Mechanism of action of Qingjie Huagong decoction reducing inflammatory response of acute pancreatitis based on PI3K/AKT/NF-κB signaling pathway
- VernacularTitle:基于PI3K/AKT/NF-κB信号通路探讨清解化攻方减轻急性胰腺炎炎症反应的作用机制
- Author:
Xiao-dong ZHU
1
;
Min-chao FENG
;
Kun-rong LIU
;
Ying BAN
;
Pan SU
;
Chuan-feng XUAN
;
Xiao-yi HUANG
;
De-wen LI
;
Xi-ping TANG
;
Guo-zhong CHEN
Author Information
- Publication Type:Journal Article
- Keywords: Qingjie Huagong decoction; PI3K/AKT/NF-κB signaling pathway; acute pancreatitis; inflam-matory response; pancreas; mechanism of action
- From: Chinese Pharmacological Bulletin 2025;41(5):978-984
- CountryChina
- Language:Chinese
- Abstract: Aim To explore the therapeutic effect and mechanism of Qingjie Huagong decoction in modulating PI3K/AKT/NF-κB signaling pathway in inflammatory response of acute pancreatitis(AP)mice.Methods Twenty-four mice were randomly divided into Blank group,Model group,Ustekin group,and Qingjie Hua-gong decoction group,with six mice in each group.The AP model was prepared by using rain frogin.Serum α-AMS,PNLP,IL-1β,IL-6,IL-8,IL-18,and TNF-α lev-els were detected by ELISA;the pancreatic pathology was detected by HE staining;the expressions of PI3K,AKT,and NF-κB-related proteins and mRNAs were de-tected by immunohistochemistry,Western blot,and RT-qPCR.Results Compared with the blank group,the model group showed obvious pathological damage to the pancreas,with significantly higher serum α-AMS,PN-LP,IL-1β,IL-6,IL-8,IL-18,and TNF-α levels(P＜0.01),and significantly higher levels of PI3K,AKT,and NF-κB-related proteins and mRNA expression(P＜0.01).Compared with the model group,both the Qingjie Huagong decoction group and the ustekin group improved the histopathological changes in the pancreas of AP mice,decreased the serum α-AMS,PNLP,IL-1β,IL-6,IL-8,IL-18,and TNF-α levels,and down-reg-ulated the expression levels of pancreatic PI3K,AKT,NF-κB-related proteins and mRNA(P＜0.05 or P＜0.01).Conclusion Qingjie Huagong decoction may inhibit the inflammatory response and protect pancreat-ic tissues by regulating the expression of PI3K/AKT/NF-κB signaling pathway.
