fed with the higher concentrations of Bryophyllum pinnatum had significant increase (p<0.05) in glutathione content (GSH), GPx, SOD and catalase activities relative to normal and standard control. However, the level of MDA was decreased (p<0.05) for the treated groups (100 and 200mg/kg). These results suggest that aqueous extracts of Bryophyllum pinnatum has active substances contributing to varied degrees of potent antioxidant activity and could serve as important source of antioxidants in food, cosmetics and pharmaceutical industries. [ABSTRACT FROM AUTHOR]

This study investigated the druggability, pharmacokinetics and ethyl acetate extract of Teucrium polium (EA T. polium), from Ha'il, and the protective effect against carbon tetrachloride (CCl4) induced liver cirrhosis in rats. The total antioxidant capacity (TAC) and scavenging activity of the extract were examined. The in vivo protective study was based on the use of an animal model of CCl4-induced liver cirrhosis. Four groups of rats have been used: Group I: control rats; Group II: received CCl4 in olive oil (0.5 mL/kg); Group III: received the EA T. polium (25 mg/kg) of pretreatment for seven days by gavage then CCl4 in olive oil by gavage for 15 days. Group IV: received the EA of T. polium for seven days (25 mg/kg). EA T. polium was found to possess significant antioxidant capacity. CCl4 caused a hepatotoxicity associated increase in both levels of AST and ALT, which were reduced back to normal values following EA T. polium pretreatment. Hepatotoxicity associated structural modifications of liver tissues and increase in thiobarbituric acid reactive substances (TBARS), conjugated dienes (CD) and carbonyl proteins (CP), associated decreases in several assessed antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT). The in vivo findings on the protective effect of T. polium were supported by its druggability, its pharmacokinetic properties and molecular docking assays. These results confirm the modulatory antioxidant and hepatoprotective potential of T. polium in this experimental liver cirrhosis model. T. polium phytochemicals are good candidates for further pharmaceutical explorations and drug design.

Research on the beneficial effects of Maillard reaction products (MRPs) and phenolic compounds derived from roasted peanut flour on the nervous system remains insufficient. This study aimed to evaluate the effect of a 28-day oral administration of defatted peanut extract rich in MPRs and polyphenolic compounds on the cognitive impairments and oxidative injury induced by scopolamine in a mouse model. Light and dark extracts from peanut flour were prepared by heating peanuts at 187°C for two different times (8.6 and 12.7 min) and defatted using soxhlet apparatus. The mice were orally pretreated with either roasted defatted peanuts extracts (100 mg/kg) or donepezil (3 mg/kg) for 21 days. On day 19 and until day 28, mice were injected subcutaneously with water or scopolamine (1 mg/kg body weight) 15 min after roasted defatted peanuts extracts/water feeding. Mice were subsequently subjected to a battery of behavioral tests including open field locomotor activity assay, and Morris water maze test. Brain tissues were collected to measure acetylcholine, acetylcholinesterase, and oxidative parameters (glutathione and malondialdehyde). Roasted defatted peanuts (light and dark) (100 mg/kg) treatment significantly ameliorated cognitive performance and reversed the oxidative damage when compared with the scopolamine group. These data demonstrate the defatted peanuts extracts exert potent anti-amnesic effects via the modulation of cholinergic and antioxidant activities. [ABSTRACT FROM AUTHOR]

The high incidence of vascular calcification (VC) in patients with chronic kidney disease (CKD) has become an important clinical subject. Hyperphosphatemia is a primary cause of CKD-related VC. Intravenous iron sucrose (IS) is commonly used to treat anemia in CKD patients, and is effective and well tolerated worldwide. However, the interaction between iron and VC remains controversial, and the underlying mechanisms are yet to be clarified. In the present study, ex vivo normal rat aortic rings were cultured with various concentrations of phosphate and IS, and the levels of calcium and iron depositions, oxidative injury, as well as phenotypic marker genes were detected. To the best of our knowledge, the present study is the first to report that IS is a double-edged sword in high phosphate media-induced VC which not only alleviates VC in a dose-dependent manner but also leads to iron overload in vasculature when in high concentration. IS is a promising agent for VC prevention in patients with hyperphosphatemia and iron deficiency. Meanwhile, the appropriate blood concentration of IS in patients with hyperphosphatemia needs to be explored clinically. [ABSTRACT FROM AUTHOR]

