Search

All drugs that can penetrate the blood-brain barrier (BBB) may lead to mental state changes, including the widely used anti-infective drug sulfamethoxazole (SMZ). Herein, we investigated whether lycopene (LYC) could ameliorate SMZ-induced brain injury and the postulated mechanisms involved. A total of 120 grass carps were exposed under SMZ (0.3 μg/L, waterborne) or LYC (10 mg/kg fish weight, diet) or their combination for 30 days. Firstly, brain injury induced by SMZ exposure was suggested by the damage of BBB (decreases of Claudins, Occludin and Zonula Occludens), and the decrease of neurotransmitter activity (AChE). Through inducing oxidative stress (elevations of malondialdehyde and 8-hydroxy-2 deoxyguanosine, inhibition of glutathione), SMZ increased the intra-nuclear level of NF-κB and its target genes (TNF-α and interleukins), creating an inflammatory microenvironment. As a positive feed-back mechanism, apoptosis begins with activation of pro-death proteins (Bax/Bcl-2) and activation of caspases (caspase-9 and caspase-3). Meanwhile, a compensatory upregulation of constitutive Nrf2 and its downstream antioxidative gene expression (NAD(P)H Quinone Dehydrogenase 1 and Heme oxygenase 1) and accelerated autophagy (increases of autophagy-related genes and p62 inhibition) were activated as a defense mechanism. Intriguingly, under SMZ stress, LYC co-administration decreased NF-κB/apoptosis cascades and restored Nrf2/autophagy levels. The neuroprotective roles of LYC make this natural compound a valuable agent for prevention SMZ stress in environment. This study suggests that LYC might be developed as a potential candidate for alleviating environmental SMZ stress in aquaculture. • Sulfamethoxazole exposure leads to oxidative stress, inflammation and apoptosis in the brain. • Lycopene supplementation ameliorates brain damage induced by Sulfamethoxazole. • Lycopene exerts neuroprotection by rebalance of NF-κB/Nrf2 pathway. [ABSTRACT FROM AUTHOR]

Microplastics (MPs) are a new type of pollutants that are widespread in nature, and their toxic effects on humans or animals are receiving attention. Birds are in a higher ecological niche in nature, and MPs may have potential bioaccumulation and biomagnification risks to birds. The mechanisms underlying the reproductive toxicity of MPs to birds are mainly unknown. To study the reproductive toxicity of MPs to birds, we randomly divided chickens into six groups and exposed polystyrene microplastics (PS-MPs) through drinking water (0, 1, and 100 mg/L) for 28 and 42 days. We found that PS-MPs caused testicular inflammatory infiltration and interstitial hemorrhage, resulting in testicular tissue damage; the expression of Claudin3 and Occludin in the blood-testis barrier (BTB) decreased and may damage the integrity of the BTB. PS-MPs exposure inhibited the expression of the Nrf2-Keap1 pathway, which in turn reduced HO-1 and NQO1, simultaneous GSH and T-AOC were also reduced, resulting in an imbalance of the redox system; in addition, the NF-κB signaling pathway was activated, increasing the expression of TNF-α, COX-2 and iNOS. Under redox system imbalance and inflammatory stress, exposure to PS-MPs led to decreased expression of Bcl-2 and increased Bax, cytc, caspase-8, and caspase-3, etc., activating apoptosis, and ultimately causing testicular damage. These results suggested that PS-MPs exposure led to an imbalance of the redox system and an inflammatory response, inducing both endogenous and exogenous apoptosis, resulting in testicular tissue damage. Our study provides a theoretical basis for reproductive injury mechanisms in chicken. [Display omitted] • PS-MPs resulted in inflammatory infiltration and hemorrhage of testicular tissue. • PS-MPs induced oxidative stress through excessive inhibition of antioxidant system. • PS-MPs caused reproductive toxicity through crosstalk NF-κB and Nrf2 pathways. • PS-MPs exposure led to apoptosis and thus reproductive toxicity. [ABSTRACT FROM AUTHOR]

