【摘要】 目的观察大黄素对细菌性腹膜炎所致多器官功能不全综合征 (MODS)大鼠结肠平滑肌细胞动力的影响 ,探讨大黄素对该平滑肌细胞钙离子的作用机制。方法制成大鼠MODS模型后观察大黄素对MODS大鼠结肠平滑肌肌条和平滑肌细胞收缩的影响 ;特异性的肌球蛋白轻链激酶抑制剂 (ML 7)和选择性的蛋白激酶C阻制剂 (CalphostinC)对大黄素收缩MODS大鼠结肠平滑肌的影响及大黄素对MODS大鼠结肠平滑肌细胞钙离子的影响。结果大黄素能直接收缩MODS大鼠结肠平滑肌肌条和平滑肌细胞 ;ML 7和CalphostinC可不同程度的抑制大黄素的收缩作用 ;MODS状态下 ,大黄素仍然能升高细胞内钙离子的浓度 ;在MODS模型组肝素〔三磷酸肌醇 (IP3)受体阻制剂 ,Heparine〕和ryanodine受体 (RyR)阻滞剂能抑制大黄素升高钙离子 ;钙离子螯和剂 (EGTA)和尼莫地平 (特异性的细胞膜电压依赖性钙通道抑制剂 ,nifedipine)没有明显作用。结论大黄素能直接收缩MODS大鼠结肠平滑肌。它是通过升高钙离子的信号途径ML CK和增加钙敏感性的PKCα信号途径来介导MODS大鼠平滑肌收缩的。升高MODS大鼠结肠平滑肌钙离子的机制主要是通过肌浆网上IP3和RyR两种钙离子通道作用的受体。更多还原

【Abstract】 ObjectiveTo observe the effect of emodin on mo tility signal transduc tion and calcium ion in colonic smooth muscle cells (SMC) in rats with bacterial peritonitis caused multiple organ dysfunction syndrome (MODS). Method sObservation was conducted in colon of MODS model rats on (1) effects of emodin on the contractio n of muscular strip and cells of colonic smooth muscle, and influences of specif ic myoglobulin light chain kinase inhibitor (ML-7) and selective proteinkinase C inhibitor (Calphostin C) on these effects; and (2) effect of emodin on calcium ion in SMC. ResultsEmodin could directly contract the m uscular strip and cells of smooth muscle; ML-7 and Calphostine could inhibit these contractile action t o some extent. Under MODS condition, emodin could still increase the intracellul ar calcium ion concentration; this effect could be inhibited by heparin (inosami ne triphosphate receptor inhibitor IP 3 and ryanodine receptor inhibitor in MOD S model but the calcium chelator EGTA and nifedipine (the specific cell membrane v oltage dependent calcium channel blocker) showed no influence on it. Co nclusionEmodin could directly contract the colonic smooth mu scle in MODS model rats, w hich is mediated by raise the signal path MLCK of calcium ion and the PKCα path for increase calcium sensibility. The mechanism of increasing calcium ion is ma inly through IP 3 and RyR the two calcium ion channel receptor in the sarcoplasm.更多还原