scholarly journals Clostridium butyricum Alleviates Enterotoxigenic Escherichia coli K88-Induced Oxidative Damage Through Regulating the p62-Keap1-Nrf2 Signaling Pathway and Remodeling the Cecal Microbial Community

2021 ◽  
Vol 12 ◽  
Author(s):  
Haihua Li ◽  
Zhiyuan Shang ◽  
Xuejiao Liu ◽  
Yingying Qiao ◽  
Kewei Wang ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Oxidative Damage ◽  
Signaling Pathway ◽  
Amplicon Sequencing ◽  
Clostridium Butyricum ◽  
Enterotoxigenic Escherichia Coli ◽  
Control Group ◽  
Starting Point ◽  
Nrf2 Signaling Pathway ◽  
16S Rdna Amplicon Sequencing

Clostridium butyricum (CB) can enhance antioxidant capacity and alleviate oxidative damage, but the molecular mechanism by which this occurs remains unclear. This study used enterotoxigenic Escherichia coli (ETEC) K88 as a pathogenic model, and the p62-Keap1-Nrf2 signaling pathway and intestinal microbiota as the starting point to explore the mechanism through which CB alleviates oxidative damage. After pretreatment with CB for 15 d, mice were challenged with ETEC K88 for 24 h. The results suggest that CB pretreatment can dramatically reduce crypt depth (CD) and significantly increase villus height (VH) and VH/CD in the jejunum of ETEC K88-infected mice and relieve morphological lesions of the liver and jejunum. Additionally, compared with ETEC-infected group, pretreatment with 4.4×106 CFU/mL CB can significantly reduce malondialdehyde (MDA) level and dramatically increase superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels in the serum. This pretreatment can also greatly increase the mRNA expression levels of tight junction proteins and genes related to the p62-Keap1-Nrf2 signaling pathway in the liver and jejunum in ETEC K88-infected mice. Meanwhile, 16S rDNA amplicon sequencing revealed that Clostridium disporicum was significantly enriched after ETEC K88 challenge relative to the control group, while Lactobacillus was significantly enriched after 4.4×106 CFU/mL CB treatment. Furthermore, 4.4×106 CFU/mL CB pretreatment increased the short-chain fatty acid (SCFA) contents in the cecum of ETEC K88-infected mice. Moreover, we found that Lachnoclostridium, Roseburia, Lactobacillus, Terrisporobacter, Akkermansia, and Bacteroides are closely related to SCFA contents and oxidative indicators. Taken together, 4.4×106 CFU/mL CB pretreatment can alleviate ETEC K88-induced oxidative damage through activating the p62-Keap1-Nrf2 signaling pathway and remodeling the cecal microbiota community in mice.

scholarly journals Clostridium butyricum Protects IPEC-J2 Cells from ETEC K88-Induced Oxidative Damage by Activating the Nrf2/ARE Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Caixia Dou ◽  
Zhiyuan Shang ◽  
Jiayun Qiao ◽  
Yimeng Wang ◽  
Haihua Li
Keyword(s):  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Signaling Pathway ◽  
Antioxidant Response ◽  
Clostridium Butyricum ◽  
Enterotoxigenic Escherichia Coli ◽  
Multiple Infection ◽  
Control Group ◽  
Related Factor ◽  
Viable Bacteria

Clostridium butyricum (CB) is a naturally occurring probiotic compound that can alleviate the oxidative damage induced by enterotoxigenic Escherichia coli K88 (ETEC K88) in porcine intestinal epithelial (IPEC-J2) cells. In this study, we investigate the molecular mechanism underlying this effect. Based on cell viability, malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPX) assessments, the optimal concentration of ETEC K88 was determined to be 1 × 10 3  cfu/mL. Viable bacteria counts in cells pretreated with CB and then infected with ETEC K88 show that CB can adhere to IPEC-J2 cells and that optimal adhesion is achieved at the multiple infection index (MOI) of 50 at 3 h of pretreatment. The results of qPCR indicate that although ETEC significantly decreases the expression levels of antioxidant enzymes regulated by NF-E2-related factor 2 (Nrf2) compared to the control group, CB reverses this effect. To confirm that Nrf2 is directly involved in the mechanism by which CB alleviates oxidative stress, siRNA was used to silence the expression of Nrf2 gene in IPEC-J2 cells. Compared to the NC+ETEC and siRNA+ETEC groups, the expressions of SOD1, SOD2, GPX1, and GPX2 in the NC+CB+ETEC and siRNA+CB+ETEC groups are significantly increased at 12 h and 24 h. This shows that CB can reduce ETEC K88-induced oxidative damage in IPEC-J2 cells by activating the expression of antioxidant enzymes implicated in the Kelch-like ECH-associated protein-1- (Keap1-) Nrf2/antioxidant response element (ARE) signaling pathway.

