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Liver fibrosis is the progressive accumulation of connective tissue in the liver, which can be caused by chronic liver injury of various etiologies. Moringa oleifera is a pan-tropical species is used in nurturing both animal and human as an excellent nutritive supplement. Colchicine is a plant that effective against gouty arthritis and other forms of rheumatic diseases (rheumatoid arthritis, familial Mediterranean fever, Bechet´s disease, etc. This study thrown light on the hepatoprotecitve effects of Moringa oleifera ethanolic leaves extract and colchicine on thioacetamide-induced liver fibrosis in rats. Liver function tests (serum ALT, AST, ALP, and Total protein) in addition to histopathological examination of the liver were performed. This study was carried out on a total number of 42 male albino rats were collocated into seven groups (6 rats per group). The experiment lasted for two months, through which all groups except for control and control positive were given Moringa oleifera ethanolic leaves extract and colchicine. Liver fibrosis was induced by intraperitoneal injection of thioacetamide (150 mg/kg) in groups II, V, VI &VII while other groups were injected with 0.9% normal saline of the same volume. Bodyweight was measured three times a week to detect the dose for each rat. The administration of thioacetamide leading a significant increase in serum liver enzyme level ALT, AST, ALP, and Total protein as compared to the control group, while treatment with colchicine and Moringa oleifera ethanolic leaves extract causing significant decreased serum liver enzyme level by (P

The present study was carried out to investigate the effects of dietary bovine lactoferrin (BLF) or chitosan nanoparticles (CHN) alone or in combinations on serum biochemical indices, antioxidative capacity, transcriptomic responses, non-specific immunity, and resistance of Nile tilapia (Oreochromis niloticus) against challenge with Aeromonas hydrophila. Fish were fed on the basal diet with no supplements and served as control (CTR), and six other experimental diets containing different levels of BLF (800 and 1200 mg per kg diet), CHN (500 and 1000 mg per kg diet), and their combinations (400 mg BLF plus 250 mg CHN per kg diet, and 600 mg BLF plus 500 mg CHN per kg diet) for 45 days. At the end of the experiment, serum, and tissue specimens (liver and kidney) were collected, fish in all groups were challenged with A. hydrophila and then observed for another ten days to calculate the RPS. Compared to the CTR group, no significant differences were recorded in TP, ALB, GLO, BUN, and CREAT values among all treatments. Serum LYZ, ALT, AST, and ALP enzyme activities were significantly increased in all experimental groups over the CTR (P 0.05), and their highest values were recorded in the combined treatments. Moreover, dietary supplementation with CHN (1000 mg/kg) and combined treatments significantly increased the SOD, CAT, and GSH-Px enzyme activities compared to other groups (P 0.05). The highest mRNA expression levels of IGF-1 gene in liver, and IL-1β, and IFN-γ genes in kidneys were found in CHN (1000 mg/kg) group and combined treatments more than other groups. Interestingly, no, or mild histopathological alterations were noticed in the hepatopancreas and posterior kidney of the treated groups. A significantly higher RPS was identified in the combined treatments challenged with A. hydrophila compared with the CTR group. This study exemplifies the positive impacts of dietary supplementation with BLF or CHN alone or combinations on the antioxidative status, immunity, and disease resistance of Nile tilapia.

Background The adverse effect of aflatoxin in broilers well known. However, dietary supplementation of nanocurcumin and/or Saccharomyces cell wall may decrease the bad effect of aflatoxin B1 because of their bio-adsorbing feature of the functional ingredients in Yeast Cell Wall and the detoxification effect of curcumin nanoparticles. The goal of this study was to see how nanocurcumin and/or Saccharomyces cell wall supplementation and/or aflatoxin affected broiler development, blood and serum parameters, carcass trait, histology, immune histochemistry, liver gene expression, and aflatoxin residue in the liver and muscle tissue of broilers. Broiler chicks with one day old were distributed into five groups according to nanocurcumin and/or saccharomyces cell wall with aflatoxin supplementation. The G1 group was given a formulated diet without any supplements. The G2 group was supplemented with aflatoxin (0.25 mg/kg diet) in the formulated diet. The G3 group was supplemented with aflatoxin (0.25 mg/kg diet) and Saccharomyces cell wall (1Kg/Ton diet) in the formulated diet. The G4 group was supplemented with aflatoxin (0.25 mg/kg diet) and nanocurcumin (400 mg/kg) in the formulated diet. The G5 group was supplemented with aflatoxin (0.25 mg/kg diet) and Saccharomyces cell wall (1Kg/Ton diet) with nanocurcumin (200 mg/kg) in the formulated diet. Results Aflatoxin supplementation had a detrimental impact on the growth performance, blood and serum parameters, carcass trait, and aflatoxin residue in the liver and muscle tissue of broilers, according to the results of this study. In addition, aflatoxin supplementation led to a liver injury that was indicated by serum biochemistry and pathological lesions in the liver tissue. Moreover, the intestinal villi, length, and width were affected. The expression of some genes in the liver tissue was affected. Conclusion Saccharomyces cell wall alone or with nanocurcumin attenuated these negative effects and anomalies, and improving all of the above-mentioned metrics.

Objective: This study aimed to explore the hepatotoxicity induced by silver nanoparticles (AgNPs) and to assess the hepatoprotective effects of α-lipoic acid (LA) against this toxicity. Methods: Thirty adult male rats were enrolled into 3 equal groups; Control, AgNPs (50 mg/kg/i.P) and LA (100 mg/kg/orally) +AgNPs. After 30 days, blood and liver tissues were collected for further studies. Results: AgNPs exposure enhanced lipid peroxidation(+281.7%) along with declines in glutathione (−58.3%) Level in hepatic tissues. The apparent hepatic oxidative damage was associated with obvious hepatic dysfunction that was ascertained by hepatopathological lesions.As, following AgNPs exposure, hepatic silver content and serum ALT, AST and ALP activities were increased, moreover allows calcium influx and induces intracellular calcium overload. Hepatic tissues treated with AgNPs showed down-regulation of all the genes considered (PGC-1α, Tfam and Nrf2).LA improved the serious effects of AgNPs on the liver tissues through its antioxidant andmetal chelator efficacy. Conclusion: Silver nanoparticles (AgNPs) can induce hepatotoxicity along with oxidative stress, substantial decrease in cell viability with concomitant increases in DNA damage. Oral treatment with LA effectively counteracted the adverse effects of AgNPs.

Silver nanoparticles (AgNPs) are noble metal nanoparticles, due to their good physicochemical properties, which have been exploited in biological applications. Nanotechnological applications advance very quickly while few literatures assessed the effects of natural products on the risks of nanoparticles in vivo. Thirty male adult rats were enrolled equally into: control, AgNPs (50 mg/kg b.w i.p 3 times/week) and GBE (100 mg/kg b.w daily per os)+AgNPs. After 30 days, the assessment of liver function, antioxidative status, mitochondrial biogenesis, and histopathological analyses were performed. AgNP exposure enhanced the hepatic lipid peroxidation (+ 281.7%) along with a decline in the reduced glutathione (- 58.3%) levels. The apparent hepatic oxidative damage was associated with obvious hepatic dysfunction that was ascertained by alteration of serum liver enzymatic biomarkers, lipid profile, and pathological hepatic lesions. Following AgNP exposure, hepatic silver and calcium contents were increased without changes in the trace element concentrations. Finally, the mRNA transcripts of hepatic PGC-1α, mtTFA, and Nrf2 were downregulated after AgNP exposure. Interestingly, GBE has the ability to alleviate AgNP-induced hepatic damage assessed by augmentation of reduced glutathione level and mitochondrial biogenesis. This study explored the potential protective role of GBE on AgNPs-induced hepatotoxicity via attenuation of oxidative stress, substantial enhancement of cell viability with concomitant mitigating DNA damage, and mitochondrial dysfunction.

