p38MAPK在低氧高二氧化碳肺动脉平滑肌中的表达及三七皂苷单体Rb_1的干预

The Expression of p38MAPK in Hypoxia Hypercapnic Pulmonary Arterial Smooth Muscle and the Intervention of Notoginsenoside Rb_1

该实验旨在探讨三七皂苷单体Rb。对低氧高二氧化碳性肺动脉收缩的作用及其与p38MAP雕号通路的关系。原代培养雄性sD大鼠肺动脉平滑肌细胞（PAsMcs），取第2～5代细胞，随机分为五组：常氧组（N组）、低氧高二氧化碳（1％02，6％C02）组（H组）、低氧高二氧化碳＋8mg／mLRbl组（RbL组）、低氧高二氧化碳＋40mg／mLRbl组（RbM组）、低氧高二氧化碳＋100mg／mLRb1组（RbH组）。孵育24h后收集细胞，分别采用免疫印迹法测定p38MAPK磷酸化蛋白的表达水平，半定量逆转录一聚合酶链反应技术检测p38MAPK基因的表达水平。p-p38MAPK蛋白在N组表达弱阳性：较之H组，Rbl干预组（RbL、RbM、Rbn组）表达均不同程度减弱，以RbM组最为显著，差异有统计学意义妒〈0．01）；p38MAPKmRNA在N组表达较弱；与H组相比，RbL、RbM和RbH组中p38MAPKmRNA表达均不同程度下降，以RbM组最为显著俨〈0．01）。上述结果表明，p38MAPK信号通路可能介导大鼠低氧高二氧化碳性肺动脉收缩；三七皂苷单体Rbl可能通过抑制p38MAPK信号通路的表达而减轻低氧高二氧化碳性肺动脉收缩。

This research will explore the mechanism of notoginsenoside Rbl to alleviate the hypoxia hy- percapnia-induced pulmonary vasoconstriction and the role of p38MAPK （extracellular singal-regulated kinase） signal pathway playing in it. The pulmonary artery smooth muscle ceils were primary cultured and the second to fifth subcultured cells were incubated with 8, 40 and 100 mg/mL notoginsenoside Rbl respectively under the hy- poxia-hypercapnia condition （1% 02, 6% CO2）. The cells were harvested in 24 h. The phosphated p38MAPK of the ceils was detected by Western blot and p38MAPK mRNA was examined by reverse transcription polymerase chain reaction （RT-PCR）. The expression of phosphated p38MAPK of control group was significant lower than that of other groups. Compared to hypoxia-hypercapnia group, the expression of phosphated p38MAPK in notogin-senoside Rbl-treated groups （RbL, RbM and RbH groups）, especially in Rbu group, was significantly lower （P〈0.01）. The expression ofp38MAPK mRNA of control group was significant lower than that of other groups. Compared to hypoxia-hypercapnia group, the expression of mRNA in notoginsenoside Rbl-treated groups （RbL, RbM and Rbn groups）, especially in Rbu group, was significantly lower （P〈0.01）. These results indicate that p38MAPK can induce hypoxia hypercapnia-induced pulmonary vasoconstriction in rats and notoginsenoside Rbl can alleviate hypoxia hypercapnia-induced pulmonary vasoconstriction by inhibiting the p38MAPK signal pathway.