Abstract
Acute pancreatitis (AP) is a life-threatening inflammatory condition of the pancreas. Gentianine (GTN), derived from Gentiana scabra, has been demonstrated to suppress inflammation in various diseases. Nonetheless, the specific effects and related pathways through which GTN influences AP progression remain unclear. Herein, we aimed to elucidate the regulatory effects of GTN on AP. Our results confirmed that the reduction in cell proliferation induced by caerulein could be reversed after GTN treatment (25 µM, 50 µM and 100 µM). Moreover, while caerulein treatment increased cell apoptosis, subsequent GTN treatment reduced this effect, as well as the inflammation provoked by caerulein. Furthermore, activation of the Toll-like receptor 4 (TLR4)/nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) pathway induced by caerulein was counteracted by GTN administration. In summary, this research revealed for the first time that GTN promotes cell proliferation and reduces inflammation and oxidative stress in AR42J cells in a caerulein-induced AP cell model, suggesting that GTN holds promise as an effective therapeutic agent for AP.