Effect and mechanism of Rabdosia rubescens on ulcerative colitis: Network pharmacology combined with in vivo experiments.
Zhang J, Zheng M, Liu X, Li L, Wang J
Summary
PubMedA traditional medicinal herb called Rabdosia rubescens can treat ulcerative colitis in mice by reducing inflammation, strengthening the gut barrier, and promoting tissue healing through a specific cellular pathway.
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Key Findings
RR significantly reduced disease activity index scores and weight loss while strengthening the intestinal barrier through increased tight junction protein expression in UC mice
RR enhanced colonic mucus production and promoted regeneration of intestinal lining cells, critical for gut protection and healing
Network pharmacology and Western blot analysis identified the PI3K/AKT signaling pathway as the mechanism, with RR reducing levels of p-PI3K and p-AKT in colon tissue
Original Abstract
Rabdosia rubescens (Hemsl.) H.Hara (RR), a medicinal and edible herb with a long history of use in the folk medicine, exhibits notable antimicrobial and anti-inflammatory effects against various inflammation-related conditions. However, contemporary pharmacological evidence supporting its therapeutic potential for ulcerative colitis (UC) remains limited. This study integrated in vivo experimentation and network pharmacology to explore the underlying mechanisms of RR in treating UC, providing a mechanistic framework for its therapeutic effects. Acute UC was induced in murine models by administration a 3 % DSS solution. RR's therapeutic efficacy was assessed through longitudinal monitoring of body weight changes, disease activity index (DAI) scoring, histopathological analysis of colonic tissues, and evaluation of tight junction protein expression. Mechanistic insights were derived from integrated network pharmacology analysis, supplemented by Western blot validation of key signaling effectors. RR effectively alleviated weight loss, reduced the DAI scores, attenuated colonic inflammation, improved tissue atrophy, and mitigated pathological damage in UC mice. Additionally, RR enhanced colonic mucus secretion vital for intestinal protection, and promoted epithelial cells regeneration, crucial for gut health. By up-regulating tight junction protein expression, RR maintained the integrity of the intestinal mucosal barrier. Network pharmacology analysis indicated that the PI3K/AKT signaling pathway as a potential molecular target of RR's anti-UC effects. Western blot analysis confirmed that RR intervention significantly reduced the expression of key signaling molecules, p-PI3K and p-AKT, involved in PI3K/AKT pathway activation within the colonic tissues of the UC model. RR shows significant therapeutic potential in DSS-induced UC models, with its efficacy linked to the suppression of PI3K/AKT pathway activation, providing critical evidence for the mechanistic basis of RR's anti-UC effects.
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