Baicalin, the main active component of Scutellaria baicalensis, has antioxidant and anti-apoptotic effects and is used to treat acute pancreatitis; however, its specific mechanism is unclear. This study aims to determine the protective effect and underlying mechanism of baicalin on AR42J pancreatic acinar cell injury. AR42J acinar cells (caerulein, 10 nmol/L) were induced in vitro to establish a cell model for acute pancreatitis. Cell relative survival was measured by thiazolyl blue tetrazolium bromide, and cell apoptosis and death were examined by flow cytometry. The expression levels of superoxide dismutase1 (SOD1), Bax, survivin, Bcl-2, caspase-3, and caspase-7 proteins were analyzed by Western blot, and those of SOD1 mRNA and miR-136-5p were determined by RT-PCR. The activities of GSH, SOD1, ROS, and MDA were also investigated. Compared with those of the caerulein group, the relative survival rate and activity of AR42J pancreatic acinar cells with different baicalin concentrations were significantly increased (p < 0.05), and the supernatant amylase level was markedly decreased (p < 0.05). In addition, the ROS and MDA activities and mir-136-5p expression were significantly decreased, and the GSH activities and SOD1 gene and protein expression levels were markedly increased (p < 0.05). These results suggest that baicalin reduced the caerulein-induced death of AR42J acinar cells and alleviated the caerulein-induced injury in pancreatic acinar cells by inhibiting oxidative stress. The mechanism may be related to the decreased expression of Mir-136-5p and the increased expression of SOD1 gene and protein.

黄芩苷是黄芩的主要活性成分，具有抗氧化、抗细胞凋亡作用，用于治疗急性胰腺炎；但其具体机​​制尚不清楚。本研究旨在确定黄芩苷对AR42J胰腺腺泡细胞损伤的保护作用及其潜在机制。体外诱导AR42J腺泡细胞（雨伞素，10 nmol/L）建立急性胰腺炎细胞模型。通过溴化噻唑蓝四唑测定细胞相对存活率，并通过流式细胞术检测细胞凋亡和死亡。采用Western blot法检测超氧化物歧化酶1（SOD1）、Bax、survivin、Bcl-2、caspase-3、caspase-7蛋白的表达水平，RT-PCR检测SOD1 mRNA和miR-136-5p的表达水平。 。还研究了 GSH、SOD1、ROS 和 MDA 的活性。与雨蛙素组相比，不同黄芩苷浓度的AR42J胰腺腺泡细胞相对存活率和活性均显着升高（p  < 0.05），上清淀粉酶水平显着降低（p  < 0.05）。此外，ROS和MDA活性以及mir-136-5p表达显着降低，GSH活性以及SOD1基因和蛋白表达水平显着升高（p  < 0.05）。这些结果表明，黄芩苷通过抑制氧化应激，减少了雨蛙素诱导的AR42J腺泡细胞死亡，并减轻了雨蛙素诱导的胰腺腺泡细胞损伤。其机制可能与Mir-136-5p表达减少、SOD1基因和蛋白表达增加有关。