Chai-Qin-Cheng-Qi Decoction Improves Intestinal Motility by Regulating Protein Kinase C-and Adenylate Cyclase-Mediated Ca<SUP>2+</SUP> Release in Colonic Smooth Muscle Cells in Rats With Acute Necrotizing Pancreatitis



Lin, ZQ, Guo, J, Chen, WW, Deng, LH, Zhang, XY ORCID: 0000-0001-9116-1253, Huang, W, Windsor, JA, Sutton, R ORCID: 0000-0001-6600-562X, Xue, P and Xia, Q
(2016) Chai-Qin-Cheng-Qi Decoction Improves Intestinal Motility by Regulating Protein Kinase C-and Adenylate Cyclase-Mediated Ca<SUP>2+</SUP> Release in Colonic Smooth Muscle Cells in Rats With Acute Necrotizing Pancreatitis. PANCREAS, 45 (10). p. 1519.

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Abstract

Chai-Qin-Cheng-Qi decoction (CQCQD) improves intestinal motility in acute pancreatitis (AP), but the mechanism(s) require elucidation. We investigated the effects of CQCQD and carbachol, a prokinetic agent, on colonic smooth muscle cells (SMCs) in L-arginine-induced necrotising AP model in rats. In treatment groups, intragastric CQCQD (20 g/kg, 2 hourly × 3 doses) or intraperitoneal carbachol (60 <i>μ</i>g/kg) was given 24 hours after induction of AP. Both CQCQD and carbachol decreased the severity of pancreatic and colonic histopathology (all <i>P</i> < 0.05). Both CQCQD and carbachol reduced serum intestinal fatty acid binding protein, vasoactive intestinal peptide, and substance P and increased motility levels. CQCQD upregulated SMC phospholipase C-beta 1 (PLC-<i>β</i>1) mRNA and PLC protein (both <i>P</i> < 0.05), while both treatments upregulated protein kinase C-alpha (PKC-<i>α</i>) mRNA and PKC protein and downregulated adenylate cyclase (AC) mRNA and protein compared with no treatment (all <i>P</i> < 0.05). Neither treatment significantly altered L-arginine-induced PKC-<i>β</i>1 and PKC-<i>ε</i> mRNA reduction. Both treatments significantly increased fluorescence intensity of SMC intracellular calcium concentration [Ca<sup>2+</sup>]<sub>i</sub> (3563.5 and 3046.9 versus 1086.9, both <i>P</i> < 0.01). These data suggest CQCQD and carbachol improve intestinal motility in AP by increasing [Ca<sup>2+</sup>]<sub>i</sub> in colonic SMCs via upregulating PLC, PKC and downregulating AC.

Item Type: Article
Uncontrolled Keywords: Digestive Diseases, 2.1 Biological and endogenous factors, 2 Aetiology, Oral and gastrointestinal
Depositing User: Symplectic Admin
Date Deposited: 23 Jan 2019 15:47
Last Modified: 16 Mar 2024 12:47
DOI: 10.1155/2017/5864945
Open Access URL: https://www.hindawi.com/journals/ecam/2017/5864945...
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URI: https://livrepository.liverpool.ac.uk/id/eprint/3031698