Houpu Sanwu decoction alleviates rat intraperitoneal adhesion by regulating macrophage polarization and inhibiting inflammatory responses.

Intraperitoneal adhesion frequently occurs after abdominal surgery, substantially affecting patients' quality of life. This study evaluated the therapeutic effect of Houpu Sanwu decoction on intraperitoneal adhesion and its possible molecular mechanism. Thirty-six male Sprague Dawley rats were randomly assigned to sham, control, fluvastatin and low-, medium-, and high-concentration Hopu Sanwu decoction groups. All groups, except for the sham group, underwent abdominal adhesion modeling. Hematoxylin and eosin staining was conducted to observe the pathological changes in peritoneal tissue. Masson staining was used to observe the development of collagen fibers within the adhesive tissues. The protein levels of MCP-1 in adhesion tissues were detected using immunohistochemistry. The serum levels of IL-1, IL-6, TNF-α, IL-4, and IL-10 were detected using ELISA. RT-PCR and western blotting were utilized to identify the expression levels of the SOCS/JAK2/STAT/PPAR-γ pathway. The occurrence of intraperitoneal adhesion decreased in the low-, medium-, and high-concentration Hopu Sanwu decoction groups compared with the control group, with the most significant decrease observed in the medium-concentration group (P < 0.05). Following Hopu Sanwu decoction treatment, MCP-1 protein expression in adhesive tissue significantly decreased (P < 0.05). Furthermore, markers associated with M1-type macrophages, such as IL-1, IL-6, and TNF-α, exhibited decreased expression levels, whereas markers of M2-type macrophages, such as IL-4 and IL-10, increased post-Hopu Sanwu decoction treatment. Additionally, Hopu Sanwu decoction can activate the SOCS1/STAT6/PPAR-γpathway, inhibit the SOCS3/JAK2/STAT1 pathway, and promote the polarization of macrophages toward M2. These results suggest that Hopu Sanwu decoction is effective in alleviating intraperitoneal adhesion, possibly by inducing M2-type macrophage polarization and modulating the SOCS/JAK2/STAT/PPAR-γ pathway.