Effect of melatonin on attenuating the isoflurane-induced oxidative damage is related to PKCα/Nrf2 signaling pathway in developing rats

2018 ◽  
Vol 143 ◽  
pp. 9-18 ◽  
Author(s):  
Bei Li ◽  
Xiu Jing Feng ◽  
Xue Yuan Hu ◽  
Yong Ping Chen ◽  
Ji Chen Sha ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Signaling Pathway ◽  
Nrf2 Signaling Pathway

scholarly journals Effects of chitooligosaccharide-zinc on mice ovarian function in premature ovarian failure via regulating the sestrin2/nrf2 signaling pathway

2020 ◽  
Author(s):  
Jia Li ◽  
Yuhang Chen ◽  
Jiayu Xu ◽  
Jiangying Liu ◽  
Jiacheng Fu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Ovarian Function ◽  
Treated Group ◽  
Control Group ◽  
Chitosan Oligosaccharide ◽  
Protective Effects ◽  
Developmental Defects ◽  
Adult Mice ◽  
Nrf2 Signaling Pathway ◽  
Significant Difference

Abstract BackgroundThe chitosan oligosaccharide-zinc (COS·Zn) is also a powerful antioxidant and anti-aging scavenger, whose anti-oxidative ability immensely exceeds that of vitamin C. Therefore, this study aimed to investigate the protective effects and potential mechanism by which COS·Zn improves ovarian function and delays aging in POF.MethodsThe female KM adult mice and POF mice were divided into treated and prevention groups; these were prophylactically or therapeutically administered COS·Zn (150mg/kg·d, 300mg/kg·d) for 21 days, respectively. ResultsThe number of antral follicles in COS·Zn-treated groups was lower in the treated and prevention groups than that in the control group, respectively. Obviously, the ovarian index, the level of FSH and LH all increased notably during the 300 mg/kg·d treated group and the prevention group compared with cy/bus groups. The expression of MVH, OCT4 and PCNA in the 300 mg/kg·d treated groups and MVH in the prevention groups were remarkably increased compared with the CY/BUS group. Meanwhile, the protein levels of P53 and P16 were markedly down-regulated in the treated groups and prevention groups compared with CY/BUS, except for the expression of P53 in the prevention groups. Furthermore, the Sestrin2 (SESN2) and SOD2 proteins were significantly higher in the 150 mg/kg·d treated group compared with the CY/BUS group, but the 300 mg/kg·d and CY/BUS group showed no significant difference in the level of SESN2. Similarly, the NRF2 and SESN2 proteins were up-regulated in the prevention groups, and the change in SOD2 was not significant. The results revealed increased GSH levels in the 150 mg/kg·d and 300 mg/kg·d treated groups compared with CY/BUS group, and the same trend was also shown in the prevention groups.1Conclusion COS·Zn improves ovarian and follicular developmental defects caused by regulating the sestrin2-nrf2 signaling pathway, and these results suggest a novel product that is effective a POF prevention and treatment drug.

scholarly journals Piceatannol inhibits pyroptosis and suppresses oxLDL-induced lipid storage in macrophages by regulating miR-200a/Nrf2/GSDMD axis

2020 ◽  
Vol 40 (9) ◽  
Author(s):  
Zhongyuan Mu ◽  
Hongling Zhang ◽  
Peng Lei
Keyword(s):  
Signaling Pathway ◽  
Bioactive Compound ◽  
Lipid Storage ◽  
Raw264.7 Cells ◽  
Control Group ◽  
Related Factor ◽  
Novel Therapy ◽  
Nrf2 Signaling Pathway ◽  
Candidate Target ◽  
First Time