Silver nanoparticles (AgNPs) are more commonly utilised in medicine, however they have negative effects on the majority of organs, including the reproductive system. AgNPs were reported to be able to reach the testes due to their small size, which allows them to pass through blood testicular barriers. The goal of this study was to see if LA (alpha lipoic acid) or GB (ginkgo biloba) might protect adult rat testes after intraperitoneal injection of AgNPs. Forty male healthy adult Wister albino rats were randomly assigned to four groups (10 rats each); control, AgNPs-intoxicated group intraperitoneally injected AgNPs 50 mg/kg b.w, 3 times a week, LA + AgNPs group intoxicated with AgNPs and orally gavaged with 100 mg LA/kg b.w, and GB + AgNPs group injected with AgNPs and orally given GB extract 120 mg/kg b.w were continued for 30 consecutive days. Biochemical changes in testicular tissue (testosterone, ACP, and Prostatic acid phosphatase), oxidative indices in testicles tissues, mRNA expression of pro-apoptotic (BAX) and anti-apoptotic (BCL-2) biomarkers, histological, and immunohistochemical changes were studied. Significant decrease in serum testosterone level and elevation in ACP and PACP enzyme activity in AgNPs treated group than in the control. In addition, lowering in tGSH, GSH GR, GPx and elevation MDA and GSSG were observed in AgNPs treated group than control. Decreasing in mRNA expression thirodexin-1 (Txn-1), transforming growth factor-1β (TGF-1β), anti-apoptic (BCL-2) and elevation the expression of proapoptic biomarkers (BAX) in the testis homogenates of rats exposed to silver nanoparticles. Strong positive action to BAX and lowering the action of Ki-67antibody were observed. Because of their antioxidant, anti-inflammatory, and anti-apoptotic properties, co-treatment with LA or GB may be beneficial in reducing the harmful effects of AgNPs on the testicles.

Silver nanoparticles (AgNPs) are commonly utilized in medicine. However, they have negative effects on the majority of organs, including the reproductive system. AgNPs were reported to be able to reach the testicular tissues due to their nano size, which allows them to pass through blood-testicular barriers. The goal of this study was to see if alpha-lipoic acid (LA) or Ginkgo biloba (GB) might protect adult rat testes after intraperitoneal injection of AgNPs. Forty male healthy adult Wister albino rats were randomly assigned to four groups: control, AgNPs-intoxicated group intraperitoneally injected AgNPs 50 mg/kg b.w, 3 times a week; LA + AgNPs group intoxicated with AgNPs and orally gavaged with 100 mg LA/kg b.w; and GB + AgNPs group injected with AgNPs and orally given GB extract 120 mg/kg b.w for 30 consecutive days. Biochemical changes (testosterone, ACP, and prostatic acid phosphatase), oxidative indices, mRNA expression of proapoptotic (BAX) and anti-apoptotic (BCL-2) biomarkers, histological, and immunohistochemical changes in testicular tissues were investigated. Significant decrease in serum testosterone level and elevation in ACP and PACP enzyme activity in AgNPs-treated rats. As well, there were lowering in tGSH, GSH GR, GPx, and elevation in MDA and GSSG values. AgNPs-exposed rats expressed downregulation of testicular thirodexin-1 (Txn-1), transforming growth factor-1β (TGF-1β), anti-apoptotic (BCL-2), and upregulaion of proapoptotic biomarkers (BAX) mRNA expressions. Strong positive action to BAX and lowering the action of Ki-67 antibody were observed. Because of their antioxidant, anti-inflammatory, and anti-apoptotic properties, cotreatment with LA or GB could be beneficial in reducing the harmful effects of AgNPs on the testicles.

Mastitis is a worldwide serious disease of the mammary gland. Curcumin is a pleiotropic polyphenol obtained from turmeric, but it is hydrophobic and rapidly eliminated from the body. However, nanoformulation of curcumin significantly improves its pharmacological activity by enhancing its hydrophobicity and oral bioavailability. Our study aimed to investigate the possible anti-oxidant and anti-inflammatory effects of nanocurcumin as a prophylactic against LPS-induced mastitis in rat model; where LPS was extracted from a field strain of Escherichia coli (bovine mastitis isolate). The study was conducted on twenty lactating Wistar female rats divided into four equal groups and the mastitis model was initiated by injection of LPS through the duct of the mammary gland. The results showed that nanocurcumin significantly attenuated the lipid peroxidation (MDA), oxidized glutathione, the release of pro-inflammatory cytokines (TNF-𝛼 and IL-1β) as well as the gene expression of TLR4, NF-κB p65, and HMGB1. Meanwhile, it improved the reduced glutathione level, Nrf2 activity and preserved the normal alveolar architecture. These findings suggested that nanocurcumin supplementation can be a promising potential protective approach for coliform mastitis.

Coliform mastitis is a worldwide serious disease of the mammary gland. Curcumin is a pleiotropic polyphenol obtained from turmeric, but it is hydrophobic and rapidly eliminated from the body. However, nanoformulation of curcumin significantly improves its pharmacological activity by enhancing its hydrophobicity and oral bioavailability. Our study aimed to investigate the possible antioxidant and anti-inflammatory effects of nanocurcumin as a prophylactic against LPS-induced coliform mastitis in rat model, where LPS was extracted from a field strain of Escherichia coli (bovine mastitis isolate). The study was conducted on twenty lactating Wistar female rats divided into four equal groups, and the mastitis model was initiated by injection of LPS through the duct of the mammary gland. The results showed that nanocurcumin significantly attenuated the lipid peroxidation (MDA), oxidized glutathione, the release of pro-inflammatory cytokines (TNF-α and IL-1β), and the gene expression of TLR4, NF-κB p65, and HMGB1. Meanwhile, it improved the reduced glutathione level and Nrf2 activity and preserved the normal alveolar architecture. These findings suggested that nanocurcumin supplementation can be a promising potential protective approach for coliform mastitis.

Iron oxide nanoparticle (IONP) therapy has diverse health benefits but high doses or prolonged therapy might induce oxidative cellular injuries especially in the brain. Therefore, we conducted the current study to investigate the protective role of quercetin supplementation against the oxidative alterations induced in the brains of rats due to IONPs. Forty adult male albino rats were allocated into equal five groups, the control received a normal basal diet, the IONP group was intraperitoneally injected with IONPs of 50 mg/kg body weight (B.W.) and quercetin-treated groups had IONPs + Q25, IONPs + Q50 and IONPs + Q100 that were orally supplanted with quercetin by doses of 25, 50 and 100 mg quercetin/kg B.W. daily, respectively, administrated with the same dose of IONPs for 30 days. IONPs induced significant increases in malondialdehyde (MDA) and significantly decreased reduced glutathione (GSH) and oxidized glutathione (GSSG). Consequently, IONPs significantly induced severe brain tissue injuries due to the iron deposition leading to oxidative alterations with significant increases in brain creatine phosphokinase (CPK) and acetylcholinesterase (AChE). Furthermore, IONPs induced significant reductions in brain epinephrine, serotonin and melatonin with the downregulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and mitochondrial transcription factor A (mtTFA) mRNA expressions. IONPs induced apoptosis in the brain monitored by increases in caspase 3 and decreases in B-cell lymphoma 2 (Bcl2) expression levels. Quercetin supplementation notably defeated brain oxidative damages and in a dose-dependent manner. Therefore, quercetin supplementation during IONPs is highly recommended to gain the benefits of IONPs with fewer health hazards.

