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Naturally Occurring Stilbenoid TSG Reverses Non-Alcoholic Fatty Liver Diseases via Gut-Liver Axis.

Lin P, Lu J, Wang Y, Gu W, Yu J, Zhao R - PLoS ONE (2015)

Bottom Line: TSG regulated gut microbiota balanced and increased the protein expression of ZO-1 and occludin, which could improve the function of the intestinal mucosal barrier and reduce serum LPS content by about 25%.TSG reduced TL4 levels by 56% and NF-κB expression by 23% relative to the NAFLD model group.This suggests that prevention of NAFLD by TSG in HFD-fed rats is mediated by modulation of the gut microbiota and TLR4/NF-κB pathway, which may alleviate chronic low-grade inflammation by reducing the exogenous antigen load on the host.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacy, Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan Province, China.

ABSTRACT
The gut-liver axis is largely involved in the development of non-alcoholic fatty liver disease (NAFLD). We investigated whether 2, 3, 5, 4'-tetrahydroxy-stilbene-2-O-β-D-glucoside (TSG) could reverse NAFLD induced by a high-fat diet (HFD) and whether it did so via the gut-liver axis. Results showed that TSG could reduce the accumulation of FFA and it did so by reducing the expression of L-FABP and FATP4. TSG regulated gut microbiota balanced and increased the protein expression of ZO-1 and occludin, which could improve the function of the intestinal mucosal barrier and reduce serum LPS content by about 25%. TSG reduced TL4 levels by 56% and NF-κB expression by 23% relative to the NAFLD model group. This suggests that prevention of NAFLD by TSG in HFD-fed rats is mediated by modulation of the gut microbiota and TLR4/NF-κB pathway, which may alleviate chronic low-grade inflammation by reducing the exogenous antigen load on the host.

No MeSH data available.


Related in: MedlinePlus

TSG and enterogenous endotoxin and intestinal mucosal barrier.(A) Contents of LPS in hepatic portal vein. LPS levels in hepatic portal vein blood samples were measured using a tachypleus amebocyte lysate test (mean±SD, n = 7). Statistical significance: * p< 0.05 vs. control;** p< 0.01 vs. control;*** p< 0.001 vs. control; # p< 0.05 vs. model; ## p< 0.01 vs. model; ### p< 0.001 vs. model. (B) Comparison of microscopic morphology in ileum tissue among CON, MOD and TSG.M group. Secional representations (100 ×magnification, haematoxylin and eosin stain) of ileum tissues. Degeneration and necrosis of ileum were relieved after TSG treatment. (C) The contents of ZO-1 and occludin. Expressions of occludin and ZO-1 in one representative intestine sample in each group were tested using flow cytometry, respectively. Single-cell suspensions were incubated with anti-occludin and anti-ZO-1 antibody for 2 h and then incubated with FITC in the dark for 1 h.Tight junctions proteins, such as occludin and ZO-1, were dramatically reduced in high fatd diet fed rats. These reductions might be lighted
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pone.0140346.g004: TSG and enterogenous endotoxin and intestinal mucosal barrier.(A) Contents of LPS in hepatic portal vein. LPS levels in hepatic portal vein blood samples were measured using a tachypleus amebocyte lysate test (mean±SD, n = 7). Statistical significance: * p< 0.05 vs. control;** p< 0.01 vs. control;*** p< 0.001 vs. control; # p< 0.05 vs. model; ## p< 0.01 vs. model; ### p< 0.001 vs. model. (B) Comparison of microscopic morphology in ileum tissue among CON, MOD and TSG.M group. Secional representations (100 ×magnification, haematoxylin and eosin stain) of ileum tissues. Degeneration and necrosis of ileum were relieved after TSG treatment. (C) The contents of ZO-1 and occludin. Expressions of occludin and ZO-1 in one representative intestine sample in each group were tested using flow cytometry, respectively. Single-cell suspensions were incubated with anti-occludin and anti-ZO-1 antibody for 2 h and then incubated with FITC in the dark for 1 h.Tight junctions proteins, such as occludin and ZO-1, were dramatically reduced in high fatd diet fed rats. These reductions might be lighted

Mentions: LPS, a cell-wall component of gram-negative bacteria, delivered to the liver via the portal vein in endotoxemia. Such endotoxin production by gut microbiota can cause chronic low-grade inflammation in patients with NAFLD. After the rats were fed HFD for 12 weeks, the LPS level in NAFLD group was significantly higher than in the normal group (P < 0.01) in both sexes (Fig 4A). Fortunately, TSG showed a satisfactory effect with respect to the inhibition of the rise of LPS, in a dose-dependent manner, especially among male rats. This inhibition effect may be related to its beneficial effects on gut microbiota equilibrium.