Abstract As a major bioactive compound from grapes, piceatannol (PIC) has been reported to exert anti-atherosclerotic activity in various studies. Nevertheless, the mechanism underlying the effect of piceatannol against atherosclerosis (AS) is elusive. Our study identified miR-200a/Nrf2/GSDMD signaling pathway as critical mediators in the effect of piceatannol on macrophages. In the present study, we confirmed that treatment of piceatannol repressed the oxLDL-induced lipid storage in macrophages. Compared with control group, piceatannol inhibited TG storage and the activity of caspase1. It is noting that in response to oxLDL challenge, piceatannol abated the pyroptosis in RAW264.7 cells, with a decreased expression of caspase1, gasdermin D (GSDMD), IL-18, IL-1β and NLRP3. Moreover, we investigated the role of microRNA (miR)-200a/Nrf2 signaling pathway in the effect of piceatannol. The results declared that after transfection of si-miR-200a or si-Nrf2 plasmids, the effects of piceatannol on macrophages were converted, including lipid storage and pyroptosis. Importantly, si-miR-200a plasmid reduced the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), indicating that miR-200a acted as an enhancer of Nrf2 in macrophages. Collectively, our findings demonstrate that piceatannol exerts anti-atherosclerotic activity on RAW264.7 cells by regulating miR-200a/Nrf2/GSDMD signaling. The present study is the first time to identify miR-200a as a candidate target in AS and declared an association between miR-200a and pyroptosis, which provides a novel therapy for the treatment of AS.

scholarly journals Composition and Diversity of the Ocular Surface Microbiota in Patients With Blepharitis in Northwestern China

2021 ◽  
Vol 8 ◽  
Author(s):  
Changhao Wang ◽  
Xiuhong Dou ◽  
Jian Li ◽  
Jie Wu ◽  
Yan Cheng ◽  
...  
Keyword(s):  
16S Rdna ◽  
Relative Abundance ◽  
Ocular Surface ◽  
Amplicon Sequencing ◽  
Northwestern China ◽  
Healthy Control Group ◽  
Control Group ◽  
Eyelid Margin ◽  
16S Rdna Amplicon Sequencing ◽  
Healthy Control

Purpose: To investigate the composition and diversity of the microbiota on the ocular surface of patients with blepharitis in northwestern China via 16S rDNA amplicon sequencing.Methods: Thirty-seven patients with blepharitis divided into groups of anterior, posterior and mixed blepharitis and twenty healthy controls from northwestern China were enrolled in the study. Samples were collected from the eyelid margin and conjunctival sac of each participant. The V3–V4 region of bacterial 16S rDNA in each sample was amplified and sequenced on the Illumina HiSeq 2500 sequencing platform, and the differences in taxonomy and diversity among different groups were compared.Results: The composition of the ocular surface microbiota of patients with blepharitis was similar to that of healthy subjects, but there were differences in the relative abundance of each bacterium. At the phylum level, the abundances of Actinobacteria, Cyanobacteria, Verrucomicrobia, Acidobacteria, Chloroflexi, and Atribacteria were significantly higher in the blepharitis group than in the healthy control group, while the relative abundance of Firmicutes was significantly lower (p < 0.05, Mann-Whitney U). At the genus level, the abundances of Lactobacillus, Ralstonia, Bacteroides, Akkermansia, Bifidobacterium, Escherichia-Shigella, Faecalibacterium, and Brevibacterium were significantly higher in the blepharitis group than in the healthy control group, while the relative abundances of Bacillus, Staphylococcus, Streptococcus, and Acinetobacter were significantly lower in the blepharitis group (p < 0.05, Mann-Whitney U). The microbiota of anterior blepharitis was similar to that of mixed blepharitis but different from that of posterior blepharitis. Lactobacillus and Bifidobacterium are biomarkers of posterior blepharitis, and Ralstonia is a biomarker of mixed blepharitis. There was no significant difference in the ocular surface microbiota between the eyelid margin and conjunctival sac with or without blepharitis.Conclusion: The ocular surface microbiota of patients with blepharitis varied among different study groups, according to 16S rDNA amplicon sequencing analysis. The reason might be due to the participants being from different environments and having different lifestyles. Lactobacillus, Bifidobacterium, Akkermansia, Ralstonia, and Bacteroides may play important roles in the pathogenesis of blepharitis.

scholarly journals Lasso Peptide Microcin J25 Effectively Enhances Gut Barrier Function and Modulates Inflammatory Response in an Enterotoxigenic Escherichia coli-Challenged Mouse Model

2020 ◽  
Vol 21 (18) ◽  
pp. 6500 ◽  
Author(s):  
Xiuliang Ding ◽  
Haitao Yu ◽  
Shiyan Qiao
Keyword(s):  
Escherichia Coli ◽  
Barrier Function ◽  
Inflammatory Responses ◽  
Intestinal Morphology ◽  
Enterotoxigenic Escherichia Coli ◽  
Control Group ◽  
Lasso Peptide ◽  
Gut Barrier Function ◽  
Microcin J25 ◽  
Etec Infection