Acrylamide (ACR) is an unsaturated monomer that entered in various fields however, it is a potent neurotoxic. The present study target is to explore the neuroprotective efficacy of allicin and melatonin on ACR-induced neurotoxicity. Thirty-six male adult rats were non-selectively separated into six groups: placebo, allicin (20 mg/kg b.w daily per os), melatonin (10 mg/kg b.w 3 times/week per os), ACR (50 mg/kg b.w daily per os), ACR + allicin and ACR + melatonin with the same doses. The assessment of brain biomarkers, neurotransmitters, antioxidative status, Nrf2 signalling pathway, and histopathological analyses were performed following 21 days. ACR exposure enhanced the brain lipid and DNA oxidative damage as well as a reduction in the GSH levels. The obvious brain oxidative injuries was contributed to distinct brain dysfunction that was assured by alteration of brain neurotransmitters (serotonin, dopamine, acetylcholine, and acetylcholinesterase), and pathological brain lesions. Furthermore, ACR exposure increased hydroxy deoxy guanosine (8-OHdG), tumor necrosis factor (TNF) and amyloid protein (AB-42). Finally, the mRNA transcripts of brain Keap-1, Nrf2, and NF-kB were up regulated after ACR intoxication. Interestingly, allicin and melatonin alleviated the ACR-induced brain damage assessed by normalization of the mentioned analyses. The present study demonstrated the protective role of both allicin and melatonin on ACR-prompted neuropathy by alleviation of redox imbalance and enhancement of neurotransmitters as well as relieving DNA damage and anti-inflammatory effect.

Aging is an oxidative stress-associated process that progresses with age. Our aim is to delay or attenuate these oxidative alterations and to keep individuals healthy as they age using natural compounds supplementation. Therefore, we conducted the present study to investigate the protective potentials of quercetin against D-galactose (D-gal)-associated oxidative alterations that were induced experimentally in male Wistar rats. Forty-five rats were randomly allocated into five groups of nine rats each. The groups were a control group that was reared on a basal diet and injected subcutaneously with 120 mg D-gal dissolved in physiological saline solution (0.9% NaCl) per kg body weight daily and quercetin-treated groups that received the same basal diet and subcutaneous daily D-gal injections were supplemented orally with 25, 50, and 100 mg of quercetin per kg body weight for 42 days. Pancreatic and renal samples were subjected to histopatholgical, immunohistochemical, and relative mRNA expression assessments. Aging (p53, p21, IL-6, and IL-8), apoptotic (Bax, CASP-3, and caspase-3 protein), proliferative (Ki67 protein), antiapoptotic (Bcl2 and Bcl2 protein), inflammatory (NF-&kappa, B, IL-1&beta, and TNF-&alpha, ), antioxidant (SOD1), and functional markers (GCLC and GCLM genes and insulin, glucagon, and podocin proteins) were determined to evaluate the oxidative alterations induced by D-gal and the protective role of quercetin. D-gal caused oxidative alterations of the pancreas and kidneys observed via upregulations of aging, apoptotic, and inflammatory markers and downregulated the antiapoptotic, proliferative, antioxidant, and functional markers. Quercetin potentially attenuated these aging-related oxidative alterations in a dose-dependent manner. Finally, we can conclude that quercetin supplementation is considered as a promising natural protective compound that could be used to delay the aging process and to maintain human health.

Aluminum (Al) had well-identified adverse influences on the nervous system mainly through the creation of reactive oxygen species (ROS). Melatonin works as an antioxidant through the inhibition of ROS and attenuating peroxidation of lipids. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a pivotal transcription factor which controls the transcription of antioxidant enzymes. This study was conducted to determine the potential neuroprophylactic impacts of melatonin in aluminum chloride (AlCl3)-initiated neurotoxicity including potential mechanism(s) of action and relevant signaling in rats. Thirty-six male rats were distributed into 4 groups: Control; AlCl3 (50 mg/kg bwt, i.p, 3 times weekly for 3 months); melatonin (5 mg/kg bwt, i.p daily for 2 weeks before AlCl3 and sustained for the next 3 months); and melatonin with AlCl3. Neuronal alterations were histopathologically and biochemically evaluated. The neuronal antioxidant-related genes and relevant Nrf2 protein expression were determined by real-time PCR and Western blotting, respectively. The current data showed a substantial increase in brain damage biomarkers, acetylecholinesterase (AchE) activity, and malondialdehyde (MDA) content while the enzymatic antioxidant expression as glutathione-s-transferase (GST), catalase (CAT), and superoxide dismutase (SOD) were substantially attenuated in the aluminum-treated group, with cleared histopathological changes as inflammatory cell infiltration with neuronal degeneration. Supplementation of melatonin resulted in an obvious amelioration in all previous abnormal alteration observed in AlCl3-treated rats rather than increased Al burden and/or altered Fe and Cu homeostasis with upregulating both total and phosphorylated Nrf2 expression. Therefore, the study concluded that melatonin has a potential ability to be neuroprophylactic against Al-induced neurotoxic effect and oxidative damage in the rat brain through upregulating and instigating Nrf2 signaling apart from metal chelation.

Objective: This study aimed to investigate the protective role of licorice on indomethacin-induced gastric ulcer in male albino rats compared to anti-ulcer drug; ranitidine. Methods: Fifty male adult rats were randomly allocated into five groups (10 rats/each); control, licorice, indomethacin, licorice/indomethacin, and ranitidine/indomethacin treated groups. Serum, gastric juice, and gastric tissues were collected for biochemical and histopathological analysis. Results: The obtained results revealed that licorice pre-treatment showed potent anti-ulcerative effect as; volume and total acidity of gastric secretion were markedly decreased, attenuated the severity of gastric lesion as confirmed by PM and histopathological examination showed preservation of gastric epithelium and ulcer healing. Moreover, gastric ulcer score, gastric MDA, and serum IL-6 were obviously decreased along with increased gastric GSH, CAT activity and NO. Interestingly licorice had no side effects on the liver and kidney evidenced by increased serum total protein, and albumin besides declined the activities of serum aminotransferases without significant changes in the serum urea, uric acid, sodium, potassium, and chloride levels. Conclusion: It was concluded that the used dose of licorice showed potent anti-ulcerative activity and more safer on the liver and kidney functions compared to the standard commercial drug; ranitidine.

The influence of tramadol (TD) on hepatic tissue and the potential efficiency of lycopene to mitigate TD-induced hepatotoxic impacts were determined. Forty male albino rats were allocated into four groups: group I, untreated (placebo); group II, injected with TD (15 mg kg−1) intraperitoneally (i.p.); group III, gastrogavaged with lycopene (10 mg kg−1) per os (p.o.); and group IV received TD with lycopene with the same mentioned doses for 15 days. The results demonstrated that TD induced augmentation in tissue lipid peroxidation biomarker and disturbance in the antioxidant homeostasis and elevated the activity of serum liver injury biomarkers and decreased serum protein, globulin, and albumin. Hepatic glutathione S-transferase (GST), superoxide dismutase (SOD), thioredoxin-1 (Txn-1), and catalase (CAT) activities and gene expression were decreased and glutathione content was reduced in the TD-challenged rats, and these effects were alleviated by lycopene. Furthermore, TD induced apoptosis in liver tissues as shown by DNA fragmentation and upregulation of proapoptotic Bax and Casp-3 while lycopene upregulated the antiapoptotic Bcl-2. The results of Western blot showed that lycopene initiated low expression of mitogen activated protein kinase pathway (MAPK) protein expression in liver tissues of TD-challenged rats. In addition, lycopene reduced fatty degeneration and necrosis of the liver in TD-challenged group. Our data demonstrate that lycopene appears to be highly efficient in mitigating the hepatotoxic impacts of TD by preventing lipid peroxidation and initiating modifications in the expression and activity of antioxidant pathways. Surprisingly, lycopene fortified liver tissue by inhibiting DNA fragmentation and apoptosis signaling induced by TD. MAPK activation may be dependent from ROS generation; due to lycopene which possessed antioxidant potential did have a substantial effect on MAPK activity.

