Anti-Fibrotic Effects of Gut-Microbiome on Liver = Anti-Fibrotic Effects of Gut-Microbiome on Liver

다국어 초록 (Multilingual Abstract)

Aims: Treatment for liver cirrhosis is intended to slow the progression and deterioration of liver function. Although many studies have shown that microbiome is an important factor in improving liver disease progression through the gut-liver axis, the exact mechanism is still unknown. The microbiome in the gut regulates nutrient metabolism and immune response and interacts closely with the host if the gut microbiome can suppress the progression of liver cirrhosis and analyze clinical data. Therefore, our study aim is to suppress the progression of liver fibrosis due to the modulation of gut-microbiome.
Methods: Liver cirrhosis in mice was induced by DDC (3,5-diethoxycarboncyl-1,4-dihydrocollidine) diet. 6-week-old male C57BL/6J mice were divided into 5 groups (n=10/group; normal, liver fibrosis-induced control, strain X, L. lactis, and UDCA). Strain X group was given the strain X twice a week [109 CFU/g, 4-week]. Gene expression was compared and analyzed through mRNA sequencing analysis of mouse hepatic stellate cells in the DDC model.
Results: The Strain X showed improvement in the Staging level and Sirius red areas compared to the fibrosis group induced by the DDC diet (P<0.05). The levels of the liver fibrosis markers TIMP1 (P=0.02), Col1a (P<0.001), and TGF-ß (P<0.001) were decreased in the Strain X group compared with fibrosis models. When HSCs were isolated, expression of TIMP1 (P=0.38) and Col1a (P=0.055) decreased in strain X. Strain X compared to DDC in the mRNA sequencing, the up-regulated gene is Ecm1, Fos, Serpina1e and the down-regulated gene is Cd5l, Cd63, Marco (P<0.03).
Conclusions: Strain X improved fibrosis by modulating the gut microbial composition in a mouse model induced cirrhosis.