急性胰腺炎(AP)是严重危害人类健康的疾病，在AP过程中腺泡细胞凋亡具有保护作用，保护机制尚未明确。微小RNA（microRNA）作为基因转录后表达调控因子，寻找凋亡相关miRNA（AAmiRNA）可能是研究AP过程中凋亡保护机制及治疗的新突破口。我们前期研究鉴定了凋亡相关 miR-22和miR-135a，鉴定靶基因分别为ERBB3 和Ptk2，miR-22和miR-135a可能通过调控靶基因诱导AP腺泡细胞凋亡，进一步研究应用染色质免疫共沉淀（ChIP）、凝胶迁移实验(EMSA)、腺相关病毒等技术研究miR-22和miR-135a 调控网络中上游转录因子、下游信号通路基因的表达，以及体内实验中诱导胰腺腺泡细胞的凋亡发挥保护机制。本项目首次从miRNA水平研究AP发病中腺泡细胞AAmiRNA，阐明miR-22和miR-135a对AP腺泡细胞凋亡的调控机制，为AP的治疗开辟了新的方向.

Acute pancreatitis is a common clinical condition with a watchable morbidity and mortality. There were two patterns of pancreatic acinar cell death: apoptosis and necrosis in acute pancreatitis. The apoptosis has protecting effect in acute pancreatitis, and the mechanism of phenomena is unclear. MicroRNAs are short non-coding RNAs and play important regulating genes expression roles in multiply processes including development, cell proliferation, cell differentiation, apoptosis, and metabolism. The finding of apoptosis associated miRNA (AAmiRNA) might be a new breakthrough for the treatment programs. The results of pilot studies indicated that miR-22 and miR-135a were identified as apoptosis associated miRNA. We also demonstrated that miR-22 and miR-135a might promote the apoptosis of pancreatic acinar cell by repressing their target genes ERBB3 and Ptk2 in vitro. But the up-stream and down-stream of the signal pathway of miR-22 and miR-135a are still unknown. In this project, We would find out the regulation mechanism that promote the apoptosis of pancreatic acinar cell of miR-22 and miR-135a in vivo and in vitro, which could provide a new therapeutic targets for the prevention and treatment of acute pancreatitis.