Full text loading...
Sepsis is a critical illness with high morbidity and mortality, particularly due to gastrointestinal complications. Despite improvements in therapeutic strategies, effective pharmacological treatments remain lacking. Banxia Xiexin Decoction (BXD), a traditional Chinese formula, has shown potential in regulating intestinal function. This study aimed to investigate the therapeutic effects and underlying molecular mechanisms of BXD in sepsis-induced intestinal injury, focusing on the PINK1/Parkin pathway.
Human intestinal epithelial cell (HIEC) injury induced by lipopolysaccharide (LPS) and a cecal ligation and perforation (CLP) rat model of sepsis were used. Experimental groups received BXD at varying doses, while PINK1 knockdown HIECs were used to assess mechanistic pathways. ELISA was employed to measure IL-6, IL-1β, IFABP, and DAO levels. Pathological changes were assessed by H&E staining, while tight junction proteins (ZO-1, Occludin), TOM20, mitochondrial membrane potential, and autophagy markers (PINK1, Parkin, LC3, p62) were analyzed via immunohistochemistry, immunofluorescence, flow cytometry, Western blot, and RT-PCR.
BXD treatment significantly reduced IL-6, IL-1β, DAO, and IFABP levels compared with controls. It restored ZO-1 and Occludin expression, improving intestinal mucosal barrier function. In septic rats, BXD enhanced TOM20 expression, preserved mitochondrial membrane potential, and upregulated the PINK1/Parkin-mediated mitophagy pathway. These effects collectively reduced inflammation, mitochondrial dysfunction, and intestinal damage.
Findings suggest that BXD exerts protective effects against sepsis-induced intestinal injury by reducing systemic inflammation and promoting mitochondrial homeostasis through the activation of PINK1/Parkin-mediated mitophagy.
BXD alleviates intestinal mucosal damage and systemic inflammation in sepsis, offering a promising therapeutic approach by targeting mitochondrial autophagy.
Article metrics loading...
Full text loading...
References
Data & Media loading...