Hepatic cancer (HCC) is a well-identified dilemma throughout the world, and hence, the molecular mechanisms and strategy for preventive protection against this malignancy are critical. S-adenosylmethionine (SAM) is a unique methyl granter in vast reactions, including DNA methylation, and secures the genome against hypomethylation, which is a hallmark of tumors. Consequently, SAM may control the rate of gene expression. The objective of this investigation was to evaluate the expression of long noncoding RNAs (lncRNAs) transcript involved in hepatic tumorigenesis, including additional coding CEBPA (ecCEBPA) and urothelial carcinoma related 1 (UCA1), antioxidant enzymes transcripts, and relevant signaling pathway in diethylnitrosamine (DEN)-prompted HCC along with their conceivable targeting by SAM at different stages of HCC in rats. Our outcomes revealed that SAM particularly when given at the starting phase downregulates ecCEBPA and UCA1 gene transcripts and ameliorate histopathological alterations in DEN-initiated HCC. Interestingly, SAM attenuates DEN-induced upregulation of PI3K/Akt protein expression. However, SAM upregulates the antioxidant enzymes mRNA transcripts and effectively diminishing DNA oxidation. The results of a DNA fragmentation assay further support the capacity of SAM to ameliorate DEN-induced hepatic malignancy. These results revealed the role of ecCEBPA and UCA1 in HCC and suggest that these lncRNAs may be helpful as prognostic and analytical biomarkers of HCC. Curiously, SAM readily targets the studied genes via inhibiting PI3K/Akt signaling pathway, which should make SAM an appealing agent for both chemoprevention and treatment of HCC.

Dietary intake of fructose corn syrup in sweetened beverages is associated with the development of metabolic syndrome and obesity. We hypothesized that inflammatory cytokines play a role in lipid storage and induction of liver injury. Therefore, this study intended to explore the expression of adipocytokines and its link to hepatic damage. Rats were assigned to drink water, cola soft drink (free access) and aspartame (240 mg/kg body weight/day orally) for 2 months. The lipid profiles, liver antioxidants and pathology, and mRNA expression of adipogenic cytokines were evaluated. Subchronic intake of soft drink or aspartame substantially induced hyperglycemia and hypertriacylglycerolemia, as represented by increased serum glucose, triacylglycerol, low-density lipoprotein and very low-density lipoprotein cholesterol, with obvious visceral fatty deposition. These metabolic syndromes were associated with the up-regulation of leptin and down-regulation of adiponectin and peroxisome proliferator activated receptor-γ (PPAR-γ) expression. Moreover, alterations in serum transaminases accompanied by hepatic oxidative stress involving induction of malondialdehyde and reduction of superoxide dismutase, catalase, and glutathione peroxidase and glutathione levels are indicative of oxidative hepatic damage. Several cytoarchitecture alterations were detected in the liver, including degeneration, infiltration, necrosis, and fibrosis, predominantly with aspartame. These data suggest that long-term intake of soft drink or aspartame-induced hepatic damage may be mediated by the induction of hyperglycemia, lipid accumulation, and oxidative stress with the involvement of adipocytokines.

Bisphenol, used in many polycarbonate plastics and epoxy resins industries, exerts toxic effects on mammalian organs. The mechanisms underlying bisphenol toxicity are well understood, however the chemoprevention effects of L-carnitine have not yet been recorded. This study aimed to explore the protective mechanism of L-carnitine against BPA-induced hepatotoxicity. Male rats were randomly distributed into 4 groups of 10 rats each: vehicle (5 mL corn oil/kg), bisphenol (50 mg/kg b.w. orally), L-carnitine (500 mg/kg b.w. i/p), and L-carnitine bisphenol pre-treated groups. Bisphenol was dissolved in corn oil and gavaged for 70 consecutive days. Up-regulation of tumor necrosis factor (6.6-fold), and interleukin 6 (3.2-fold) mRNA transcript, along with suppression of nuclear factor erythroid 2-like 2 (0.4-fold), were recorded, following bisphenol administration. Subsequently, bisphenol provoked oxidative stress and attenuated the antioxidative molecules. Finally, hepatic dysfunction was assessed by elevated serum aminotransferases, alkaline phosphatase, lactate dehydrogenase, glutamyl transferase activities and ammonia levels, with the subsequent decline in serum albumin concentration, which confirmed the inflammatory cell infiltration and hydropic degeneration, and the impairment of lipid profile. Interestingly, co-administration of L-carnitine improved liver function and lipid profile, which was explained by the activation of nuclear factor erythroid 2-like 2 (1.5-fold) mRNA transcript, which augmented the antioxidant levels and suppressed oxidative stress, tumor necrosis factor (2.6- fold), and interleukin 6 (1.5-fold) gene expression. In conclusion, L-carnitine exerted hepatoprotective activity against bisphenol toxicity via antioxidant and anti-inflammatory effects., Bisfenol, koji se koristi u mnogim industrijama polikarbonatne plastike i epoksidnih smola, ima toksične učinke na organe sisavaca. Mehanizmi na kojima se temelji toksičnost bisfenola dobro su razumljivi, međutim učinci L-karnitina na kemoprevenciju još nisu zabilježeni. Cilj ovog ispitivanja bio je istražiti zaštitni mehanizam L-karnitina protiv hepatotoksičnosti izazvane BPA-om. Mužjaci štakora slučajnim su odabirom podijeljeni u su u 4 skupine od po 10 štakora: kontrolna skupina (5 mL kukuruznog ulja/kg tjelesne težine), duga skupina (50 mg bisfenol/kg tjelesne težine peroralno), teća skupina (500 mg L-karnitin/kg tjelesne težine i/p) i četvrta skupina (L-karnitin apliciran skupini prethodno tretiranoj bisfenolom). Bisfenol je otopljen u kukuruznom ulju kojim su štakori hranjeni 70 uzastopnih dana. Nakon primjene bisfenola zabilježeno je povećanje mRNK transkripta za stvarnje faktora tumorske nekroze i interleukina 6 uz supresiju nukleotidnog faktora sličnog eritroidu 2, povezanog s faktorom 2. Nakon toga bisfenol je izazvao oksidativni stres i oslabio antioksidativne molekule. Naposljetku, disfunkcija jetre procjenjivana je povišenim razinama aminotransferaza u serumu, alkalne fosfataze, laktat dehidrogenaze, aktivnosti glutamiltransferaze i amonijaka, uz naknadno smanjenje koncentracije serumskog albumina, što je potvrdilo infiltraciju upalnih stanica i hidropičnu degeneraciju, te narušavanje lipidnog statusa. Zanimljivo je da je istodobna primjena L-karnitina poboljšala funkciju jetre i lipidni status, što je objašnjeno aktivacijom transkripta mRNK tipa 2 povezanog s faktorom 2, koji je povećao razine antioksidansa i potisnuo oksidativni stres, te ekspresiju gena faktora tumorske nekroze i interleukina 6. Zaključno, L-karnitin je pokazao hepatozaštitnu aktivnost protiv toksičnosti bisfenola antioksidativnim i protuupalnim učincima.

DOI: 10.20286/ajlsr-040292 Background: Micro-minerals imbalances have a great impact on animal’s physiology and cause various problems. Trace mineral deficiency is not recognized easily, especially in the sheep and goats as the deficiency exists in the flocks in sub-clinical form and affects the fertility and animal welfare. Rationale for The Study: This study was carried out to detect trace elements deficiency through behavioral observation, haematological and biochemical analysis in sheep with a trial of treatment with a trace elements mixture. Methods and Results: A total number of fifteen diseased baladi ewes were used, blood samples were obtained at the beginning and also ewes were behaviorally observed two weeks before treatment for ascertain trace elements deficiency. Ewes were then treated with mineral mixture drug for two weeks during which they were behaviorally observed. Blood samples were obtained again after treatment for haematological and biochemical analysis. The obtained results following treatment showed significant increased drinking and licking frequencies; copper, cobalt, selenium and magnesium levels and also haemoglobin and red blood cells count, while feeding and lateral recumbancy time, movement frequency, zinc and calcium levels and also white blood cells count and packed cell volume percent were non-significant increased. Furthermore, rumination and standing time and iron and phosphorus levels were non-significantly decreased. However, sodium and potassium levels were significantly decreased. Conclusions: It can be concluded that trace elements deficiency in sheep could cause behavioural, haematological and biochemical changes which respond to treatment but need long time for complete curns so it is recommended to provide trace element supplementation in ration.