The therapeutic potentials of Cannabis sativa L. on oxidative-induced testicular dysfunction were investigated in isolated testes of male albino rats. C. sativa leaves were subjected to sequential extraction to yield the hexane, dichloromethane (DCM), and ethanol extracts. Oxidative injury was induced by incubating testicular tissue homogenate with 0.1 mM FeSO4 for 30 min at 37 °C. Treatment was done by incubating the tissues with C. sativa extracts and 0.1 mM FeSO4 under same conditions. Induction of oxidative injury led to significant (p < 0.05) depleted levels of glutathione, superoxide dismutase, catalase, and ecto-nucleoside triphosphate diphosphohydrolase (E-NTPDase) activities, while elevating malondialdehyde and nitric oxide levels, acetylcholinesterase, ATPase, glucose 6-phosphatase, fructose 1,6-biphosphatase, and amylase activities. These levels and activities were significantly (p < 0.05) reversed following treatment with the extracts. The extracts also displayed cytotoxic effect against human DU-145 prostate cancer cells. These results indicate the protective potentials of C. sativa extracts against oxidative-mediated testicular injury as shown by their ability to attenuate testicular oxidative stress, and modulate cholinergic and purinergic activities, while suppressing testicular carbohydrate dysmetabolism. [ABSTRACT FROM AUTHOR]

Severe complications have been observed and established for Plasmodium falciparum as well as P. vivax infections worldwide. Although P. vivax infection is not fully acknowledged as malignant malaria, recently life-threatening complications have been reported to occur in many studies. The recognition of biomarkers with excellent sensitivity and reliability plays a prime role in disease management. Acute inflammatory response and oxidative stress are observed in malaria due to the production of reactive oxygen species. Lipid and protein oxidative injuries are prospective biomarkers for disease severity owing to the damage caused by the parasite. We have tried to find out whether protein carbonylation (PC), lipid peroxidation (LPO) and superoxide dismutase (SOD) could suffice as a biomarker for severe vivax malaria or not. Blood samples were collected from the individuals attending Jawaharlal Nehru Medical College of Aligarh Muslim University during the wet season of malaria transmission. Microscopy and rapid diagnostic kits were used as a tool for malaria diagnosis. A total of 214 subjects were enrolled for the study: 30 febrile controls and 184 subjects with vivax malaria. Protein carbonylation and lipid peroxidation were found to be directly associated with parasite count and total antioxidant status (TAS). Increase in oxidative stress was also observed in severe vivax malaria patients. Levels of uric acid and bilirubin too were raised in complicated cases. Protein carbonylation was found to be a more reliable indicator of vivax malaria severity than lipid peroxidation. [ABSTRACT FROM AUTHOR]

