NF-κB/Bcl-2/Caspase 3信号通路与吲哚美辛作用机制的综述与假说：急性胰腺炎胃肠道功能受损的潜在机制研究

Review and Hypothesis on the NF-κB/Bcl-2/Caspase 3 Signaling Pathway and the Mechanism of Action of Indomethacin: Research on the Potential Mechanism of Gastrointestinal Dysfunction in Acute Pancreatitis

摘要: 急性胰腺炎是一种严重的炎症性疾病，可导致胃肠道功能障碍，增加病死率。NF-κB信号通路在急性胰腺炎的炎症反应中起关键作用，其激活可诱导多种炎症因子和抗凋亡蛋白的表达，加剧炎症并影响细胞存活。Bcl-2/Caspase 3信号通路也与急性胰腺炎的发展密切相关，调节细胞凋亡过程。NF-κB信号通路与Bcl-2/Caspase 3信号通路存在联系，NF-κB的激活可影响Bcl-2家族蛋白的表达，进而调控细胞凋亡。吲哚美辛是一种非甾体类抗炎药，已被发现可降低急性胰腺炎的风险并减轻胰腺损伤，但其具体机制尚不明确。吲哚美辛是否可以抑制NF-κB信号通路的激活还有待探索，未来可进一步研究吲哚美辛在调节NF-κB和Bcl-2/Caspase 3信号通路中的作用，从而缓解急性胰腺炎引起的胃肠道损伤。

Abstract: Acute pancreatitis is a severe inflammatory condition that can lead to gastrointestinal dysfunction and increased mortality. The NF-κB signaling pathway plays a key role in the inflammatory response of acute pancreatitis; its activation induces the expression of various inflammatory cytokines and anti-apoptotic proteins, thereby exacerbating inflammation and affecting cell survival. The Bcl-2/Caspase 3 signaling pathway is also closely associated with the progression of acute pancreatitis, regulating the process of cell apoptosis. There is crosstalk between the NF-κB and Bcl-2/Caspase 3 pathways—activation of NF-κB can influence the expression of Bcl-2 family proteins, thereby modulating apoptosis. Indomethacin, a nonsteroidal anti-inflammatory drug, has been found to reduce the risk of acute pancreatitis and alleviate pancreatic injury, but its precise mechanism remains unclear. Whether indomethacin can suppress the activation of the NF-κB signaling pathway warrants further investigation. Future studies may explore the role of indomethacin in modulating both the NF-κB and Bcl-2/Caspase 3 pathways to mitigate gastrointestinal damage caused by acute pancreatitis.