Bovine coliform mastitis is a global serious disease of the mammary gland (MG). The current study aimed to investigate the therapeutic effects of nanocurcumin on inflammatory and redox alterations caused by lipopolysaccharide (LPS) induced mastitis in a rat model. Twenty early lactating albino rats were allocated into four identical groups; control, nanocurcumin (35mg/kg bwt orally), LPS (30ug through the duct of the MG), LPS+ nanocurcumin treated group. After 15 days rats were euthanized and MG tissue was collected for determination of inflammatory and oxidative indices. LPS significantly elevated the level of malondialdehyde (MDA), oxidized glutathione (GSSG), tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, while reduced the level of reduced glutathione (GSH) and nuclear factor erythroid-2 factor2 (Nrf2), with up-regulation of toll-like receptor 4 (TLR4), nuclear factor kappa B (NF-κB) and high mobility group box 1 (HMGB1). Nanocurcumin post-treatment ameliorated the damaging impact induced by LPS on MG tissue as denoted by a low level of MDA, GSSG, pro-inflammatory cytokines as well as improved level of GSH and Nrf2 and the down-regulation of TLR4, NF-κB and HMGB1 mRNA transcription. Our findings suggested that nanocurcumin could be a promising potential therapeutic approach for LPS induced mastitis.

This study was conducted to investigate the effect of moringa olifera and colchicine on thioacetamide induced liver fibrosis in rats. One hundred and fife rats were randomly divided into equal seven groups of fifteen animals each for 60 days as follows: The first group (control) was kept on basal diet and water, the second group hepatotoxicity was induced by i.p injection of TAA (150 mg/kg of body weight, i.p.), for three times/week for two months and the third group was given colchicine (COL) orally with stomach tube (50 μ/kg day ) the fourth group was given MOEL( moringa olifera ethanolic leaves extract) also by stomach tube ( 400 mg/kg) ,the fifth group was given TAA(150 mg/kg) + COL(50 μ/kg day ), the six group was given TAA(150 mg/kg) +MOEL(400mg/kg), the seven group was given (TAA(150 mg/kg) + COL(50 μ/kg day )+ MOEL 400mg/kg) for 3times/week for 2 months. We studied liver fibrosis from three point of view biochemical effect, molecular effect and histopathological effect. Blood samples were collected and serum was separated for the determination of the following biochemical tests as liver enzymatic function ALT (Alanin aminotransferase),AST (Aspartateaminotransferase),GGT, ALP (Alkaline phosphatase ) , total protein ,albumin. The total antioxidant capacity (TAC), reduced glutathione (GSH) and malondialdehyde (MDA) in liver tissue homogenates, molecular view point as measuring BAX (bacl2associated X, Apoptosis Regulator) Bcla2 (B-celleymphoma 2) for detection apoptosis occurred then histopathological effect of liver fibrosis on liver tissue. The induction of TAA revealed a significant increase in liver enzymes, bilirubin, MDA, BAX, and a significant decrease in TP, Alb ,Bacl2 by p

The current study aimed to explore the protective roles of ginseng against dexamethasone liver devastating effects. Sixty male rats were equally allocated into six groups; G1: control, G2: ginseng aqueous extract (200 mg/kg B.W. orally /4 weeks), G3: dexamethasone (1mg/kg B.W. i.p/one week then decapitated), G4: dexamethasone- withdrawal group (1mg/kg B.W. i.p/one week and decapitated at the end of experiment), G5: dexamethasone ginseng treated group (injected with dexamethasone/one week then treated with ginseng/other 3weeks), and G6: ginseng-dexamethasone-ginseng group (received ginseng/two weeks followed by dexamethasone/one week then ginseng/another week). Dexamethasone significantly increased serum liver enzymatic activities alongside with mild to moderate hepatic vacuolation, and periportal mononuclear infiltration suggesting liver damage. The level of hepatic malondialdehyde (MDA) was elevated markedly with subsequent decline in the reduced glutathione concentration following challenged with dexamethasone. Moreover, the hepatic expression of thioredoxin mRNA transcript was down-regulated while BCL2-associated X protein (Bax) mRNA transcript was up-regulated providing imbalance in antioxidant and apoptosis pathway. Ginseng treatment ameliorated the damaged effects of dexamethasone on the liver as indicated by attenuation of elevated liver enzymatic activities, augmentation the reduced glutathione level, up-regulation thioredoxin mRNA transcription along with down-regulation of Bax mRNA expression in liver tissue. Conclusively, ginseng exerted a protective action on dexamethasone hepatic side effects through anti-apoptotic and antioxidant properties.

Nile tilapia (Oreochromis niloticus) is the most common aquaculture fish, but is exposed to various pollutants and may be susceptible to infectious diseases due to reduction in their antioxidant status and immune defense. Therefore, researchers have tried to find feed supplements of natural origin to increase the health status of fish and decrease the incidence of drug resistance. The current study was conducted to investigate the effect of dietary supplementation of Miswak (Salvadora persica, SP) on Nile tilapia. Fish were randomly allocated into four experimental groups (30 fish each); the control fish were fed on the basal commercial diet and the SP-treated groups were fed basal diet supplemented with different concentrations 0.5, 1, and 2% for 30 days. The SP supplementations had no significant effects of SP on fish growth performance traits and lipid profiles but augmented the serum protein and globulin levels. The SP significantly improved the hepatic antioxidant status through the significant decrease of malondialdehyde (MDA) and the increases of reduced glutathione (GSH) levels and the activities of total superoxide dismutase (T.SOD), catalase (CAT) and glutathione peroxidase (GPx), especially in the SP 1% group, while glutathione S-transferase (GST) activities were significantly increased due to SP in a dose-dependent manner. The same results were obtained for the mRNA expression of CAT and GPx. Regarding the nonspecific immune status of the fish kidneys, SP, especially SP1, significantly increased interleukin-1 beta (IL-1β) and interferon-gamma (INF-γ). The data of the present study revealed the protective effect of SP on Nile tilapia health status. Therefore, SP can be considered as a promising feed additive for Nile tilapia.

Aims This study explored whether silver nanoparticles (AgNPs) can disrupt tight-junctions integrity resulted in blood-brain barrier dysfunction along with oxidative stress, pro-inflammation, and apoptosis induction. Additionally, neuroprotective activities of α-lipoic acid (LA) and Ginkgo biloba (GB) were investigated. Main methods Forty adults rats were enrolled into; Control, AgNPs (50 mg/kg), LA (100 mg/kg) + AgNPs, and GB (120 mg/kg) + AgNPs. After 30 days, neuronal changes were assessed biochemically and histopathologically. Brain tissues oxidative indices, mRNA expression of proinflammatory cytokines and tight-junction proteins and pro-apoptotic biomarker, caspase-3 were investigated. Key findings AgNPs exposure enhanced lipid peroxidation (+195%) along with declines in glutathione (−43%), glutathione peroxidase (−34%), glutathione S-transferase (−31%), catalase (−43%), and superoxide dismutase (−38%) activities in brain tissues. The apparent brain oxidative damage was associated with obvious neuronal dysfunction that was ascertained by neuropathological lesions. AgNPs lowered serum acetylcholine esterase, iron and copper levels, and increased creatine phosphokinase and creatine phosphokinase–brain type activities. Following AgNPs exposure, brain silver and iron contents were increased, but the copper level was decreased. AgNPs up-regulated TNF-α (6.5-fold) and IL-1β (8.9-fold) transcript levels, and simultaneously over-expressed the caspase-3 protein in cerebrum and cerebellum inducing cell apoptosis. Moreover, AgNPs down-regulated the transcript levels of tight-junction proteins; JP-1 (0.65-fold) and JAM-3(0.81-fold). Significance LA and relatively GB improved the serious effects of AgNPs on the blood-brain barrier function and tight-junction proteins through their antioxidants, anti-inflammatory, and anti-apoptotic efficacies. Co-treatment with LA or GB may be favorable in ameliorating the neurotoxic side effects of AgNPs.

