上睑下垂
活力测定
雷公藤甲素
化学
免疫印迹
腺泡细胞
药理学
细胞凋亡
体内
体外
分子生物学
生物
程序性细胞死亡
胰腺
生物化学
生物技术
基因
作者
MinChao Feng,Baijun Qin,Luo Fang,Hui Li,Kunrong Liu,Kai Li,Dong-yang Wu,Xiping Tang,Guozhong Chen
出处
期刊:Phytomedicine
[Elsevier]
日期:2023-12-01
卷期号:: 155265-155265
被引量:1
标识
DOI:10.1016/j.phymed.2023.155265
摘要
Safer and more effective drugs are needed for the treatment of acute pancreatitis (AP). Qingjie Huagong decoction (QJHGD) has been applied to treat AP for many years and has shown good clinical effects. However, the potential mechanism has not yet been determined. To investigate the role and underlying mechanism of the effects of QJHGD on AP both in vitro and in vivo. QJHGD was characterized by UHPLC-Q-Orbitrap-MS. The protective effect of QJHDG and the underlying mechanism were investigated in MPC-83 cells in vitro. A caerulein-induced AP model was established to evaluate the protective effect of QJHGD in mice. CCK-8 assays were used to detect cell viability. The contents of inflammatory mediators were determined by ELISA. Expression levels of circRNA, miRNA and mRNA were determined by qRT-PCR. Protein expression was determined using Western blot. Pancreatic tissues were assessed by hematoxylin and eosin staining as well as immunohistochemical and immunofluorescence analyses. Pull-down and luciferase activity assays were performed to determine the regulatory relationships of circHipk3, miR-193a-5p and NLRP3. Our results confirmed that mmu-miR-193a-5p was sponged by mmu-circHipk3, and NLRP3 was a target of miR-193a-5p. In vitro experiments showed that QJHGD enhanced MPC-83 cell viability by regulating circHipk3 sponging mir-193a-5 targeting NLRP3 and inhibiting pyroptosis-related factors. Finally, we showed that QJHGD ameliorated pancreatic tissue injury in AP mice via this pathway. This study demonstrate that QJHDG exerted its anti-AP effects via the circHipk3/miR-193a-5p/NLRP3 pathway, revealing a novel mechanism for the therapeutic effect of QJHDG on AP.
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