• Effects of L-theanine on the colonic injury in DSS induced-colitis mice were investigated. • L-theanine ameliorated the inflammation-associated damage in DSS induced-colitis mice. • Nitric oxide synthase, cyclooxygenase-2, TLR-2, TLR-4, TLR-6, and TLR-9 were inhibited by L-theanine. • L-theanine reduced lipopolysaccharides and increased the production of short-chain fatty acids. This study investigated the effects of L-theanine supplementation on the colonic mucosa injury in C57BL/6J male mice treated with dextran sulfate sodium (DSS)-induced colitis. Treatment with L-theanine significantly decreased the disease activity index and ameliorated the inflammation-associated pathological damage in colon length, as well as the histopathological features of DSS-induced colitis. L-Theanine administration also inhibited DSS-induced changes in the colonic tissue that included myeloperoxidase by 4.5-fold and malondialdehyde by 2.3-fold in comparison to the DSS group. In addition, GSH was increased by 85% and lipopolysaccharides level was decreased by 55% in comparison to the DSS group. Proinflammatory cytokines expression, including interleukin (IL)-1β, IL-6, and tumor necrosis factor-α, at the both protein and mRNA levels were also decreased significantly. Notably, the increase in serum content of lipopolysaccharides and colonic expressions of inducible nitric oxide synthase, cyclooxygenase-2, toll like receptor (TLR)-2, TLR-4, TLR-6, and TLR-9 induced by DSS were also significantly inhibited by L-theanine administration. In addition, L-theanine also attenuated the reduction of serum contents of diamine oxidase and the production of short-chain fatty acids in the colonic tissue, and gene expression of mucosal barrier zonula occludens-1 and claudin-1 in DSS-induced colitis. Furthermore, 16S rRNA phylogenetic sequencing revealed a shift in microbial community composition induced by DSS, but no significant difference was observed following L-theanine supplementation. Overall, our findings demonstrated that L-theanine inhibits intestinal inflammation and protects against intestinal barrier disruption in mice with DSS-induced colitis. Further clinical trials should be considered to assess the effects of L-theanine supplementation on oxidative and inflammatory responses in humans. [ABSTRACT FROM AUTHOR]

Plant-derived dietary lectins have been reported to be involved in the pathogenesis of several inflammatory diseases, including hepatitis, inflammatory bowel disease, diabetes, and celiac disease. In this present study, we aimed to assess whether green tea polyphenols (GTPs) exerts protective effects against plant lectins-induced liver inflammation and immunological reaction in mice. The C57BL/6 mice received intragastric GTPs (200 mg/kg b.w.) once per day for 7 consecutive days prior to plant lectins stimulation (50 mg/kg b.w., intraperitoneally). GTPs supplementation alleviated the histopathological changes of liver and the disorder of serum biochemical parameters in plant lectins-challenged mice. GTPs supplementation also alleviated plant lectins-induced oxidative stress and liver inflammation, decreasing protein contents and gene expression levels of pro-inflammatory cytokines in the plasma and hepatic tissue and increasing antioxidant capacity in the liver. GTPs decreased the protein expression levels of myeloperoxidase, F4/80 and neutrophil, as determined by immunohistochemical analysis, and T lymphocytes (CD4 and CD8) contents as determined by immunofluorescence analysis, in the liver. Moreover, we found that GTPs inhibited Nod-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome expression and increased nuclear factor erythroid 2-related factor 2 (Nrf2) pathways in the liver tissues of plant lectins-challenged mice. Taken together, these results show that GTPs alleviates hepatic inflammatory damage and immunological reaction after plant lectins challenge, and GTPs (or green tea intake) supplements can be beneficial for people exposed to plant lectins. • GTPs ameliorated plant lectins-induced inflammation and increasing antioxidant capacity in the liver. • GTPs alleviated the histopathological changes in plant lectins-challenged mice. • GTPs decreased the expression of MPO, F4/80, neutrophil and T lymphocytes in plant lectins-challenged mice. • GTPs inhibited NLRP3 inflammasome activation and increased Nrf2 pathway in the liver. [ABSTRACT FROM AUTHOR]