Gastric ulcers are among the most broadly perceived illnesses affecting individuals. Alcohol consumption is the main cause of gastric ulceration. This study assessed the protective effects of Salvadora persica (SP) extract against ethanol-induced gastric ulcer and elucidated the conceivable underlying mechanisms involved. For this purpose, 40 rats were allotted into 4 equal groups (control, ethanol- (EtOH-) treated, and SP-treated “SP200 and SP400” groups). The control and EtOH-treated groups were given phosphate buffer saline (PBS), and both the SP200 and SP400 groups were given SP extract dissolved in PBS at doses of 200 and 400 mg/kg b.w., respectively. All treatments were given orally for 7 constitutive days. On the 8th day, all rats were fasted for 24 h followed by oral gavage of PBS in the control group and chilled absolute ethanol solution (5 ml/kg b.w.) in the EtOH- and SP-treated groups to induce gastric lesions. One hour later, the rats were sacrificed and the stomachs were harvested. Gross and microscopic examinations of the EtOH-treated group showed severe gastric hemorrhagic necrosis, submucosal edema, destruction of epithelial cells, and reduced glycoprotein content at the mucus surface. These pathological lesions were defeated by SP extract treatment. Administration of SP extract modulated the oxidative stress and augmented the antioxidant defenses. The elevated ethanol-expressed tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) genes, as well as bcl-2-like protein 4 (Bax) and inducible nitric oxide synthase (iNOS), were diminished in the SP-treated group. Curiously, SP extract upregulated endothelial nitric oxide synthase (eNOS) and transforming growth factor-β1 (TGF-β1) gene expression comparable to that of the EtOH-treated rats. Aggregately, SP exerted antiulcer activities in ethanol-induced gastric ulcer rat models via modulation of oxidant/antioxidant status, mitigation of proinflammatory cytokines, and apoptosis, as well as remodeling of both NOS isoforms.

The potential antifibrotic effects of melatonin against induced hepatic fibrosis were explored.Rats were allocated into four groups: placebo; thioacetamide (TAA) (200mg/kg bwt, i.p twice weekly for two months); melatonin (5mg/kgbwt, i.p daily for a week before TAA and continued for an additional two months); and melatonin plus TAA. Hepatic fibrotic changes were evaluated biochemically and histopathologically. Hepatic oxidative/antioxidative indices were assessed. The expression of hepatic proinflammatory cytokines (tumor necrosis factor-α, and interleukin-1β), fibrogenic-related genes (transforming growth factor-1β, collagen I, collagen, III, laminin, and autotaxin) and an antioxidant-related gene (thioredoxin-1) were detected by qRT-PCR.In fibrotic rats, melatonin lowered serum aspartate aminotransferase, alanine aminotransferase, and autotaxin activities, bilirubin, hepatic hydroxyproline and plasma ammonia levels. Melatonin displayed hepatoprotective and antifibrotic potential as indicated by mild hydropic degeneration of some hepatocytes and mild fibroplasia. In addition, TAA induced the depletion of glutathione, glutathione s-transferase, glutathione peroxidase, superoxide dismutase, catalase, and paraoxonase-1 (PON-1), while inducing the accumulation of malondialdehyde, protein carbonyl (C=O) and nitric oxide (NO), and DNA fragmentation. These effects were restored by melatonin pretreatment. Furthermore, melatonin markedly attenuated the expression of proinflammatory cytokines and fibrogenic genes via the upregulation of thioredoxin-1 mRNA transcripts.Melatonin exhibits potent anti-inflammatory, antioxidant and fibrosuppressive activities against TAA-induced hepatic fibrogenesis via the suppression of oxidative stress, DNA damage, proinflammatory cytokines and fibrogenic gene transcripts. In addition, we demonstrate that the antifibrotic activity of melatonin is mediated by the induction of thioredoxin-1 with attenuation of autotaxin expressions.

Thiamethoxam (TMX) is a non-mutagenic neonicotinoid insecticide that is widely used to combat different types of insects. The hepatotoxicity and carcinogenicity of TMX have been approved previously in mice but not in rats. However, the TMX-induced hepatotoxic and pro-carcinogenic effects on rabbits remain unclear. The present study elucidated the roles of oxidative stress, pro-inflammatory cytokines, and apoptosis-related genes in the hepatotoxic and carcinogenic effects of TMX on rabbits. Sixteen male rabbits were equally divided into two groups; eight rabbits orally treated with TMX at a dose of 250 mg/kg b.w for 90 successive days. Hepatotoxic effects of TMX were evidenced by attenuation of liver enzyme activities, elevation of bilirubin levels, and alterations in the hepatic architecture, including hepatocyte death by necrosis and apoptosis, lymphocyte infiltration and fibrosis. TMX induced oxidative stress, as evidenced by the significant increases in malondialdehyde levels and antioxidant enzyme (glutathione transferase and catalase) activities along with a decrease in glutathione levels. TMX also up-regulated the mRNA levels of interleukin-6 (1.6-fold) and B cell lymphoma-2 (1.8-fold) and down-regulated the mRNA level of the tumor necrosis factor-α (0.8-fold), indicating its effects on cell survival and proliferation through the inhibition of apoptosis. Interestingly, the elevated level of carcinoembryonic antigen and the appearance of ground glass-like hepatocytes suggested that TMX exerted a pro-carcinogenic effect. In conclusion, TMX exerts potentially hepatotoxic and pro-carcinogenic effects on rabbits by modulating oxidative/antioxidative status and pro-inflammatory cytokine production, inhibiting apoptosis and activating cell survival pathways.

Cadmium (Cd) exposure leads to production of reactive oxygen species (ROS), which are associated with Cd-induced neurotoxicity and nephrotoxicity. Selenium nanoparticles (Se-NPs) have high bioavailability and antioxidant activities so it attracted wide spread attention. The present study examined the possible ameliorative effect of Se-NPs with diameters of 3-5 nm and 10-20 nm against cadmium chloride (CdCl2)-induced neuro- and nephrotoxicity in rats. Rats were treated with Se-NPs (0 or 0.5 mg/kg BW, s.c.) one hour prior to the CdCl2 (0 or 5 mg/kg BW, p.o.). Pretreatment with Se-NPs significantly decreased CdCl2-induced elevation of serum kidney and brain damage biomarkers; lipid peroxidation; the percent of DNA fragmentation and nearly normalized the activity of acetylcholinesterase (AchE) and significantly increased the activity and expression of antioxidant biomarkers in the RNA and protein levels. Se-NPs also attenuated CdCl2-induced upregulation of kidney and brain pro-apoptotic B-cell CLL/lymphoma 2 associated X (Bax) RNA and protein levels with preventing the increased body burden of Cd and the altered Fe and Cu homeostasis. Histopathological analysis confirmed the biochemical and molecular outcomes. Our data stated that Se-NPs appear to be effective in ameliorating the adverse neurological and nephrotoxic effects induced by CdCl2 partially through the scavenging of free radicals, metal ion chelation, averting apoptosis and altering the cell-protective pathways. The results indicated that Se-NPs could potentially included as an additive to Cd-based industries to control Cd-induced brain and renal injury.

