IMR Press / FBL / Volume 24 / Issue 5 / DOI: 10.2741/4754

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Qingyi Decoction amerliorates acute biliary pancreatitis by targeting Gpbar1/NF-kb pathway
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1 General Surgery Department, The First Affiliated Hospital of Dalian Medical University, Dalian, China
2 Institute of Integrative Medicine of Dalian Medical University, Dalian, China
*Correspondence: zgx0109@yeah.net (Gui-xin Zhang)
Front. Biosci. (Landmark Ed) 2019, 24(5), 833–848; https://doi.org/10.2741/4754
Published: 1 March 2019
(This article belongs to the Special Issue Leader sequences of coronavirus are altered during infection)
Abstract

Acute biliary pancreatitis (ABP) is a potentially life-threatening disease that is induced by the common bile duct (CBD) sludge or stones. This study aimed to investigate protective effects of Qingyi Decoction (QYT) on deoxycholic-acid-sodium salt (DCA) induced ABP in rats. Gpbar1 is a G-protein coupled receptor that can be activated by DCA. Both Gpbar1 overexpression vector and Gpbar1 RNAi were constructed and transfected into ABP cell models. Functional assays reveal that DCA significantly induced AR42J apoptosis and triggered Gpbar1 expression. Gpbar1 significantly activated caspase 8 and caspase 9 as compared to LV5-NC and LV3-NC (p<0.05). Gpbar1 significantly triggered apoptosis associated inflammatory factors as compared to LV5-NC and LV3-NC (p<0.05). Gpbar1 significantly induced calcium flux as compared to LV5-NC and LV3-NC (p<0.05). Gpbar1 up-regulated caspases and inflammatory factors in DCA treated pancreatic acinar cells. QYT reversed DCA induced apoptosis and inflammatory response. QYT significantly reduced Gpbar1 levels compared to no-QTY treated cells (p<0.05). In conclusion, QYT protects against DCA induced pancreatic acinar cell damage in ABP by inhibiting Gpbar1/NF-kB/p-RIP signaling pathway.

Keywords
Acute biliary pancreatitis
Qingyi Decoction
Gpbar1
NF-kB
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