Epigallocatechin gallate but not catechin prevents nonalcoholic steatohepatitis in mice similar to green tea extract while differentially affecting the gut microbiota

Dey, Priyankar; Olmstead, Bryan D.; Sasaki, Geoffrey Y.; Vodovotz, Yael; Yu, Zhongtang; Bruno, Richard S.

doi:10.1016/j.jnutbio.2020.108455

Cited by 60 publications

(55 citation statements)

References 57 publications

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“…In recent years, many studies have confirmed that intestinal microorganisms can affect liver health through the gut-liver axis. Green tea extract can limit the inflammatory response of LPS-TLR4-NFκB and reduce the occurrence of nonalcoholic steatohepatitis through the intestinal hepatic axis pathway ( Dey et al., 2020 ). Mesenteric congestion caused by portal blood flow interruption can induce endotoxin mediated toll-like receptor 4 expression, leading to an increased burden of liver cancer ( Orci et al., 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Therapeutic effect of Schisandrin A on avian colibacillosis through gut-liver axis

Bao

Zhang

et al. 2021

Poultry Science

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This study evaluated the therapeutic efficacy of Schisandrin A on systemic colibacillosis of chickens. One hundred and eighty, 1-day-old Hailan Brown chickens were divided into 6 groups of 30 chickens each and assigned to the following treatments: 1) uninfected/untreated control; 2) infected Escherichia coli ; 3) infected-plus low dose of Schisandrin A therapy (50 mg/kg); 4) infected-plus medium dose of Schisandrin A therapy (100 mg/kg); 5) infected-plus high dose of Schisandrin A therapy (200 mg/kg) and 6) infected-plus antimicrobial therapy (florfenicol). Each group of chickens was placed in cages with a photoperiod of 12 h of light and 12 h of dark. Feed and water for all groups were provided ad libitum for the duration of the study. On d 14, all the chickens except the uninfected control group were intraperitoneally inoculated with a fresh culture of E. coli containing 1 × 10 8 CFU/mL. The parameters measured included: average daily weight gain ( ADG ), percent survivability, liver index, serum activity of enzymes (ALT and AST), hepatic and intestinal concentrations of TNF-α, IL-1β, IL-6, IL-8, and LPS, expression of tight junction proteins (occludin, ZO-1, and claudin-1), relative abundance of bacterial species and histopathological changes in hepatic and intestinal tissue. The results showed that the medium and high doses of Schisandrin A ameliorated the detrimental effects of colibacillosis on weight gain. Regarding organ indexes, E. coli infection induced a significant increase in liver index, all the doses of Schisandrin A produced a significant reduction of liver index in comparison to the E. coli infected control. Serum activity of ALT and AST enzymes significantly increased due to E. coli infection, with the exception of the low dose of Schisandrin A for AST enzyme activity, all the Schisandrin A treatments significantly lowered enzyme activity in comparison to the E. coli infected control. Regarding concentrations of inflammatory markers in hepatic and intestinal, E. coli infection caused a significant increase in TNF-α, IL-1β, IL-6, and IL-8, except the lowest dose of Schisandrin A for IL-1β, the rest of the doses tested were able to significantly reduced the concentrations of inflammatory markers. Concentrations of LPS in hepatic and intestinal tissues were significantly increased by E. coli infection, all doses of Schisandrin A significantly reduced the concentration of LPS in hepatic and intestinal tissue. E. coli infection significantly reduced the expression of 2 tight junction proteins (ZO-1 and Claudin-1), the higher doses of Schisandrin A were effective in significantly increasing the expression of these tight junction proteins when compared with the E. coli infected control. Taken together, these results show that...

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Section: Introductionmentioning

confidence: 99%

Therapeutic effect of Schisandrin A on avian colibacillosis through gut-liver axis

Bao

Zhang

et al. 2021

Poultry Science

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“…[ 40 ] These catechin‐derived microbial metabolites are likely to also possess anti‐inflammatory activity at the intestinal‐level to limit NASH‐associated liver injury. [ 10,37 ] Thus, future studies are needed to consider the tissue‐specific role of aberrant TLR4 signaling on NASH risk and also integrate the complex interactions between green tea catechins and their metabolites, the hepatic metabolome, and the gut microbiome.…”

Section: Discussionmentioning

confidence: 99%

“…[ 7–9 ] While its catechins provide anti‐inflammatory activity, epigallocatechin gallate (EGCG) is the principle bioactive constituent of GTE that is responsible for alleviating endotoxin‐TLR4‐NFκB‐mediated NASH. [ 10 ] Studies in TLR4 mut mice suggest that GTE attenuates hepatic NFκB‐mediated inflammation in NASH in a TLR4‐dependent manner. [ 6 ] In support, GTE in wild‐type (WT) mice fed a HF diet decreased expression levels of hepatic TLR4 in association with reduced NFκB activation, lipid peroxidation, and histological evidence of NASH compared with WT controls.…”