Spirulina platensis (SP) is a microalga with antioxidant, antidiabetic and anti-inflammatory properties. The present study explored the ability and potential mechanism(s) by which SP induced glucose lowering impact in diabetic rat model. Forty rats were allocated into four groups: control; streptozotocin (STZ)-induced diabetes (STZ, 45mg/kg b.w., intraperitoneally); SP (500mg/kg b.w., orally twice weekly for 2 months) and STZ-induced diabetes+SP group. In the STZ-induced diabetic rats, SP significantly decreased (P>0.05) serum glucose, glycated hemoglobin (HbA1c), malondialdehyde (MDA) levels and significantly increased (P>0.05) serum insulin, the activity of antioxidant enzymes and normalized their mRNA gene expression. Furthermore, SP attenuates STZ-induced upregulation of the gluconeogenic enzyme pyruvate carboxylase (PC), the pro-apoptotic Bax and caspase-3 (CASP-3), tumor necrosis factor alpha (TNF-α) gene expression. The Western blot results revealed that, SP induced downregulation of mitogen activated protein kinase pathway (MAPK) protein expression in hepatic tissues of diabetic rats. Additionally, SP reestablished the typical histological structure of the liver and pancreas of diabetic rats. Acute toxicity study further shows that SP is relatively safe. This study demonstrates that SP is rich in antioxidant compounds and has powerful glucose lowering effect through the normalization of increased hepatic PC gene expression. Interestingly, SP induced recovery of damaged hepatocytes and pancreatic β-cells via its anti-inflammatory, antioxidant and anti-apoptotic properties. The MAPK signaling cascade is a pivotal component of the proapoptotic signaling pathway induced by diabetes mellitus. MAPK activation may be dependent from ROS production, since SP which exhibited antioxidant activities did have a significant impact on MAPK activity.

A significant association between fructose corn syrup in sweetened beverages consumption and increased risk of detrimental central nervous system effects has been recently reported. We hypothesized that the aspartame and soft drink induced disturbances in energy production and endocrine function, which play a role in the induction of brain damage. Therefore, we aimed to assess the effect of aspartame and soft drink on brain function and the link between energy status in the brain, oxidative stress and molecular pathways of apoptosis. Thirty rats were randomly assigned to drink water, aspartame (240 mg/kg orally) and cola soft drinks (free access) daily for two months. Subchronic intake of aspartame and soft drink significantly disrupted the brain energy production, as indicated by inhibited serum and brain creatine kinase, specifically in soft drink-received rats. Moreover, they substantially altered serum electrolytes (increased Ca and Na, and depleted Cu, Fe, Zn and K levels), and accordingly the related hormonal status (increased T4 and PTH, and lowered T3 and aldosterone levels), particularly in soft drink-received rats reflecting brain damage. Additionally, significant increment of acetylcholine esterase activity concomitant with the reduction of antioxidant molecules (SOD, CAT, GSH-Px and GSH), and induction of malondialdehyde level are precisely indicative of oxidative brain damage. Brain mRNA transcripts of target genes showed that aspartame and soft drink induced upregulation of BAX, Casp3, P27 and Mdm2 (1.5-fold) and down-regulation of Bcl2, suggesting an activation of cellular apoptosis. Collectively, subchronic aspartame and soft drink-induced brain damage in rats may be driven via a mechanism that involves energy production disruption, electrolytes and hormonal imbalance, increased oxidative stress and activation of molecular pathway of neuronal apoptosis.

The ability of Cichorium intybus root extract (chicory extract) to protect against carbon tetrachloride (CCl4)-induced oxidative stress and hepatotoxicity was evaluated in male rats. The rats were divided into four groups according to treatment: saline (control); chicory extract (100 mg/kg body weight daily, given orally for 2 weeks); CCl4 (1 ml/kg body weight by intraperitoneal injection for 2 consecutive days only); or chicory extract (100 mg/kg body weight daily for 2 weeks) + CCl4 injection on days 16 and 17. The levels of hepatic lipid peroxidation, antioxidants, and molecular biomarkers were estimated twenty-four hours after the last CCl4 injection. Pretreatment with chicory extract significantly reduced CCl4-induced elevation of malondialdehyde levels and nearly normalized levels of glutathione and activity of glutathione S-transferase, glutathione peroxidase (GPx), glutathione reductase, catalase (CAT), paraoxonase-1 (PON1), and arylesterase in the liver. Chicory extract also attenuated CCl4-induced downregulation of hepatic mRNA expression levels of GPx1, CAT and PON1 genes. Results of DNA fragmentation support the ability of chicory extract to ameliorate CCl4-induced liver toxicity. Taken together, our results demonstrate that chicory extract is rich in natural antioxidants and able to attenuate CCl4-induced hepatocellular injury, likely by scavenging reactive free radicals, boosting the endogenous antioxidant defense system, and overexpressing genes encoding antioxidant enzymes.

Excess manganese (Mn) is potentially toxic resulting in a permanent neurodegenerative disorder, clinically known as “manganism” that is distinctive for hepaticencephalopathy. The present study was designed to explore the toxic impacts of subacute Mn exposure on brain and liver tissues, and the relative abilities of lycopene in averting such neurohepatic damage. Rats were daily injected with MnCl2 (0 or 6 mg/kg, i.p.) 20 days after lycopene administration (0 or 10 mg/kg, p.o.), and killed 4 weeks after MnCl2 exposure. MnCl2-induced lipid peroxidation and perturbation in antioxidant system, increase of acetylcholinesterase, aminotransferases, and decrease alkaline phosphatase, and lactate dehydrogenase activities with hyperglycemia as demonstrated by Alzheimer type II astrocytosis, and periportal hepatic necrosis and apoptosis were prevented by lycopene. However, lycopene did not prevent the increased body burden of Mn and the altered Fe and Cu homeostasis induced by MnCl2. Glutathione S-transferase and catalase activities, and glutathione content were reduced in MnCl2-challenged rats, and sustained by lycopene. Our results indicate that although lycopene failed to reduce Mn concentration or retain disturbed elemental status; it appears to be a highly effective in alleviating its neurohepatic deleterious effects by preventing lipid peroxidation, hyperglycemia and changes in the activity of acetylcholinesterase and hepatobiliary enzymes, and antioxidant pathways.

Objective The objective of the this study is to investigate the protective effect of curcumin on paracetamol induced hepatotoxicity in rats through determination of, serum protein concentration, ammonia, bilirubin, liver enzymes activities, liver lipid peroxidation and antioxidants. The study was carried on 70 male rats weighing 140± 10 divided into equal 7 groups as following: GI: control, GII: control corn, GIII: curcumin (200mg/kgb.wt/gavage), GIV: curcumin (400mg/kgb.wt/gavage), GV: paracetamol (500mg/kgb.wt/gavage), GVI: Curcumin (200mg/kgb.wt/gavage) + paracetamol (500mg/kgb.wt/gavage) and GVII: curcumin (400mg/kgb.wt/ gavage)+ paracetamol (500mg/kgb.wt/ gavage). After 30 days, blood was collected for biochemical examination. Results: Paracetamol at dose (500 mg/kg b.wt) caused marked liver damage as there was pronounced increase in bilirubin, ammonia and MDA levels along with marked elevation in liver enzyme activities while levels of serum proteins, GSH and Catalase activity markedly decreased. Interestingly, curcumin was able to ameliorate hepatic deterioration caused by paracetamol via restoring depleted glutathione, rebalanced antioxidants and improved damage as curcumin (200 mg/ kg b.wt) successfully decreased degree of hepatic vacuolation with best improvent via curcumin (400 mg/ kg b.wt). Conclusion: Curcumin showed protective effect on paracetamol induced hepatotoxicity as it successfully improved the altered hepatic parameters and through its powerful antioxidant properties.