To investigate the impact of the ethanoic fractions of Periploca forrestii Schltr. (P. forrestii) in ameliorating the liver injury caused by fluoride ingestion and to explore the potential mechanisms. Initially, an in vitro fluorosis cell model was constructed using the human normal liver cell line (L-02) induced by fluoride. Cell viability was assessed using the CCK-8 assay kit. The lactate dehydrogenase (LDH) assay kit was utilized to measure LDH content in the cell supernatant, while the malonic dialdehyde (MDA) assay kit was employed to determine MDA levels within the cells. Subsequently, a fluorosis rat model was established, and LDH content in the cell supernatant was measured using the LDH assay kit. Various parameters, including MDA, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and reactive oxygen species (ROS) content within the cells, were detected using appropriate assay kits. Additionally, cell apoptosis rate was determined using the Annexin V-FITC/PI cell apoptosis assay kit. The protein expression levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), Caspase-3, Cleaved Caspase-3, Caspase-9, and Cleaved Caspase-9 were analyzed through Western blotting. Compared to the model group, the ethanolic fraction D of P.forrestii (Fr.D) increased cell viability (P < 0.01) and decreased LDH and MDA levels (P < 0.01). In the high-dose Fr.D treatment group of fluoride-poisoned rats, serum ALT, AST, LDH and MDA levels significantly decreased (P < 0.01). Results from rat primary cells exhibited that the Fr.D administration group exhibited significantly higher cell survival rates than the fluoride group (P < 0.01). Similarly, primary rat cells treated with Fr.D showed enhanced cell viability (P < 0.05) and reduced apoptosis rate, LDH, MDA, SOD, GSH-Px, CAT, and ROS levels (P < 0.05) compared to the model group. Western blot analysis indicated that the Fr.D treatment group elevated the Bcl-2/Bax protein expression ratio and reduced Caspase-3 and Caspase-9 activation levels (P < 0.01) compared to the model group. The results suggest that components within the Fr.D from Periploca forrestii may alleviate fluoride-induced liver injury by potentially counteracting oxidative stress and cell apoptosis. [Display omitted] • Ethanoic Fr.D from P. forrestii alleviates fluoride-induced liver injury in rats. • Fr.D affects fluorosis-induced liver changes and serum markers. • Fr.D counteracts oxidative stress and apoptosis, offering therapeutic potential. • Fr.D alleviates fluorosis liver injury by modulating oxidative stress and apoptosis. [ABSTRACT FROM AUTHOR]

Exposure to organophosphorus during different phases of pregnancy induces many adverse impacts on the developing foetuses due to their immature detoxification system. We have estimated the potential amelioration role of quercetin against hepatic injury-induced apoptosis in rat foetuses following gestational exposure to fenitrothion and probable involvement of paraoxonase-1. Forty pregnant rats were allocated into four groups; the first one kept as control, the second intubated with quercetin (100 mg/kg), the third orally administrated fenitrothion (4.62 mg/kg) and the last group received quercetin two hours before fenitrothion intoxication. Fenitrothion significantly elevated the foetal hepatic levels of thiobarbituric acid reactive substances, protein carbonyl, and nitric oxide, but it reduced the enzymatic activities of glutathione-S-transferase, superoxide dismutase, catalase, and acetylcholinesterase. Furthermore, fenitrothion provoked many histopathological changes in the foetal liver and markedly up-regulated the mRNA gene expression of p53, caspase-9 along with elevation in the immunoreactivity of Bax and caspase-3, but it down-regulated the expression level of paraoxonase-1. Remarkably, quercetin co-treatment successfully ameliorated the hepatic oxidative injury and apoptosis prompted by fenitrothion. Dietary supplements with quercetin can be used to reduce the risk from organophosphorus exposure probably through paraoxonase-1 up-regulation and enhancement of the cellular antioxidant system. [ABSTRACT FROM AUTHOR]

