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本文对吴茱萸次碱的收缩血管效应及其机制进行了研究。结果表明,吴茱萸次碱体外可明显的引起大鼠胸主动脉血管平滑肌收缩。与血管平滑肌收缩相关的信号蛋白Rho激酶(RhoA)和IP3受体(IP3R)的抑制剂可以抑制吴茱萸次碱的缩血管效应。血管平滑肌细胞A7r5的实验发现,吴茱萸次碱(300μg/L)可以明显升高胞内Ca2+浓度,促进IP3R的mRNA表达,而后者与胞内Ca2+浓度升高有关。预先使用RhoA抑制剂H-1152,吴茱萸次碱仍能使RhoA mRNA表达升高。此外,吴茱萸次碱能够促进肌球蛋白轻链磷酸酶(MLCP)以及肌球蛋白轻链(MLC)的磷酸化。提示吴茱萸次碱的缩血管效应与RhoA/MLCP-MLC信号转导通路有关。本工作对于深入认识吴茱萸次碱的药理活性具有重要的意义。
This article studies the vasoconstrictor effect of rutaecarpine and its mechanism. The results showed that rutaecarpine significantly induced thoracic aortic smooth muscle contraction in vitro. Inhibitors of Rho kinase (RhoA) and IP3R (IP3R), a signal protein involved in vascular smooth muscle contraction, inhibit the vasoconstrictive effect of rutaecarpine. Vascular smooth muscle cells A7r5 experiments found that rutaecarpine (300μg / L) can significantly increase intracellular Ca2 + concentration, and promote IP3R mRNA expression, while the latter with the intracellular Ca2 + concentration. Ruthenium ethane could still increase RhoA mRNA expression by using RhoA inhibitor H-1152 in advance. In addition, rutaecarpine promotes the phosphorylation of myosin light chain phosphatase (MLCP) and myosin light chain (MLC). Prompt vasolarine vasoconstrictor effect and RhoA / MLCP-MLC signal transduction pathway. This work is of great significance for the further understanding of the pharmacological activity of rutaecarpine.