Chai-Qin-Cheng-Qi Decoction and Carbachol Improve Intestinal Motility by Regulating Protein Kinase C-Mediated Ca(2+) Release in Colonic Smooth Muscle Cells in Rats with Acute Necrotising Pancreatitis.
Chai-Qin-Cheng-Qi Decoction and Carbachol Improve Intestinal Motility by Regulating Protein Kinase C-Mediated Ca(2+) Release in Colonic Smooth Muscle Cells in Rats with Acute Necrotising Pancreatitis.
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柴芩承气汤和卡巴胆碱通过调节蛋白激酶C介导的急性坏死性胰腺炎大鼠结肠平滑肌细胞Ca2+释放来改善肠蠕动
DOI：
10.1155/2017/5864945
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Xia Q
中科院分区：
文献类型：
--
作者：
Zhang CL;Lin ZQ;Luo RJ;Zhang XX;Guo J;Wu W;Shi N;Deng LH;Chen WW;Zhang XY;Bharucha S;Huang W;Sutton R;Windsor JA;Xue P;Xia Q
柴芩承气汤（CQCQD）改善急性胰腺炎（AP）患者肠道蠕动，但其作用机制尚不清楚。我们研究了CQCQD和促动力学剂carbachol对l -精氨酸诱导的大鼠坏死性AP模型结肠平滑肌细胞（SMCs）的影响。治疗组在AP诱导24 h后灌胃CQCQD （20 g/kg， 2 h × 3剂量）或腹腔灌胃carbachol (60 μg/kg)， CQCQD和carbachol均可降低胰腺和结肠组织病理的严重程度（均P < 0.05）。CQCQD和carbachol均可降低血清肠脂肪酸结合蛋白、血管活性肠肽和P物质，并增加运动性水平。CQCQD上调SMC磷脂酶c -β1 (PLC-β1) mRNA和PLC蛋白（均P < 0.05），上调蛋白激酶c -α (PKC-α) mRNA和PKC蛋白，下调腺苷酸环化酶（AC） mRNA和蛋白（均P < 0.05）。两种处理均未显著改变l -精氨酸诱导的PKC-β1和PKC-ε mRNA的减少。两种处理均显著提高了SMC细胞内钙浓度[Ca2+]i的荧光强度（3563.5和3046.9比1086.9，P均< 0.01）。这些数据表明，CQCQD和carbachol通过上调PLC、PKC和下调AC来增加结肠SMCs中的[Ca2+]i，从而改善AP的肠道运动。
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 μg/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-β1) 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-β1 and PKC-ε mRNA reduction. Both treatments significantly increased fluorescence intensity of SMC intracellular calcium concentration [Ca2+]i (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 [Ca2+]i in colonic SMCs via upregulating PLC, PKC and downregulating AC.