Naturally Occurring Stilbenoid TSG Reverses Non-Alcoholic Fatty Liver Diseases via Gut-Liver Axis.

Lin P, Lu J, Wang Y, Gu W, Yu J, Zhao R - PLoS ONE (2015)

TSG and enterogenous endotoxin and intestinal mucosal barrier.(A) Contents of LPS in hepatic portal vein. LPS levels in hepatic portal vein blood samples were measured using a tachypleus amebocyte lysate test (mean±SD, n = 7). Statistical significance: * p< 0.05 vs. control;** p< 0.01 vs. control;*** p< 0.001 vs. control; # p< 0.05 vs. model; ## p< 0.01 vs. model; ### p< 0.001 vs. model. (B) Comparison of microscopic morphology in ileum tissue among CON, MOD and TSG.M group. Secional representations (100 ×magnification, haematoxylin and eosin stain) of ileum tissues. Degeneration and necrosis of ileum were relieved after TSG treatment. (C) The contents of ZO-1 and occludin. Expressions of occludin and ZO-1 in one representative intestine sample in each group were tested using flow cytometry, respectively. Single-cell suspensions were incubated with anti-occludin and anti-ZO-1 antibody for 2 h and then incubated with FITC in the dark for 1 h.Tight junctions proteins, such as occludin and ZO-1, were dramatically reduced in high fatd diet fed rats. These reductions might be lighted
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4608713&req=5

pone.0140346.g004: TSG and enterogenous endotoxin and intestinal mucosal barrier.(A) Contents of LPS in hepatic portal vein. LPS levels in hepatic portal vein blood samples were measured using a tachypleus amebocyte lysate test (mean±SD, n = 7). Statistical significance: * p< 0.05 vs. control;** p< 0.01 vs. control;*** p< 0.001 vs. control; # p< 0.05 vs. model; ## p< 0.01 vs. model; ### p< 0.001 vs. model. (B) Comparison of microscopic morphology in ileum tissue among CON, MOD and TSG.M group. Secional representations (100 ×magnification, haematoxylin and eosin stain) of ileum tissues. Degeneration and necrosis of ileum were relieved after TSG treatment. (C) The contents of ZO-1 and occludin. Expressions of occludin and ZO-1 in one representative intestine sample in each group were tested using flow cytometry, respectively. Single-cell suspensions were incubated with anti-occludin and anti-ZO-1 antibody for 2 h and then incubated with FITC in the dark for 1 h.Tight junctions proteins, such as occludin and ZO-1, were dramatically reduced in high fatd diet fed rats. These reductions might be lighted
Mentions: LPS, a cell-wall component of gram-negative bacteria, delivered to the liver via the portal vein in endotoxemia. Such endotoxin production by gut microbiota can cause chronic low-grade inflammation in patients with NAFLD. After the rats were fed HFD for 12 weeks, the LPS level in NAFLD group was significantly higher than in the normal group (P < 0.01) in both sexes (Fig 4A). Fortunately, TSG showed a satisfactory effect with respect to the inhibition of the rise of LPS, in a dose-dependent manner, especially among male rats. This inhibition effect may be related to its beneficial effects on gut microbiota equilibrium.

Bottom Line: TSG regulated gut microbiota balanced and increased the protein expression of ZO-1 and occludin, which could improve the function of the intestinal mucosal barrier and reduce serum LPS content by about 25%.TSG reduced TL4 levels by 56% and NF-κB expression by 23% relative to the NAFLD model group.This suggests that prevention of NAFLD by TSG in HFD-fed rats is mediated by modulation of the gut microbiota and TLR4/NF-κB pathway, which may alleviate chronic low-grade inflammation by reducing the exogenous antigen load on the host.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacy, Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan Province, China.

ABSTRACT
The gut-liver axis is largely involved in the development of non-alcoholic fatty liver disease (NAFLD). We investigated whether 2, 3, 5, 4'-tetrahydroxy-stilbene-2-O-β-D-glucoside (TSG) could reverse NAFLD induced by a high-fat diet (HFD) and whether it did so via the gut-liver axis. Results showed that TSG could reduce the accumulation of FFA and it did so by reducing the expression of L-FABP and FATP4. TSG regulated gut microbiota balanced and increased the protein expression of ZO-1 and occludin, which could improve the function of the intestinal mucosal barrier and reduce serum LPS content by about 25%. TSG reduced TL4 levels by 56% and NF-κB expression by 23% relative to the NAFLD model group. This suggests that prevention of NAFLD by TSG in HFD-fed rats is mediated by modulation of the gut microbiota and TLR4/NF-κB pathway, which may alleviate chronic low-grade inflammation by reducing the exogenous antigen load on the host.

No MeSH data available.


Related in: MedlinePlus