scholarly journals Preventive Effect of Resveratrol on Caerulein-induced Acute Pancreatitis in High-fat diet-feeding Mice

2021 ◽  
Author(s):  
Xiaoying Zhang ◽  
Guodong Yang
Keyword(s):  
Gut Microbiota ◽  
Signaling Pathway ◽  
Therapeutic Effect ◽  
High Fat Diet ◽  
Histopathological Examination ◽  
Underlying Mechanism ◽  
Mice Model ◽  
High Fat ◽  
Tnf Α ◽  
Related Proteins

Abstract Background: The aim of this study was to investigate the therapeutic effect and the underlying mechanism of resveratrol in high fat diet (HFD) and hyperlipidemia AP (HTG-AP) mice model. Methods: Following successful establishment of the HFD and HTG-AP mice model, resveratrol was administrated. 16sRNA sequencing of gut microbiota in colonic fecal, the LPS, MCP-1, TNF-α, and IL-6 expressions in serum, and MCP-1 expression of the pancreatic tissues were measured in HFD model. The MDA, SOD, T-AOC, TNF-α, and MCP-1 expressions; the NF‑κB proinflammatory signaling pathway‑related proteins in pancreatic tissues were determined. Histopathological examination was evaluated in both models.Results: Resveratrol effectively inhibited pancreatic pathological injury in both models. It reduced the MDA, SOD, T-AOC, TNF-α, and MCP-1 expressions and changed composition of gut microbiota in feces compared with the HFD model. Resveratrol also reduced oxidative stress by decreasing the level of MDA and increasing the levels of SOD and T-AOC. TNF-α and MCP-1 were decreased following the administration of resveratrol. Furthermore, resveratrol suppressed the NF‑κB proinflammatory signaling pathway in pancreatic tissues.Conclusions: The study suggested that resveratrol had therapeutic effect on HFD and HTG-AP mice model by regulating the gut microbiota, promoting antioxidant capacity and inhibiting proinflammatory cytokines via the NF‑κB inflammatory pathway. The results can provide evidence that resveratrol might be regarded as a promising therapeutic agent for HTG-AP.

scholarly journals Chlorogenic Acid and Geniposide Combination Prevents NASH in Rats Fed High-fat diet via Microbiota and TLR4-LPS Pathway

2021 ◽  
Author(s):  
Zhijia Zhou ◽  
Lingxia Xu ◽  
Shaoliang Zhang ◽  
Shilin Xu ◽  
Yanmiao Yang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Chlorogenic Acid ◽  
Inflammatory Cytokines ◽  
High Fat Diet ◽  
Oral Treatment ◽  
Variable Region ◽  
High Fat ◽  
Tnf Α ◽  
Abundance And Diversity ◽  
Factor Α

Abstract Objective: Chlorogenic acid and geniposide (CG) are derived from traditional Chinese medicine, Yinchenhao Recipe (QCHR), and can improve the clinical efficacy of NASH patients. This study investigated the effects of CG on NASH and expounded its Potential mechanism of action through the LPS-TLR4 pathway and microbiota. Methods: Rats were randomized into Control (C), Model (M), Chlorogenic Acid and Geniposide (CG), Pioglitazone (PH) and Bifico (B) groups. After an 8-week high-fat diet (HFD), CG, PH and B oral treatment were initiated and carried out for a further 8 weeks. The stool samples were used in a16S rDNA V4 highly variable region measurement method in order to regulate the role of CG in gut microbiota. The concentrations of triglyceride (TG), cholesterol (CHO), interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) in LPS were detected by the corresponding methods. Results: Observations were made that CG significantly improved the pathology of the liver and terminal ileum tissue. The accumulation of TG and the content of inflammatory cytokines in the liver were significantly decreased and the abundance of Proteobacteria was significantly down-regulated. The expression of TLR4, AP-1, MyD88, and phosphorylated NF-κB p65 were significantly decreased. All the findings above indicated that CG was highly effective in improving the composition of gut microbiota, decreasing the production of endogenous LPS, and reducing the secretion of inflammatory cytokines through the gut-liver axis.Conclusion: CG can regulate the abundance and diversity of the intestinal microbial community and improve liver inflammation and steatosis in NASH rats by reducing LPS-TLR4-mediated inflammation.

scholarly journals Propofol Alleviates Neuropathic Pain in CCI Rat Model via the miR-140-3p/JAG1/Notch Signaling Pathway

