大黄素对豚鼠结肠收缩性的影响及其机制的研究

目的研究大黄素对豚鼠离体远端结肠平滑肌收缩活动的影响及其可能机制。方法急性分离豚鼠远端结肠平滑肌,采用生理记录仪记录不同浓度大黄素对远端结肠收缩的影响;木瓜蛋白酶消化分离豚鼠近端结肠平滑肌细胞,采用全细胞膜片钳技术记录钾电流。结果不同浓度的大黄素（1～50μmol.L-1）对豚鼠远端结肠具有双向调节作用,且其效应呈剂量依赖的趋势1～10μmol.L-1大黄素可浓度依赖性地增强豚鼠远端结肠平滑肌的收缩10μmol.L-1浓度时,大黄素的作用达到平台期。当大黄素的浓度大于10μmol.L-1时,逐渐呈现明显的抑制作用,且其抑制作用与浓度正相关10μmol.L-1硝苯地平孵育肌条后,大黄素不能增强肌条的收缩。大黄素（1～30μmol.L-1）浓度依赖性地抑制豚鼠近端结肠平滑肌细胞钾电流。结论大黄素增强豚鼠结肠的收缩作用可能与L-型钙通道及钾通道有关。

The effect of emodin on guinea-pig's colon contractility and aprimary study of the effecting mechanism

OBJECTIVE The paper was in order to observe the effect of emodin on guinea-pig′s colonic contractility and the pharmacological mechanism.METHODS Colon muscle strips were used to take contractile tension recording.Smooth muscle cells were freshly isolated from the proximal colon by means of papain treatment.Potassium currents were measured using whole-cell patch clamp techniques.RESULTS Emodin affected colonic contractility in a concentration-dependent manner with bilateral way.Emodin(1～10μmol·L-1)enhanced colonic contractility,and its effect was maximal value at 10μmol·L-1.Then it relaxed colon with the concentration increasing.Preincubation with 10μmol·L-1 Nifedipine,emodin didn′t enhance colonic contractility.Emodin inhibited potassium current of proximal colon smooth muscle cell in a concentration-dependent manner(1～30μmol·L-1).CONCLUSION Emodin enhances colonic contractility via L-type calcium channel and potassium channel pathway.