The Expression of p38MAPK in Hypoxia Hypercapnic Pulmonary Arterial Smooth Muscle and the Intervention of Notoginsenoside Rb1

Abstract: This research will explore the mechanism of notoginsenoside Rb1 to alleviate the hypoxia hypercapnia-induced pulmonary vasoconstriction and the role of p38MAPK (extracellular singal-regulated kinase) signal pathway playing in it. The pulmonary artery smooth muscle cells were primary cultured and the second to fifth subcultured cells were incubated with 8， 40 and 100 mg/mL notoginsenoside Rb1 respectively under the hypoxia-hypercapnia condition (1% O2， 6% CO2). The cells were harvested in 24 h. The phosphated p38MAPK of the cells 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 Rb1-treated groups (RbL， RbM and RbH groups)， especially in RbM group， was significantly lower (P<0.01).The expression of p38MAPK mRNA of control group was significant lower than that of other groups. Compared to hypoxia-hypercapnia group， the expression of mRNA in notoginsenoside Rb1-treated groups (RbL， RbM and RbH groups)， especially in RbM group， was significantly lower (P<0.01). These results indicate that p38MAPK can induce hypoxia hypercapnia-induced pulmonary vasoconstriction in rats and notoginsenoside Rb1 can alleviate hypoxia hypercapnia-induced pulmonary vasoconstriction by inhibiting the p38MAPK signal pathway.

CSTR: 32200.14.cjcb.2014.12.0006