Paracetamol can cause a life threating renal damage and there is no specific treatment for it. Therefore, the current study aims to investigate the nepheroprotective effect of curcumin against paracetamol nephrotoxicity in rats through determination of kidney function parameters, minerals concentration, kidney lipid peroxidation and antioxidants. To achieve this aim, seventy adult male albino rats were divided into equal seven groups as following, Group I served as control,Group II (corn oil treated group), Group III (curcumin200 mg/kg b.wt/orally), Group IV (Curcumin 400 mg/kg b.wt/orally), Group V served as positive control (Paracetamol 500 mg/kg b.wt/orally), Group VI (Curcumin 200 mg/kg b.wt and paracetamol 500 mg/kg b.wt/orally), and Group VII (Curcumin 400 mg/kg b.w and paracetamol 500 mg/kg b.w/orally). At the end of experiment (after 30 days), blood and tissue samples were collected for biochemical, and histopathological analysis.

The objective of the current study is to investigate the hypolipidemic activity of green tea in induced hyperlipidemic rats through determination of lipid profile, atherogenic indices and to throw light on its liver and kidney protection ability in such condition. To achieve this aim, forty adult male albino rats (150±10 g) were used in which they were divided into equal four groups; Group I (control group) received free access to basal diet and water, Group II (sucrose rich diet) received ( 650g basal diet mixed with 350 g of sucrose), Group III (hyperlipidemic treated group with green tea) received sucrose rich diet and green tea extract at dose of ( 100 mg /kg B.W by stomach tube) , Group IV received basal diet with green tea extract ( 100 mg /kg B.W by stomach tube ). the experiment lasted for one month . Finally, blood samples were collected for biochemical analysis .

The present study aimed to explore the protective effects of L-carnitine on the oxidative stress induced by Bisphenol A (BPA) in rat kidneys. Forty male adult rats were allocated into four groups (10 rats each); placebo, BPA (50 mg/kg bwt per os), L-carnitine (500 mg/kg bwt i.p), and the BPA/L-carnitine-treated group. After 70 days, blood and kidneys were collected for measurement of renal function, oxidative/antioxidative status, histopathological analyses, and gene expression of nrf2. BPA significantly increased serum urea and carnitine levels suggesting renal damage evidenced by hydropic degenerative changes and hydronephrosis. The level of malondialdehyde (MDA) in kidney was elevated along with decline in renal total antioxidant capacity (TAC) and reduced glutathione (GSH) concentrations following challenged with BPA. Notably, the expression of nrf2 mRNA transcript in kidney tissues was down-regulated after BPA-induced toxicity. L-carnitine treatment ameliorates the damaged effects of BPA on kidneys as indicated by low levels of serum urea and carnitine, and renal MDA. Further, L-carnitine enhances the antioxidants (TAC, and GSH), with up-regulation of nrf2 expression in kidney tissues. Our results suggest the renoprotective activity of L-carnitine in BPA-induced kidney injuries through induction of antioxidant system and modulation of oxidative stress

Hyperlipidemia has been ranked as one of the greatest risk factors contributing to the prevalence and severity of coronary heart diseases which considered as the primary causes of death.As hypolipidemic drugs are expensive and of harmful sideffects so, medicinal plant products have been used as an alternative to current management of hyperlipidemia and obesity to some extent as fenugreek leaves and seeds (Trigonella foenum graecum) which were used during Hippocrates and ancient Egyptian times and also, its hypocholesterolemic effect was reported in rats. So, this study aimed to investigate the effect of Fenugreek (Trigonella foenum Graceum) seed powder on hyperlipidemia,atherogenic indices and sexual hormons in induced hyperlipidemic rats.Forty adult male albino rats were used in which they were divided into four groups as : Group I(control group) received basal diet ,GroupII (fenugreek group) received basal diet mixed with 5 % fenugreek seed powder (95 ration diet + 5 gm fenugreek seed powder),GroupIII(hyperlipidemic group) received basal diet, with induction of hyperlipidemia via intraperitoneal injection of triton at adose of (250 mg/kg),GroupIV received basal diet + 5 % fenugreek seed powder after induction of hyperlipidemia via intraperitoneal injection of triton by the same previous method.After 8 weeks, Blood samples were collected (after overnight fasting) , for biochemical analysis and statistical analysis. Result: Triton caused significant increase in serum level of Totalcholesterol(TC) ,Triglycerides(TG), LowDenisityLipoprotein(LDL-c) , very low density lipoprotein (vLDL) ingroup 3(hyperlipidemic group) , with significant decrease in high density lipoprotein (HDL-c).Meanwhile,serum level of TC.,TG.,LDL-c.vLDL-c were significantly decreased in hyperlipidemic group after treating with fenugreek seed powder in group 4 (Hypolipidemic effect) with increasing serum level of high density lipoprotein (HDL-c) with significant improvement in Atherogenic Index as:Cardiac Risk Factors (CRR), Atherogenic Coefficient (AC) and Atherogenic Indices (AI). Also, sexual hormons were improved with fenugreek administration especially group 2 (fenugreek group) compared to group1 (controlgroup). Conclusion: Fenugreek has hypolipidemic effect when added to diet by 5% with improving atherogenic index and sexual hormons.

This study was conducted to evaluate the effect of Parsley (Petroselinum crispum) on some biochemical profiles in streptozotocin diabetic rats. For this purpose, 40 male albino rats were divided into 4 groups according to the program assigned 10 rats per group: Group 1: control group kept on basal ration, Group 2: Parsley group kept on basal ration + Parsley 2gm/kg body weight, Group 3: Diabetic group rats injected intra peritoneal with STZ 45mg/kg body weight and kept on basal diet, Group 4: Diabetic + Parsley rats injected intra peritoneal with STZ 45mg/kg body weight and kept on basal diet + Parsley 2gm/kg body weight. Results showed that: Treatment of the STZ induced diabetic rats with parsley resulted in significant decrease in fasting blood glucose and glycated haemoglobin compared to control group but there is no significant difference within all groups in fructose amine, Alanine aminotransferase, aspartate aminotransferase, Total protein, Albumin, Urea and Creatinine also in Total cholesterol, Triglyceride and HDL while STZ resulted in significant increase in liver antioxidants compared to Parsley treated group.

The ability of Cichorium intybus root extract (chicory extract) to protect against carbon tetrachloride (CCl4)-induced oxidative stress and hepatotoxicity was evaluated in male rats. The rats were divided into four groups according to treatment: saline (control); chicory extract (100 mg/kg body weight daily, given orally for 2 weeks); CCl4 (1 ml/kg body weight by intraperitoneal injection for 2 consecutive days only); or chicory extract (100 mg/kg body weight daily for 2 weeks) + CCl4 injection on days 16 and 17. The levels of hepatic lipid peroxidation, antioxidants, and molecular biomarkers were estimated twenty-four hours after the last CCl4 injection. Pretreatment with chicory extract significantly reduced CCl4-induced elevation of malondialdehyde levels and nearly normalized levels of glutathione and activity of glutathione S-transferase, glutathione peroxidase (GPx), glutathione reductase, catalase (CAT), paraoxonase-1 (PON1), and arylesterase in the liver. Chicory extract also attenuated CCl4-induced downregulation of hepatic mRNA expression levels of GPx1, CAT and PON1 genes. Results of DNA fragmentation support the ability of chicory extract to ameliorate CCl4-induced liver toxicity. Taken together, our results demonstrate that chicory extract is rich in natural antioxidants and able to attenuate CCl4-induced hepatocellular injury, likely by scavenging reactive free radicals, boosting the endogenous antioxidant defense system, and overexpressing genes encoding antioxidant enzymes.