2021 ◽  
Author(s):  
Fang Cheng ◽  
Wei Qin ◽  
Ai-xing Yang ◽  
Feng-feng Yan ◽  
Yu chen ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Notch Pathway ◽  
Thermal Hyperalgesia ◽  
Underlying Mechanism ◽  
Notch Signaling Pathway ◽  
Mechanical Threshold ◽  
Tnf Α ◽  
Related Proteins

Abstract As a renowned anesthetic, propofol exerts excellent analgesic function in nerve injury. However, the underlying mechanism of propofol on neuropathic pain (NP) remains unknown. The research aims to analyze propofol’s analgesia mechanism to alleviate NP in CCI rats. The chronic constriction injury (CCI) of sciatic nerve was used to established NP rat models. CCI rats were treated with propofol and its paw withdrawal mechanical threshold (PMWT) and paw withdraw thermal latency (PWTL) were measured. The expressions of TNF-α, IL-1β and IL-10 were detected. CCI rats with propofol treatment were injected with antagomiR-140-3p. After the targeting relationship between miR-140-3p and JAG1 was checked, JAG1 expression was detected. Propofol-treated CCI rats were further injected with Ad-JAG1. Finally, the levels of JAG1 and Notch pathway-related proteins were detected. As a result, propofol could alleviate NP, including thermal hyperalgesia and mechanical pain threshold, and ameliorate neuroinflammation. Mechanically, propofol enhanced the level of miR-140-3p in CCI rats. JAG1 was a direct target of miR-140-3p. The downregulation of miR-140-3p or upregulation of JAG1 could reduce the protective effect of propofol against NP. Propofol inhibited activation of Notch signaling via miR-140-3p/JAG1. Overall, Propofol could inhibit the neuroinflammation and Notch signaling pathway via miR-140-3p/JAG1 to alleviate NP.

scholarly journals The Regulation Effect of Crude Polysaccharides from Cordyceps Militaris on Obesity Control and Gut Microbiota Community via High-Fat Diet-Fed Mice Model

2020 ◽  
Author(s):  
Minglei Yu ◽  
Nan Hui ◽  
Kashif Hayat ◽  
Xijia Yang ◽  
Shaohua Chu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
Liver Steatosis ◽  
Serum Triglyceride ◽  
Cordyceps Militaris ◽  
High Yield ◽  
Serum Triglyceride Level ◽  
Mice Model ◽  
High Fat ◽  
Brown Adipose

Administration of crude polysaccharides extract from natural product is a promising gut microbiota-targeted approach to preventing obesity and associated metabolic disorders. Dietary restrictions can change the type and number of gut bacteria, which is an important factor in delaying the onset and burden of diseases. This study aimed to investigate the effects of high-yield crude polysaccharides from Cordyceps militaris (CMP) on high-fat diet (HFD) mice model and the gut microbiota community assembly, and to identify whether selenium (Se) addition would improve CMP action mode during cultivation. We found that the CMP treatment ameliorated adipose and liver pathologic morphology and fat accumulation in obese mice, while, SeCMP intervention was not superior than CMP in body mass gain, but notably decreasing serum triglyceride level increased by HFD. The upregulated expression of gene Cyp7a1 in liver and protein UCP1 in brown adipose tissue (BAT) preliminary indicated that the effect might relate to bile acids (BAs) metabolism pathway and thermogenesis. In addition, CMP showed a drastic decrease in the gut microbes which positively correlated with dyslipidemia parameters. Our result reveals the potential of CMP to be used as functional food in the prevention of diet-induced adipose and liver steatosis, so does SeCMP has outstanding capacity of improving dyslipidemia.

scholarly journals Broccoli Florets Supplementation Improves Insulin Sensitivity and Alters Gut Microbiome Population—A Steatosis Mice Model Induced by High-Fat Diet

2021 ◽  
Vol 8 ◽  
Author(s):  
Gil Zandani ◽  
Sarit Anavi-Cohen ◽  
Nina Tsybina-Shimshilashvili ◽  
Noa Sela ◽  
Abraham Nyska ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Gut Microbiota ◽  
Gut Microbiome ◽  
High Fat Diet ◽  
Serum Insulin ◽  
Normal Diet ◽  
Receptor Expression ◽  
Mice Model ◽  
High Fat ◽  
Significant Difference

