OBJECTIVETo explore the protective function and mechanism of notoginsenoside Rb1 against hypoxia hypercapnia-induced pulmonary vasoconstriction (HHPV).

METHODSThe pulmonary artery smooth muscle cells of healthy male SD rats were primarily cultured and the second to the fifth subcultured cells were incubated with 8, 40, and 100 mg/L notoginsenoside Rb1 respectively under the hypoxia-hypercapnia condition (1% O2 and 6% CO2). The cells were harvested for 24 h. The phosphated extracellular signal-regulated kinase (p-ERK) protein expression of the cells was detected by Western blot. The mRNA expressions of ERK1 and ERK2 were detected using half quantitative reverse transcription polymerase chain reaction (RT-PCR).

RESULTSThe expression of p-ERK protein, the mRNA expressions of ERK1 and ERK2 were weakly positive in the control group. Their expressions in the hypoxia-hypercapnia group were obviously enhanced (P < 0.01). After intervention of Rb1 at different concentrations, their expressions were obviously lowered (P < 0.05, P < 0.01) in a dose-dependent manner. The optimal effects were obtained at the dose of 100 mg/L. The expression of p-ERK protein was significantly positively correlated with mRNA expressions of ERK1 and ERK2 in notoginsenoside Rbl-treated groups (r = 0.500, P < 0.01; r = 0.977, P < 0.01).

CONCLUSIONSERK1/2 pathway might play a role in the rat HHPV. Notoginsenoside Rb, could alleviate HHPV by inhibiting the ERK1/2 pathway.