Perfluorodecanoic acid (PFDA) is a highly toxic food contaminant that is extensively used in food applications as surface antifouling agent. In this present study, we aimed to assess whether green tea polyphenols (GTPs) and epigallocatechin-3-gallate (EGCG) exert protective effects against PFDA-induced liver damage and inflammation in mice. A mouse model to evaluate liver toxicity was established by giving mice drinking water containing different concentrations of PFDA. GTPs or EGCG (0.32%, w / v) were co-administered to mice exposed to PFDA in drinking water. Overall, GTPs and EGCG extended the survival time and inhibited weight loss among mice who received a lower dose of PFDA. Moreover, GTPs and EGCG ameliorated hepatic oxidative stress, cell apoptosis, necrosis, steatosis, edema, and degeneration, reduced hepatic inflammation and NLRP3 inflammasome activation caused by a moderate dose of PFDA. Taken together, these results show that GTPs or EGCG (or green tea intake) supplements can be beneficial for people exposed to PFDA. Unlabelled Image • GTPs and EGCG reduced mortality of mice exposed to PFDA • GTPs extended survival time and inhibited weight loss among mice caused by PFDA. • GTPs and EGCG ameliorated PFDA-induced liver toxicity and inflammation. • GTPs and EGCG inhibited PFDA-induced NLRP3 inflammasome activation. [ABSTRACT FROM AUTHOR]

This study aims to evaluate the effect of berberine-based carbon quantum dots (Ber-CDs) on improving 5-fluorouracil (5-FU)-induced intestinal mucositis in C57BL/6 mice, and explored the mechanisms behind this effect. Thirty-two C57BL/6 mice were divided into four groups: normal control (NC), 5-FU-induced intestinal mucositis model (5-FU), 5-FU + Ber-CDs intervention (Ber-CDs), and 5-FU + native berberine intervention (Con-CDs). The Ber-CDs improved body weight loss in 5-FU-induced mice with intestinal mucositis compared to the 5-FU group. The expressions of IL-1β and NLRP3 in spleen and serum in Ber-CDs and Con-Ber groups were significantly lower than those in the 5-FU group, and the decrease was more significant in the Ber-CDs group. The expressions of IgA and IL-10 in the Ber-CDs and Con-Ber groups were higher than those in the 5-FU group, but the up-regulation was more significant in the Ber-CDs group. Compared with the 5-FU group, the relative contents of Bifidobacterium, Lactobacillus and the three main SCFAs in the colon contents were significantly increased the Ber-CDs and Con-Ber groups. Compared with the Con-Ber group, the concentrations of the three main short-chain fatty acids in the Ber-CDs group were significantly increased. The expressions of Occludin and ZO-1 in intestinal mucosa in the Ber-CDs and Con-Ber groups were higher than those in the 5-FU group, and the expressions of Occludin and ZO-1 in the Ber-CDs group were more higher than that in the Con-Ber group. In addition, compared with the 5-FU group, the damage of intestinal mucosa tissue in the Ber-CDs and Con-Ber groups were recovered. In conclusion, berberine can attenuate intestinal barrier injury and oxidative stress in mice to mitigate 5-fluorouracil-induced intestinal mucositis, moreover, the above effects of Ber-CDs were more significant than those of native berberine. These results suggest that Ber-CDs may be a highly effective substitute for natural berberine. [ABSTRACT FROM AUTHOR]