Nonalcoholic fatty liver disease (NAFLD) is linked to obesity, type 2 diabetes, hyperlipidemia, and gut dysbiosis. Gut microbiota profoundly affects the host energy homeostasis, which, in turn, is affected by a high-fat diet (HFD) through the liver-gut axis, among others. Broccoli contains beneficial bioactive compounds and may protect against several diseases. This study aimed to determine the effects of broccoli supplementation to an HFD on metabolic parameters and gut microbiome in mice. Male (7–8 weeks old) C57BL/J6 mice were divided into four groups: normal diet (ND), high-fat diet (HFD), high-fat diet+10% broccoli florets (HFD + F), and high-fat diet + 10% broccoli stalks (HFD + S). Liver histology and serum biochemical factors were evaluated. Alterations in protein and gene expression of the key players in lipid and carbohydrate metabolism as well as in gut microbiota alterations were also investigated. Broccoli florets addition to the HFD significantly reduced serum insulin levels, HOMA-IR index, and upregulated adiponectin receptor expression. Conversely, no significant difference was found in the group supplemented with broccoli stalks. Both broccoli stalks and florets did not affect fat accumulation, carbohydrate, or lipid metabolism-related parameters. Modifications in diversity and in microbial structure of proteobacteria strains, Akermansia muciniphila and Mucispirillum schaedleri were observed in the broccoli-supplemented HFD-fed mice. The present study suggests that dietary broccoli alters parameters related to insulin sensitivity and modulates the intestinal environment. More studies are needed to confirm the results of this study and to investigate the mechanisms underlying these beneficial effects.

scholarly journals Lactic Acid Bacteria Strains Differently Modulate Gut Microbiota and Metabolic and Immunological Parameters in High-Fat Diet-Fed Mice

2021 ◽  
Vol 8 ◽  
Author(s):  
Emanuel Fabersani ◽  
Antonela Marquez ◽  
Matías Russo ◽  
Romina Ross ◽  
Sebastián Torres ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lactic Acid ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Ex Vivo ◽  
Obese Mice ◽  
High Fat ◽  
Immunological Parameters ◽  
Tnf Α ◽  
Obese Control

Background: Dietary strategies, including the use of probiotics as preventive agents that modulate the gut microbiota and regulate the function of adipose tissue, are suitable tools for the prevention or amelioration of obesity and its comorbidities. We aimed to evaluate the effect of lactic acid bacteria (LAB) with different adipo- and immuno-modulatory capacities on metabolic and immunological parameters and intestinal composition microbiota in high-fat-diet-induced in mice fed a high-fat dietMethods: Balb/c weaning male mice were fed a standard (SD) or high-fat diet (HFD) with or without supplementation with Limosilactobacillus fermentum CRL1446 (CRL1446), Lactococcus lactis CRL1434 (CRL1434), or Lacticaseibacillus casei CRL431 (CRL431) for 45 days. Biochemical and immunological parameters, white-adipose tissue histology, gut microbiota composition, and ex vivo cellular functionality (adipocytes and macrophages) were evaluated in SD and HFD mice.Results: CRL1446 and CRL1434 administration, unlike CRL431, induced significant changes in the body and adipose tissue weights and the size of adipocytes. Also, these strains caused a decrease in plasmatic glucose, cholesterol, triglycerides, leptin, TNF-α, IL-6 levels, and an increase of IL-10. The CRL1446 and CRL1434 obese adipocyte in ex vivo functionality assays showed, after LPS stimulus, a reduction in leptin secretion compared to obese control, while with CRL431, no change was observed. In macrophages from obese mice fed with CRL1446 and CRL1434, after LPS stimulus, lower levels of MCP-1, TNF-α, IL-6 compared to obese control were observed. In contrast, CRL431 did not induce modification of cytokine values. Regarding gut microbiota, all strain administration caused a decrease in Firmicutes/Bacteroidetes index and diversity. As well as, related to genus results, all strains increased, mainly the genera Alistipes, Dorea, Barnesiella, and Clostridium XIVa. CRL1446 induced a higher increase in the Lactobacillus genus during the study period.Conclusions: The tested probiotic strains differentially modulated the intestinal microbiota and metabolic/immunological parameters in high-fat-diet-induced obese mice. These results suggest that CRL1446 and CRL1434 strains could be used as adjuvant probiotics strains for nutritional treatment to obesity and overweight. At the same time, the CRL431 strain could be more beneficial in pathologies that require regulation of the immune system.