Section: Introductionmentioning

confidence: 99%

Catechin‐Rich Green Tea Extract and the Loss‐of‐TLR4 Signaling Differentially Alter the Hepatic Metabolome in Mice with Nonalcoholic Steatohepatitis

Sasaki

Cichon

et al. 2020

Molecular Nutrition Food Res

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Scope Catechin‐rich green tea extract (GTE) limits inflammation in nonalcoholic steatohepatitis (NASH) consistent with a Toll‐like receptor 4 (TLR4)‐dependent mechanism. It is hypothesized that GTE supplementation during NASH will shift the hepatic metabolome similar to that attributed to the loss‐of‐TLR4 signaling. Methods and results Wild‐type (WT) and loss‐of‐function TLR4‐mutant (TLR4mut) mice are fed a high‐fat diet containing 0% or 2% GTE for 8 weeks prior to performing untargeted mass spectrometry‐based metabolomics on liver tissue. The loss‐of‐TLR4 signaling and GTE shift the hepatic metabolome away from that of WT mice. However, relatively few metabolites are altered by GTE in WT mice to the same extent as the loss‐of‐TLR4 signaling in TLR4mut mice. GTE increases acetyl‐coenzyme A precursors and spermidine to a greater extent than the loss‐of‐TLR4 signaling. Select metabolites associated with thiol metabolism are similarly affected by GTE and the loss‐of‐TLR4 signaling. Glycerophospholipid catabolites are decreased by GTE, but are unaffected in TLR4mut mice. Conversely, the loss‐of‐TLR4 signaling but not GTE increases several bile acid metabolites. Conclusion GTE limitedly alters the hepatic metabolome consistent with a TLR4‐dependent mechanism. This suggests that the anti‐inflammatory activities of GTE and loss‐of‐TLR4 signaling that regulate hepatic metabolism to abrogate NASH are likely due to distinct mechanisms.

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“…Dey et al [ 69 ] fed C57BL/6J mice with either high-fat diet or low-fat diet and added catechin, EGCG, or green tea extract. The idea was to trigger nonalcoholic steatohepatitis and study whether green tea polyphenols would exert any protection.…”

Section: Influence Of Green Tea On Health Via Gut Microbiotamentioning

confidence: 99%

“…They observed how both polyphenols and green tea extract shaped gut microbiota and its functionality at the same time, and either of the treatments were able to protect reducing inflammation. However, they noticed that each treatment had a different effect on the gut microbiota, suggesting that the benefits observed in the liver were not, at least entirely, dependent on the gut microbiota [ 69 ]. Conversely, Ning et al [ 70 ] suggested that shifts caused in gut microbiome by EGCG could be related to benefits against nonalcoholic steatohepatitis.…”

Section: Influence Of Green Tea On Health Via Gut Microbiotamentioning

confidence: 99%

Green Tea and Its Relation to Human Gut Microbiome

et al. 2021

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Green tea can influence the gut microbiota by either stimulating the growth of specific species or by hindering the development of detrimental ones. At the same time, gut bacteria can metabolize green tea compounds and produce smaller bioactive molecules. Accordingly, green tea benefits could be due to beneficial bacteria or to microbial bioactive metabolites. Therefore, the gut microbiota is likely to act as middle man for, at least, some of the green tea benefits on health. Many health promoting effects of green tea seems to be related to the inter-relation between green tea and gut microbiota. Green tea has proven to be able to correct the microbial dysbiosis that appears during several conditions such as obesity or cancer. On the other hand, tea compounds influence the growth of bacterial species involved in inflammatory processes such as the release of LPS or the modulation of IL production; thus, influencing the development of different chronic diseases. There are many studies trying to link either green tea or green tea phenolic compounds to health benefits via gut microbiota. In this review, we tried to summarize the most recent research in the area.

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Epigallocatechin gallate but not catechin prevents nonalcoholic steatohepatitis in mice similar to green tea extract while differentially affecting the gut microbiota

Cited by 60 publications

References 57 publications

Therapeutic effect of Schisandrin A on avian colibacillosis through gut-liver axis

Therapeutic effect of Schisandrin A on avian colibacillosis through gut-liver axis

Catechin‐Rich Green Tea Extract and the Loss‐of‐TLR4 Signaling Differentially Alter the Hepatic Metabolome in Mice with Nonalcoholic Steatohepatitis

Green Tea and Its Relation to Human Gut Microbiome

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