Baicalin ameliorates acute pancreatitis through inhibiting the activation of cGAS/STING signaling pathway

Baicalin, a compound derived from natural sources, has demonstrated potential for alleviating inflammation and pain associated with acute pancreatitis (AP). This study aimed to evaluate the therapeutic efficacy and underlying mechanisms of baicalin in AP.

The role of baicalin in AP was evaluated both in vivo and in vitro. Pancreatic damage was assessed via histopathological examinations and serum enzyme measurements. The activation of the cGAS/STING signaling pathway was investigated under AP conditions both in vivo and in vitro. Knockdown of cGAS was employed to validate the involvement of the cGAS/STING signaling pathway in AP. Additionally, overexpression of cGAS and an agonist of STING were utilized to explore the mechanisms through which baicalin alleviates AP. Baicalin significantly reduced serum levels of lipase and amylase and alleviated pancreatic edema. Following treatment with baicalin, apoptosis and reactive oxygen species (ROS) levels in AP mice were diminished, as indicated by results from TUNEL and DHE staining assays. In both in vivo and in vitro studies, baicalin notably inhibited the expression of the cGAS/STING signaling pathway, along with downstream factors, including NLRP3, IL-1β, and IL-18. Knockdown of cGAS resulted in a significant reduction of apoptosis and inflammation in the pancreatic acinar cell line AR42J. Conversely, both genetic and pharmacological overexpression of cGAS/STING pathway negated the protective effects of baicalin on anti-apoptosis and anti-inflammation.

In conclusion, our data suggest that baicalin may attenuate AP by suppressing the cGAS/STING signaling pathway.