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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

SIBO inhibition effects of TSG.Blended intestinal content sample in each group (45 mg) was cultivated at 37°C for 72 h on blood agar plates. The numbers of colonies were significantly higher in MOD group than CON group in both sexes. TSG treatment reduced the numbers of colonies in a dose-dependent manner. In the meantime, hemolysis extent was also alleviated after TSG treatment. Colony counts (CFU/mL) of each sample were listed below.
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pone.0140346.g002: SIBO inhibition effects of TSG.Blended intestinal content sample in each group (45 mg) was cultivated at 37°C for 72 h on blood agar plates. The numbers of colonies were significantly higher in MOD group than CON group in both sexes. TSG treatment reduced the numbers of colonies in a dose-dependent manner. In the meantime, hemolysis extent was also alleviated after TSG treatment. Colony counts (CFU/mL) of each sample were listed below.

Mentions: At the end of the study, the intestinal contents of rats were cultivated for 72 h on blood agar plates (Fig 2). The number of colonies was significantly higher in the model group, whose members also experienced obvious hemolysis. SIBO was diagnosed in the model group and found to be inhibited in the TSG groups in a dose-dependent manner.


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)

SIBO inhibition effects of TSG.Blended intestinal content sample in each group (45 mg) was cultivated at 37°C for 72 h on blood agar plates. The numbers of colonies were significantly higher in MOD group than CON group in both sexes. TSG treatment reduced the numbers of colonies in a dose-dependent manner. In the meantime, hemolysis extent was also alleviated after TSG treatment. Colony counts (CFU/mL) of each sample were listed below.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0140346.g002: SIBO inhibition effects of TSG.Blended intestinal content sample in each group (45 mg) was cultivated at 37°C for 72 h on blood agar plates. The numbers of colonies were significantly higher in MOD group than CON group in both sexes. TSG treatment reduced the numbers of colonies in a dose-dependent manner. In the meantime, hemolysis extent was also alleviated after TSG treatment. Colony counts (CFU/mL) of each sample were listed below.
Mentions: At the end of the study, the intestinal contents of rats were cultivated for 72 h on blood agar plates (Fig 2). The number of colonies was significantly higher in the model group, whose members also experienced obvious hemolysis. SIBO was diagnosed in the model group and found to be inhibited in the TSG groups in a dose-dependent manner.

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