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BACKGROUND: Exhaustive exercise is a vigorous physical activity performed by an organism beyond its physiological limits, and it causes a series of histological changes in the body. Myocardial exercise-induced oxidative stress injury means that the organism generates free radicals through oxidative stress signal pathway to damage myocardial cells under exhaustive exercise. OBJECTIVE: To explore the mechanism of oxidative stress injury in rat myocardium caused by one-time exhaustive exercise based on the protein kinase C (PKC)/ NOX pathway. METHODS: Thirty adult male Sprague-Dawley rats were randomly divided into a control group, an exhaustive exercise group, and an exhaustive exercise+drug group, with 10 rats in each group. The exhaustive exercise+drug group was injected with PKC inhibitor chelerythrine (5 mg/kg body weight) for 3 consecutive days. Rats in the two exercise groups exercised at a speed of 25 m/min on a 0° incline treadmill until exhaustion. Immediately after exercise, blood sample was collected from each rat, and then the rat’s left ventricle was removed for hematoxylin-eosin staining to observe the morphological changes of myocardial cells. Serum and myocardial malondialdehyde and myocardial reactive oxygen species levels were detected. The protein expressions of PKC, NOX2, NOX4 and 3-NT in rat myocardial tissue were determined by western blot. RESULTS AND CONCLUSION: The myocardial tissues in the exhaustive exercise and exhaustive exercise+drug groups were damaged, but the damage was significantly eased in the exhaustive exercise+drug group compared with the exhaustive exercise group. Compared with the control group, the reactive oxygen species level in the myocardial tissue of the exhaustive exercise group increased significantly (P < 0.05). Compared with the control group, the content of malondialdehyde in the myocardial tissues of the exhaustive exercise and exhaustive exercise+drug groups was significantly increased (P < 0.01), and the concentration of serum malondialdehyde in the exhaustive exercise group was significantly increased (P < 0.05). Compared with the control group, the expression levels of PKC, NOX2, NOX4 and 3-NT proteins in the myocardium of rats after exhaustive exercise were significantly increased (P < 0.01). Compared with the exhaustive exercise group, the expression levels of NOX2 and NOX4 in the myocardial tissue of rats significantly decreased in the exhaustive exercise+drug group (P < 0.01), and the expression of 3-NT significantly decreased (P < 0.05). Therefore, one-time exhaustive exercise can activate PKC and increase its protein expression in rat myocardial cells, which in turn induces an increase in the expression of NOX2 and NOX4 proteins in the myocardium, catalyzes the generation of large amounts of reactive oxygen species, and leads to the excessive production of peroxynitrite anions, thereby causing oxidative damage to the myocardium. [ABSTRACT FROM AUTHOR]

Silicon (Si), a major contributing constituent for plant resistance against abiotic stresses. In spite of this, the detailed mechanisms underlying the potential of Si in mitigating salt toxicity in maize (Zea mays L.) are still poorly understood. The present study deals with the response of Si application on growth, gaseous exchange, ion homeostasis and antioxidant enzyme activities in two maize cultivars (P1574 and Hycorn 11) grown under saline conditions. Salt stress remarkably reduced the plant tissue (roots and shoots) biomass, relative water contents (RWC), membrane stability index (MSI), gaseous exchange characteristics, and antioxidant enzymatic activities i.e., superoxide dismutase (SOD), peroxidase (POD), ascorbate peroxidase (APX) and catalase (CAT). However, salt-induced phytotoxicity increased the plant tissue concentration of malondialdehyde (MDA), hydrogen peroxide (H 2 O 2), Na+/K+ ionic ratio, Na+ translocation (root to shoot), and its uptake. The detrimental effects were more prominent in Hycorn 11 cultivar than the P1574 cultivar at higher salinity level (S2; 160 mM NaCl). The addition of Si alleviated salt toxicity, which was more obvious in P1574 relative to Hycorn 11 as demonstrated by an increasing trend in RWC, MSI, and activities of SOD, POD, APX and CAT. Besides, Si-induced mitigation of salt stress was due to the depreciation in Na+/K+ ratio, Na+ ion uptake at the surface of maize roots, translocation in plant tissues and thereby significantly reduced Na+ ion accumulation. The findings showed a new dimension regarding the beneficial role of Si in maize plants grown under salt toxicity. • Salt stress reduced maize growth, increased oxidative stress and sodium uptake by plants. • Silicon (Si) supply increased plant biomass through alleviating salt-induced phytotoxicity. • Silicon decreased Na+/K+ ratio in plants under salt stress • Silicon reduced sodium uptake, translocation and bioaccumulation by plants. [ABSTRACT FROM AUTHOR]