Bacterial resistance leads to severe public health and safety issues worldwide. Alternatives to antibiotics are currently needed. A promising lasso peptide, microcin J25 (MccJ25), is considered to be the best potential substitute for antibiotics to treat pathogen infection, including enterotoxigenic Escherichia coli (ETEC). This study evaluated the efficacy of MccJ25 in the prevention of ETEC infection. Forty-five female BALB/c mice of clean grade (aged seven weeks, approximately 16.15 g) were randomly divided into three experimental groups as follows: (i) control group (uninfected); (ii) ETEC infection group; (iii) MccJ25 + ETEC group. Fifteen mice per group in five cages, three mice/cage. MccJ25 conferred effective protection against ETEC-induced body weight loss, decrease in rectal temperature and increase in diarrhea scores in mice. Moreover, in ETEC-challenged mice model, MccJ25 significantly improved intestinal morphology, decreased intestinal histopathological scores and attenuated intestinal inflammation by decreasing proinflammatory cytokines and intestinal permeability, including reducing serum diamine oxidase and D-lactate levels. MccJ25 enhanced epithelial barrier function by increasing occludin expression in the colon and claudin-1 expression in the jejunum, ultimately improving intestinal health of host. MccJ25 was further found to alleviate gut inflammatory responses by decreasing inflammatory cytokine production and expression via the activation of the mitogen-activated protein kinase and nuclear factor κB signaling pathways. Taken together, the results indicated that MccJ25 protects against ETEC-induced intestinal injury and intestinal inflammatory responses, suggesting the potential application of MccJ25 as an excellent antimicrobial or anti-inflammation agent against pathogen infections.

scholarly journals Proanthocyanidins Protect against β-Hydroxybutyrate-Induced Oxidative Damage in Bovine Endometrial Cells

Molecules ◽  
2019 ◽  
Vol 24 (3) ◽  
pp. 400 ◽  
Author(s):  
Xi Cheng ◽  
Shuhua Yang ◽  
Chuang Xu ◽  
Lanzhi Li ◽  
Yi Zhang ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Signaling Pathway ◽  
Manganese Superoxide Dismutase ◽  
Metabolic Diseases ◽  
Heme Oxygenase 1 ◽  
Endometrial Cells ◽  
Manganese Superoxide ◽  
Nrf2 Signaling Pathway ◽  
Mrna And Protein Expression ◽  
Stress Damage

Metabolic diseases, such as ketosis, are closely associated with decreased reproductive performance (such as delayed estrus and decreased pregnancy rate) in dairy cows. The change of β-hydroxybutyrate (BHBA) concentration in dairy cattle is an important mechanism leading to ketosis, and its blood concentration in ketotic cows is always significantly higher than in nonketotic cows. Many studies indicated that BHBA can induce oxidative damage in liver and other organs. Proanthocyanidins (PCs) have gained substantial attention in the last decade as strong antioxidative substances. This study aimed to demonstrate a protective effect of PCs against BHBA-induced oxidative stress damage in bovine endometrial (BEND) cells by activating the nuclear erythroid2-related factor2 (Nrf2) signaling pathway. Our research show that PCs could significantly increase activities of catalase (CAT) and glutathione peroxidase (GSH-PX), glutathione (GSH) content, and antioxidant capacity (T-AOC), while significantly decreasing malondialdehyde (MDA) content in BEND cells. Both mRNA and protein expression levels of Nrf2 were significantly increased in BEND cells, and glutamate–cysteine ligase catalytic subunit (GCLC), heme oxygenase 1 (HO-1), manganese superoxide dismutase (Mn-SOD), and NAD(P)H quinone dehydrogenase 1 (NQO-1) were also significantly increased. These results indicate that PCs can antagonize BHBA-induced oxidative damage by activating the Nrf2 signaling pathway to exert an antioxidant effect.

Biogenic selenium nanoparticles synthesized by Lactobacillus casei ATCC 393 alleviate diquat-induced intestinal barrier dysfunction in C57BL/6 mice through their antioxidant activity

2020 ◽  
Vol 11 (4) ◽  
pp. 3020-3031 ◽  
Author(s):  
Lei Qiao ◽  
Xina Dou ◽  
Shuqi Yan ◽  
Baohua Zhang ◽  
Chunlan Xu
Keyword(s):  
Antioxidant Activity ◽  
Oxidative Damage ◽  
Signaling Pathway ◽  
Lactobacillus Casei ◽  
Intestinal Barrier ◽  
Selenium Nanoparticles ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction ◽  
Nrf2 Signaling Pathway ◽  
Biogenic Selenium Nanoparticles

Biogenic SeNPs synthesized by Lactobacillus casei ATCC 393 reversed diquat-induced oxidative damage to the epithelium by activating the Nrf2 signaling pathway.

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