Chai‐Qin‐Cheng‐Qi Decoction and Carbachol Improve Intestinal Motility by Regulating Protein Kinase C‐Mediated Ca²⁺ Release in Colonic Smooth Muscle Cells in Rats with Acute Necrotising Pancreatitis

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 μ g/kg) was given 24 hours after induction of AP. Both CQCQD and carbachol decreased the severity of pancreatic and colonic histopathology (all P < 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‐ β 1) mRNA and PLC protein (both P < 0.05), while both treatments upregulated protein kinase C‐alpha (PKC‐ α ) mRNA and PKC protein and downregulated adenylate cyclase (AC) mRNA and protein compared with no treatment (all P < 0.05). Neither treatment significantly altered L‐arginine‐induced PKC‐ β 1 and PKC‐ ε mRNA reduction. Both treatments significantly increased fluorescence intensity of SMC intracellular calcium concentration (3563.5 and 3046.9 versus 1086.9, both P < 0.01). These data suggest CQCQD and carbachol improve intestinal motility in AP by increasing in colonic SMCs via upregulating PLC, PKC and downregulating AC.