Traumatic spinal cord injury is a devastating insult followed by progressive cord atrophy and neurodegeneration. Dysregulated or non-resolving inflammatory processes can disturb neuronal homeostasis and drive neurodegeneration. Here, we provide an in-depth characterization of innate and adaptive inflammatory responses as well as oxidative tissue injury in human traumatic spinal cord injury lesions compared to non-traumatic control cords. In the lesion core, microglia were rapidly lost while intermediate (co-expressing pro- as well as anti-inflammatory molecules) blood-borne macrophages dominated. In contrast, in the surrounding rim, TMEM119+ microglia numbers were maintained through local proliferation and demonstrated a predominantly pro-inflammatory phenotype. Lymphocyte numbers were low and mainly consisted of CD8+ T cells. Only in a subpopulation of patients, CD138+/IgG+ plasma cells were detected, which could serve as candidate cellular sources for a developing humoral immunity. Oxidative neuronal cell body and axonal injury was visualized by intracellular accumulation of amyloid precursor protein (APP) and oxidized phospholipids (e06) and occurred early within the lesion core and declined over time. In contrast, within the surrounding rim, pronounced APP+/e06+ axon-dendritic injury of neurons was detected, which remained significantly elevated up to months/years, thus providing mechanistic evidence for ongoing neuronal damage long after initial trauma. Dynamic and sustained neurotoxicity after human spinal cord injury might be a substantial contributor to (i) an impaired response to rehabilitation; (ii) overall failure of recovery; or (iii) late loss of recovered function (neuro-worsening/degeneration). [ABSTRACT FROM AUTHOR]

Diabetic nephropathy (DN), as the most common microvascular complication of diabetes mellitus (DM), has become one of the leading causes of end-stage renal disease (ESRD). Numerous studies have indicated that podocyte loss plays an important role in the development of DN and can even cause proteinuria in the early stage of DN. In the study, we found that Huidouba (HDB) significantly decreased the level of fasting blood glucose (FBG), the ratio of microalbumin to urine creatine (mAlb/Ucr), serum creatine (Scr), serum urea nitrogen (BUN), and malondialdehyde (MDA) in the kidney and downregulated the expression of Nox4 predominantly located in glomerular tissue while upregulating nephrin and WT1 expression in DN rats. In addition, HDB could also reduce podocyte damage and glomerular basement membrane (GBM) pathologic changes, as shown by transmission electron microscopy (TEM). In vitro study showed that HDB could inhibit high glucose (HG)-induced Reactive Oxygen Species (ROS) production and protect against podocyte apoptosis by downregulated Nox4 expression in podocytes. These results may provide a scientific basis for developing HDB as a potential folk medicine for the treatment of DN.

