To investigate the intervention effects of Astragalus polysaccharide on peritoneal fibrosis related to peritoneal dialysis in mice and its possible mechanisms.

Male C57BL/6 mice were randomly divided into a blank control group (Control), a model group (Model), a low-dose group of Astragalus polysaccharide (APS 100 mg/kg) and a high-dose group of Astragalus Polysaccharide (APS 200 mg/kg), with 10 mice in each group. A mouse model of peritoneal fibrosis was established using high-glucose peritoneal dialysis fluid, and the treatment was administered daily for 28 days. After the final treatment, peritoneal function (glucose transport and urea nitrogen levels) was assessed. Hematoxylin-eosin staining (HE) and Masson staining were performed to observe the pathological changes, fibrosis and peritoneal thickness. Western blot analysis was conducted to detect the expressions of epithelial-mesenchymal transition (EMT) related proteins in peritoneal tissue. The immunohistochemistry and flow cytometry methods were used to assess the expressions of macrophage polarization-related proteins in peritoneal tissue.

Compared to the Control group, the Model group showed significant increases in peritoneal thickness and collagen fiber deposition, elevated glucose transport and higher urea nitrogen levels. The expressions of EMT-related proteins[α-smooth muscle actin (α-SMA), collagen Ⅲ, fibronectin)]significantly increased, while E-cadherin protein expression significantly decreased, and M2 macrophage markers[Arginase-1 (Arg-1), CD163]were significantly elevated. In comparison to the Model group, the treatment with Astragalus polysaccharide led to significant improvements in the above indicators, with the high-dose group showing better effects than the low-dose group. After the clearance of macrophages, the inhibitory effect of Astragalus polysaccharide on the peritoneal fibrosis was weakened.

Astragalus polysaccharide inhibits the peritoneal fibrosis in mice by suppressing epithelial-mesenchymal transition and regulating M2 macrophage polarization.