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作 者:宋张娟[1] 唐兰兰[1,2] 黎关龙[1] 赵珊[1] 王园园[1] 刘亚坤[1] 王淑君[1] 周俊辉[1] 王万铁[1]
机构地区:[1]温州医学院病理生理学教研室,浙江325035 [2]浙江中医药大学附属第二医院病理科,杭州310005
出 处:《中国中西医结合杂志》2012年第10期1380-1384,共5页Chinese Journal of Integrated Traditional and Western Medicine
基 金:浙江省中医药科技计划重点项目(No.2008ZA017)
摘 要:目的探讨三七皂苷单体Rb1在低氧高二氧化碳性肺动脉收缩(hypoxia hypercapnia-induced pulmonary vasoconstriction,HHPV)中的保护作用及机制。方法原代培养健康雄性SD大鼠肺动脉平滑肌细胞,取第2~5代细胞至低氧高二氧化碳(1%O2,6%CO2)条件下继续培养,并分别用8、40、100mg/LRb1孵育24h后收集细胞,分别采用Westernblot测定磷酸化细胞外调节蛋白激酶(ERK)蛋白表达,半定量RT-PCR检测ERK1和ERK2mRNA表达。结果常氧组p-ERK蛋白及ERK1、ERK2mRNA表达均呈弱阳性,低氧高二氧化碳组p-ERK蛋白及ERK1、ERK2mRNA表达均明显增加(P<0.01);经不同浓度Rb1干预后,p-ERK蛋白及ERK1、ERK2mRNA表达均明显降低(P<0.05,P<0.01),并呈剂量依赖关系,以100mg/L效果最好。Rb1各浓度组p-ERK蛋白表达与ERK1和ERK2mRNA表达均呈显著正相关(r分别为0.500、0.977,P<0.01)。结论 ERK1/2信号通路可能介导大鼠HHPV;三七皂苷单体Rb1可能通过抑制ERK1/2通路减轻HHPV。Objective To explore the protective function and mechanism of notoginsenoside Rbl against hypoxia hypercapnia-induced pulmonary vasoconstriction (HHPV). Methods The 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 Rbl respectively under the hypoxia-hypercapnia condition (1% 02 and 6% CO2). The cells were harvested for 24 h. The phosphated extracellular signal-regulated kinase (p-ERK) pro- tein expression of the cells was detected by Western blot. The mRNA expressions of ERK1 and ERK2 were detec- ted using half quantitative reverse transcription polymerase chain reaction (RT-PCR). Results The expression of p-ERK protein, the mRNA expressions of ERK1 and ERK2 were weakly positive in the control group. Their expres- sions in the hypoxia-hypercapnia group were obviously enhanced (P 〈0. 01 ). After intervention of Rb~ 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 ). Conclusions ERK1/2 pathway might play a role in the rat HHPV. Notoginsenoside Rb1 could alleviate HHPV by inhibiting the ERK1/2 pathway.
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