The utilization of traditional Chinese medicine (TCM) for disease treatment dates back thousands of years. Atractylodis rhizoma (AR) is recognized as a premier TCM and has effective therapeutic properties for gastrointestinal disorders. Nonetheless, the underlying mechanisms by which the ethanolic extract of Atractylodis rhizoma (EEAR) addresses ulcerative colitis (UC) remain ambiguous. This study aimed to clarify the potential molecular mechanisms by which EEAR ameliorated dextran sodium sulfate (DSS)-induced UC in mouse models and Caco-2 cells. EEAR exhibited significant therapeutic effects in UC mice, including decreasing symptoms and reducing inflammation. It also upregulated the expressions of tight junction (TJ) proteins, which enhanced UC intestinal mucosal barrier protection. In addition, EEAR inhibited the expressions of matrix metalloprotein (MMP)-2/9 proteins and inactivated the RhoA/ROCK (Rho-associated kinase)/MLC (myosin light chain) pathway in UC mice. Consistent with the results of in vivo experiments, EEAR significantly increased cell viability and improved the barrier disruption in DSS-induced Caco-2 cells. EEAR increased the expressions of TJ proteins, regulated F-actin cytoskeletal remodeling, and inhibited the expressions of MMP-2/9 proteins and the RhoA/ROCK/MLC pathway. EEAR significantly decreased intestinal pathological injury. Its potential mechanism was related to its inhibition of the RhoA/ROCK/MLC pathway, decreased activation of MMP-2/9, and increased expressions of TJ proteins, thereby regulating cytoskeleton remodeling.
Keywords: RhoA/ROCK/MLC; ethanolic extract of Atractylodis rhizoma; intestinal barrier; tight junction; ulcerative colitis.