In recent years, sodium butyrate has gained increased attention for its numerous beneficial properties. However, whether sodium butyrate could alleviate inflammatory damage by macrophage activation and its underlying mechanism remains unclear. The present study used an advanced glycosylation products- (AGEs-) induced inflammatory damage model to study whether sodium butyrate could alleviate oxidative stress, inflammation, and metabolic dysfunction of human monocyte-macrophage originated THP-1 cells in a PI3K-dependent autophagy pathway. The results indicated that sodium butyrate alleviated the AGEs-induced oxidative stress, decreased the level of reactive oxygen species (ROS), increased malondialdehyde (MDA) and mRNA expression of pro-inflammatory cytokines of interleukin (IL)-1β and tumor necrosis factor (TNF)-α, and increased the content of superoxide dismutase (SOD). Sodium butyrate reduced the protein expression of the NLR family, pyrin domain-containing protein 3 (NLRP3) and Caspase-1, and decreased the nucleus expression of nuclear factor-kappaB (NF-κB). Sodium butyrate decreased the expression of light-chain-associated protein B (LC3B) and Beclin-1, and inhibited autophagy. Moreover, sodium butyrate inhibited the activation of the PI3K/Akt pathway in AGEs-induced THP-1 cells. In addition, the metabolomics analysis showed that sodium butyrate could affect the production of phosphatidylcholine, L-glutamic acid, UDP-N-acetylmuraminate, biotinyl-5'-AMP, and other metabolites. In summary, these results revealed that sodium butyrate inhibited autophagy and NLRP3 inflammasome activation by blocking the PI3K/Akt/NF-κB pathway, thereby alleviating oxidative stress, inflammation, and metabolic disorder induced by AGEs. [ABSTRACT FROM AUTHOR]

[Display omitted] • Aqueous extract (AE) of butterfly pea petals has mainly flavonoids (anthocyanins). • AE ameliorated the oxidative stress and inflammation mediators in obese mice. • AE reduced plasma leptin, free fatty acid, LDL, and hepatic MDA contents. • AE reduced total cholesterol and ameliorated insulin resistance in obese mice. • AE exert hypolipidemic/anti-inflammatory effects by promoting reverse cholesterol transport. This study examined the chemical compounds and bioactivity of the aqueous extract of Clitoria ternatea blue petals and investigated its beneficial effects in vivo on a mouse model of obesity and metabolic syndrome. The extract mainly contained flavonoids, and nine compounds were tentatively identified. Male C57BL/6J mice were either fed a standard diet (SD) or a high-fat, high-fructose diet (HFFD) for 16 weeks, and HFFD-fed animals were treated with 0.25%, 0.5%, and 2% (w/w) of the aqueous extract in drinking water. The aqueous extract ameliorated oxidative stress and inflammation mediators. Furthermore, the aqueous extract reduced plasma leptin, free fatty acid, low-density lipoprotein cholesterol levels and hepatic malondialdehyde content. The aqueous extract significantly reduced total cholesterol and ameliorated insulin resistance. The results demonstrated that the aqueous extract of C. ternatea blue petals contains bioactive anthocyanins that exert substantial hypolipidemic and anti-inflammatory effects by promoting reverse cholesterol transport in HFFD-fed mice. [ABSTRACT FROM AUTHOR]

Microplastics (MPs) are a novel environment pollutant widespread among the natural environment, also causing damage to aquatic animals and mammals. However, their effects on the kidney of poultry are still unclear. In this study, chickens were exposure to the different doses of PS-MPs (1, 10, 100 mg/L) for six weeks, with 1 mg/L being the environmental concentration. The effects of PS-MPs on renal tissue damage in chicken were analyzed. Our results suggested that MPs exposure causes mitochondrial morphology and dysbiosis (MFN1/2, OPA1, Drp1), mitochondrial structural damage by triggering imbalance in mitochondrial dynamics. Antioxidant enzyme (SOD, CAT, MDA, GSH, T-AOC) activity was significantly altered, which in turn caused oxidative stress. H&E staining results showed damage and inflammation of chicken kidney. Mechanistically, the inflammation featured by activated NF-κB P65 and increased expression of pro-inflammatory factors (TNFα, iNOs, IL-1β and IL-6). Moreover, PS-MPs intake induced necroptosis through activated RIP1/RIP3/MLKL signaling pathway. In conclusion, our study was the first to show that oral intake of PS-MPs induced inflammation and necroptosis in chicken kidney and the differences in damage were linked to the concentration of PS-MPs. The purpose of this study provided theoretical support for the environmental risk assessment of PS-MPs. [Display omitted] • Exposure to the PS-MPs induced renal injury in chicken. • Oxidative stress was the key event of PS-MPs induced renal injury. • PS-MPs promoted kidney inflammation by mediating NF‑κB pathway. • PS-MPs activated kidney necroptosis via RIP1/RIP3/MLKL pathway. [ABSTRACT FROM AUTHOR]