scholarly journals Dahuang Zexie Decoction Protects against High-Fat Diet-Induced NAFLD by Modulating Gut Microbiota-Mediated Toll-Like Receptor 4 Signaling Activation and Loss of Intestinal Barrier

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Jing Fang ◽  
Xiaoqi Sun ◽  
Boyu Xue ◽  
Nanyuan Fang ◽  
Min Zhou
Keyword(s):  
Gut Microbiota ◽  
Signaling Pathway ◽  
High Fat Diet ◽  
Intestinal Barrier ◽  
Toll Like Receptor ◽  
High Fat ◽  
Toll Like Receptor 4 ◽  
Tlr4 Signaling ◽  
Tlr4 Signaling Pathway ◽  
Signaling Activation

Increasing evidence suggests that intestinal dysbiosis, intestinal barrier dysfunction, and activated Toll-like receptor 4 (TLR4) signaling play key roles in the pathogenesis of NAFLD. Dahuang Zexie Decoction (DZD) has been verified to be effective for treating NAFLD, but the mechanisms remain unclear. In this study, we investigated the effects of DZD on NAFLD rats and determined whether such effects were associated with change of the gut microbiota, downregulated activity of the TLR4 signaling pathway, and increased expressions of tight junction (TJ) proteins in the gut. Male Sprague Dawley rats were fed high-fat diet (HFD) for 16 weeks to induce NAFLD and then given DZD intervention for 4 weeks. We found that DZD reduced body and liver weights of NAFLD rats, improved serum lipid levels and liver function parameters, and relieved NAFLD. We further found that DZD changed intestinal bacterial communities, inhibited the intestinal TLR4 signaling pathway, and restored the expressions of TJ proteins in the gut. Meanwhile ten potential components of DZD had been identified. These findings suggest that DZD may protects against NAFLD by modulating gut microbiota-mediated TLR4 signaling activation and loss of intestinal barrier. However, further studies are needed to clarify the mechanism by which DZD treats NAFLD.

scholarly journals Effects of probiotic Lactobacillus rhamnosus GG and Propionibacterium freudenreichii ssp. shermanii JS supplementation on intestinal and systemic markers of inflammation in ApoE*3Leiden mice consuming a high-fat diet

2012 ◽  
Vol 110 (1) ◽  
pp. 77-85 ◽  
Author(s):  
Anna Oksaharju ◽  
Teake Kooistra ◽  
Robert Kleemann ◽  
Wim van Duyvenvoorde ◽  
Minja Miettinen ◽  
...  
Keyword(s):  
Mast Cells ◽  
Gut Microbiota ◽  
Plasma Levels ◽  
High Fat Diet ◽  
Lactobacillus Rhamnosus ◽  
Probiotic Bacteria ◽  
Propionibacterium Freudenreichii ◽  
High Fat ◽  
Markers Of Inflammation ◽  
Tnf Α

A high-fat diet disturbs the composition and function of the gut microbiota and generates local gut-associated and also systemic responses. Intestinal mast cells, for their part, secrete mediators which play a role in the orchestration of physiological and immunological functions of the intestine. Probiotic bacteria, again, help to maintain the homeostasis of the gut microbiota by protecting the gut epithelium and regulating the local immune system. In the present study, we explored the effects of two probiotic bacteria, Lactobacillus rhamnosus GG (GG) and Propionibacterium freudenreichii spp. shermanii JS (PJS), on high fat-fed ApoE*3Leiden mice by estimating the mast cell numbers and the immunoreactivity of TNF-α and IL-10 in the intestine, as well as plasma levels of several markers of inflammation and parameters of lipid metabolism. We found that mice that received GG and PJS exhibited significantly lower numbers of intestinal mast cells compared with control mice. PJS lowered intestinal immunoreactivity of TNF-α, while GG increased intestinal IL-10. PJS was also observed to lower the plasma levels of markers of inflammation including vascular cell adhesion molecule 1, and also the amount of gonadal adipose tissue. GG lowered alanine aminotransferase, a marker of hepatocellular activation. Collectively, these data demonstrate that probiotic GG and PJS tend to down-regulate both intestinal and systemic pro-inflammatory changes induced by a high-fat diet in this humanised mouse model.

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