OBJECTIVE To investigate the protective effects and potential mechanism of alisol B 23-acetate on acute alcoholic liver injury in mice. METHODS Fifty male Kunming mice were divided into the blank group， model group， and alisol B 23-acetate low-， medium- and high-dose groups （10， 20， 40 mg/kg）， with 10 mice in each group. Each group was given relevant drug solution or normal saline intragastrically， once a day， for 2 consecutive weeks. On the 15th day， mice in the blank group were given normal saline intragastrically， while the other four groups were given 12 mL/kg white wine intragastrically， twice at six-hour intervals， to establish an acute alcoholic liver injury model. On the 16th day of the experiment， the liver indexes of mice in each group were calculated； the serum levels of alanine transaminase （ALT）， aspartate transaminase （AST）， total cholesterol （TC）， triglycerides （TG）， malondialdehyde （MDA） and glutathione （GSH） were also determined. The histopathological morphology of their liver tissues was observed and scored. The protein expressions of cytochrome P450 2E1 （CYP2E1）， Kelch-like ECH-associated protein 1 （Keap1）， nuclear factor erythroid 2-related factor 2 （Nrf2） and NAD（P）H： quinone oxidoreductase 1 （NQO1） were measured in liver tissue. RESULTS Compared with model group， mice in each dosage group of alisol B 23-acetate showed varying degrees of recovery in body weight， along with improvements in pathological changes in liver tissues such as inflammatory cell infiltration and fatty vacu oles. Their liver indexes， histopathological scores of liver tissue， serum levels of ALT， AST， TC， TG and MDA， as well as the protein expressions of CYP2E1 and Keap1 in liver tissue， were all significantly decreased （ P ＜0.05 or P ＜0.01）. The serum GSH levels and the protein expressions of Nrf2 （except for the alisol B 23-acetate low-dose group） and NQO1 in liver tissue were significantly increased （ P ＜0.05 or P ＜0.01）， and the changes in the above quantitative indicators showed a dose-dependent pattern. CONCLUSIONS Alisol B 23-acetate can ameliorate acute alcoholic liver injury in mice， and its mechanism may be related to improving antioxidant capacity by regulating the Keap1/Nrf2/NQO1 signaling pathway while simultaneously improving liver lipid metabolism-related indexes.

Liver cirrhosis is the final stage of the progression of various chronic liver diseases， often accompanied by serious complications and high mortality rates. Recent studies have shown that the interaction between gut microbiota and bile acid metabolism （the gut microbiota-bile acid axis） is closely associated with liver cirrhosis. This article systematically reviews the mechanism of action of the gut microbiota-bile acid axis in the progression of liver cirrhosis， elaborates on the pathological features of liver cirrhosis and its harm to the body， and summarizes the association of the gut microbiota-bile acid axis with the development and progression of liver cirrhosis. It also analyzes the key regulatory role of this axis in the progression of liver cirrhosis and explores its potential application value as a therapeutic target for liver cirrhosis， in order to provide a theoretical basis for exploring more effective clinical intervention methods.

Objective To explore the effect of NPY on activation of primary microglia and the production of in?terleukin-1β. Methods Rat primary cortical microglia was cultured and divided into control group, LPS group, NPY+LPS group, NPY group and BIBP3226+NPY+LPS group. Microglia in control group were incubated with serum-free me?dium for 6 h;microglia in LPS group were incubated with serum-free medium plus LPS for 6 h;microglia in NPY+LPS group were incubated with serum-free medium plus NPY and LPS for 6 h; microglia cells in NPY group were incubat?ed in serum-free medium plus NPY for 6 h; microglia cells in BIBP3226+NPY+LPS group were incubated in se?rum-free medium including BIBP3226 、NPY and LPS for 6 h. After 6 h , Primary cultured microglia were stained us?ing IBA-1 antibody and examined under the fluorescence microscope. The protein levels of IL-1βin the culture media and the mRNA expression levels of IL-1βin the microglia of different groups were detected using the methods of Elisa and RT-PCR. Results After 6 h, the contents of IL-1 βin the culture media and the mRNA expression levels of IL-1βin the cells of LPS group increased remarkably compared with control group (P<0.05) and the microglia were activat? ed. Compared with LPS group, the contents of IL-1 βin the culture media. the mRNA expression levels of IL-1β and the activity of microglia in LPS+NPY group were significantly decreased .Compared with LPS+NPY group, the contents of IL-1βin the culture media. the mRNA expression levels of IL-1β and the activity of microglia in BIBP3226+NPY+LPS group were increased (P<0.05). There were no significant differences in the contents of IL-1βin the culture media. the mRNA expression levels of IL-1βand the activity of microglia between BIBP3226+NPY+LPS group and LPS group or between NPY group and the control group. Conclusion NPY can inhibit the biological activity of microglia and IL-1βproduction through NPY Y1 receptorin the microglia.