Carp has a wide range of edible value. As a vital organ that plays a crucial role in the innate immunity and respiratory system, gill may cause pollutants to enter fish during gas exchange. The negative effects of arsenic (As) pollution in the aquaculture industry cannot be ignored. Zinc (Zn) has the potential to replace endogenous antioxidants. This study aimed to investigate the comprehensive effects of As 2 O 3 and ZnCl 2 on carp gills. The obtained results found that: 1) As3+ can cause significant gill damage; fortunately, Zn co-administration significantly recovered the histopathological damage, antioxidant function and barrier function of carp gill tissue (Occludin, Claudins and Zonula Occludens (ZOs)); 2) from the perspective of mRNA and protein levels, after the Zn2+ pretreatment, heat shock response (HSPs), endoplasmic reticulum stress (glucose regulatory protein 78 (GRP78), phosphorylated PKR-like ER Kinase (p-PERK), phosphorylated eukaryotic initiation factor 2 α (p -eIF2α)), apoptosis (cysteyl aspartate specific protease 3/9 (Cas 3/9), B cells Lymphoma-2 (Bcl-2), BCL2-related X (Bax)) and autophagy (microtubule-associated protein 1 light chain 3 (LC3) and sequestosome 1 (P62) caused by As3+) have decreased. In conclusion, this study preliminarily showed that As3+ and Zn2+ have antagonistic effects on carp gill tissues. These informations emphasized the importance of assessing the injury and recovery ability of organisms after the input of heavy metal and elements, and enhanced the understanding of the potential impact of As3+ and Zn2+ to freshwater ecosystems and aquaculture. [Display omitted] • Arsenic-induced toxicity is reflected in the gill tissues. • Zinc and arsenic have potential antagonistic effects. • Due to direct contact with pollutants, gill become one of the organs with a higher degree of susceptibility. [ABSTRACT FROM AUTHOR]

• Arsenic poses a serious threat to the aquatic environment and aquatic organisms. • Arsenic induces redox imbalance and reactive oxygen species (ROS) burst in the foregut and midgut of carp. • Arsenic induces apoptosis and autophagy through phosphatidylinositol 3 kinase (PI3K)/protein kinase b (AKT)/mammalian target of rapamycin (mTOR) pathway and mitogen-activated protein kinase (MAPK) pathway. • Zinc can antagonize the toxicity of arsenic by protecting the antioxidant system, as well as the PI3K/AKT/mTOR pathway and MAPK pathway. Arsenic (As) pollution is a serious and longstanding problem, which has obvious threaten to aquatic organisms. The study aimed to explore the mitigation effect of natural antioxidant zinc (Zn) on As toxicity in the foregut and midgut of common carp (Cyprinus carpio L.), and in-depth disclose related signal cascade. Carps were treated with Zn2+ (1 mg/L) and/or As3+ (2.83 mg/L) for a period of 30 days. Under As exposure, the foregut and midgut showed obvious burst of reactive oxygen species (ROS) and breakdown of antioxidant system. What followed is the activation of the endogenous and exogenous apoptotic pathways, and the rise of autophagy level prompted by the increase in LC3 II and the down-regulation of p62. Mitochondrial swelling, cristae fragmentation and autophagosomes were observed under the electron microscope, which also means the occurrence of apoptosis and autophagy. In addition, As induced the activation of p38 mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK) and the inhibition of extracellular signal-related kinase (ERK) in MAPK signaling, and up-regulated the level of autophagy through the inhibition of the phosphatidylinositol 3 kinase (PI3K)/AKT/ mammalian target of rapamycin (mTOR) signaling cascade. However, Zn supplementation has clearly reversed the above phenomenon, and it basically has no effect on foregut and midgut. In conclusion, this study shows that Zn can alleviate the damage caused by subchronic As exposure, which provides a reference for the use of Zn preparations in aquaculture. [Display omitted] [ABSTRACT FROM AUTHOR]