Objective: To investigate the role of gut microbiota in the amelioration of liver fibrosis induced by CCl4 in mice by 3-methyladenine (3-MA). Methods: Fifteen mice were randomly divided into normal control group, liver fibrosis group and 3-MA treatment group. The liver fibrosis model was established by injecting CCl4, and the mice in the 3-MA treatment group were injected 3-MA additionally from the third week onwards. After 8 weeks, all of the mice were sacrificed and their blood, liver tissue and fecal samples were collected to analyze serum ALT, AST, GGT levels, liver histopathology and gut microbiota. Results: Compared with the liver fibrosis group, serum ALT and AST levels in 3-MA treatment group decreased obviously ([68.6±4.2] U/L vs [111.0±7.8] U/L, [179.0±12.9] U/L vs [253.2±26.7] U/L, P＜0.01), and the degree of hepatic histopathological changes was reduced. The intestinal flora in three groups were distinguished by principal coordinate analysis (PCoA) and non-metric multi-dimensional scaling (NMDS) analysis. Compared with the normal control group, there were decreased Alpha diversity of intestinal community, reduced significantly abundance of Lachnospiraceae, and increased obviously abundance of Actinobacteria and Desulfovibrionacea in the liver fibrosis group (P＜0.05). Compared with the liver fibrosis group, there were increased Alpha diversity of intestinal community, increased significantly abundance of Lachnospiraceae and Blautia, and reduced abundance of Bifidobacteriaceae in the 3-MA treatment group (P＜0.05). In addition, the abundance of Lactobacillaceae in the 3-MA treatment group was significantly higher than that in the normal control group (P＜0.05). Conclusion 3-MA improves the liver fibrosis of mice induced by CCl4, and gut microbiota may play an active role in this process.

Polycystic ovary syndrome （PCOS） is a reproductive endocrine disorder characterized by coexisting reproductive dysfunction and glucolipid metabolic disturbance， affecting 8%-13% of women of reproductive age and 3%-11% of adolescent females. Due to the highly heterogeneous clinical features， symptom-oriented individualized strategies are commonly adopted for the treatment of PCOS. Chronic low-grade inflammation is one of the core mechanisms for the occurrence of PCOS. Macrophages， as foundational cells of innate immunity， play an indispensable role in modulating systemic inflammatory responses. The imbalance of macrophage M1/M2 polarization is involved in chronic low-grade inflammation in PCOS via pathways such as activating pro-inflammatory responses， disrupting ovarian tissue repair， stimulating excessive synthesis of androgens， and promoting the occurrence of insulin resistance. Reshaping the phenotype of macrophages might serve as a potential therapeutic strategy for PCOS. Traditional Chinese medicine （TCM） holds that spleen deficiency and phlegm dampness is a crucial pathogenesis of PCOS. The spleen， being in charge of defensive function， plays a key role in ensuring normal physiological functions such as transportation and defense against external pathogen during the occurrence and development of PCOS. The imbalance of macrophage polarization resembles the transition from spleen being in charge of defensive function to spleen losing its defensive role in TCM. Therefore， this paper， for the first time， explores the deep connection between macrophage polarization and the pathogenesis of chronic low-grade inflammation in PCOS from the TCM theory of spleen being in charge of defensive function， providing theoretical support and new research directions for the treatment and drug research of PCOS.