Salinity is persistently a decisive feature confining agricultural sustainability and food security in arid and semi-arid regions. Biochar (Bi) has been advocated as a means of lessening climate changes by sequestering carbon, concurrently supplying energy and rising crop productivity under normal or stressful conditions. Melatonin (Mt) has been shown to mediate numerous biochemical pathways and play important roles in mitigating multi-stress factors. However, their integrated roles in mitigating salt toxicity remain largely inexpressible. A completely randomized design was conducted to realize the remediation potential of Bi and/or Mt in attenuation salinity injury on borage plants by evaluating its effects on growth, water status, osmotic adjustment, antioxidant capacity, ions, and finally the yield. Salinity stress significantly decreased the plant growth and attributed yield when compared with non-salinized control plants. The depression effect of salinity on borage productivity was associated with the reduction in photosynthetic pigment and ascorbic acid (AsA) concentrations, potassium (K+) percentage, K+-translocation, and potassium/sodium ratio as well as catalase (CAT) activity. Additionally, borage plants’ water status was disrupted by salinity through decreasing water content (WC), relative water content (RWC), and water retention capacity (WTC), as well as water potential (Ψw), osmotic potential (Ψs), and turgor potential (Ψp). Moreover, salinity stress evoked oxidative bursts via hyper-accumulation of hydrogen peroxide (H2O2) and malondialdehyde (MDA), as well as protein carbonyl, which is associated with membrane dysfunction. The oxidative burst was connected with the hyper-accumulation of sodium (Na+) and chloride (Cl−) in plant tissues, coupled with osmolytes’ accumulation and accelerating plants’ osmotic adjustment (OA) capacity. The addition of Bi and/or Mt had a positive effect in mitigating salinity on borage plants by reducing Cl−, Na+, and Na+-translocation, and oxidative biomarkers as well as Ψw, Ψs, and Ψp. Moreover, Bi and/or Mt addition to salt-affected plants increased plant growth and yield by improving plant water status and OA capacity associated with the activation of antioxidant capacity and osmolytes accumulation as well as increased photosynthetic pigments, K+, and K+/Na+ ratio. Considering these observations, Bi and/or Mt can be used as a promising approach for enhancing the productivity of salt-affected borage plants due to their roles in sustaining water relations, rising solutes synthesis, progressing OA, improving redox homeostasis, and antioxidant aptitude.

Phytoremediation with hyperaccumulator plants has been recognized as a potential way for the clearing of cadmium (Cd)-contaminated soil. In this study, hyperaccumulator Tagetes patula was treated with seven concentrations of Cd, ranging from 0 to 300 mg kg−1. The Cd enrichment and nutrient contents in different organs during different growth phases were investigated. Under Cd concentrations ≤75 mg kg-1, the morphological growth of T. patula did not change significantly regardless of growth stage. However, when Cd concentration exceeded 150 mg kg−1, the morphological growth was remarkedly inhibited. The root/shoot ratio remained unchanged except for at 300 mg kg−1. In addition, Cd negatively influenced the flowering process at the concentration of 300 mg kg−1. Cd content increased significantly in Cd-treated plants. Nitrogen absorption was increased under Cd treatments, and phosphorus content was also increased under concentration ≤150 mg·kg−1. However, the potassium content in the flower was decreased under 300 mg kg−1. Furthermore, the contents of H2O2, O2− and malondialdehyde were increased during the seedling phase, especially when Cd concentration was ≥150 mg kg−1. In summary, T. patula showed a strong ability to tolerate Cd, and such ability might be explained by nutrient absorption and reactive oxygen clearness.

Antioxidant peptides were purified from Hydrilla verticillata (Linn. f.) Royle ( HVR ) protein hydrolysate by ultrafiltration, gel filtration chromatography, and semipreparative reversed-phase HPLC and identified by UPLC-ESI-MS/MS. Therein, TCLGPK and TCLGER were selected to be synthesized, and they displayed desirable radical-scavenging activity to ABTS (99.20 ± 0.56-99.20 ± 0.43%), DPPH (97.32 ± 0.59-97.56 ± 0.97%), hydroxyl radical (54.32 ± 1.27-70.42 ± 2.01%), and superoxide anion (42.93 ± 1.46-52.62 ± 1.11%) at a concentration of 0.96 μmol/mL. They possessed a cytoprotective effect against H 2 O 2 -induced oxidative stress in HepG2 cells in a dose-dependent manner. 1.6 μmol/mL of the two peptides could perfectly protect HepG2 cells from H 2 O 2 -induced injury. The TCLGPK exhibited higher antioxidant activity and cytoprotective effect than TCLGER. Western blot and molecular docking results indicated that the two peptides achieved antioxidant ability and cytoprotective effect by combining with Kelch-like ECH-associated protein 1 (Keap1) to activate the Keap1-nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response elements signaling pathway, leading to the activity and expression of the related antioxidases in the pathway significantly up-regulating and the intracellular reactive oxygen species level, lipid peroxidation, and cell apoptosis rate significantly down-regulating.