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作 者:唐兰兰[1,2] 王淑君[1] 黎关龙[1] 王园园[1] 周俊辉[1] 赵珊[1] 刘亚坤[1] 王万铁[1]
机构地区:[1]温州医学院病理生理学教研室 [2]浙江中医药大学附属第二医院病理科
出 处:《中国临床药理学与治疗学》2011年第11期1216-1221,共6页Chinese Journal of Clinical Pharmacology and Therapeutics
基 金:浙江省中医药科技计划重点项目(2008ZA017)
摘 要:目的:探讨三七皂苷单体R1减轻低氧高二氧化碳性肺动脉收缩(hypoxia hypercapnia-in-duced pulmonary vasoconstriction,HHPV)的作用及其与细胞外信号调节激酶(ERK)1/2信号通路的关系。方法:原代培养雄性SD大鼠肺动脉平滑肌细胞(PASMCs),随机分为6组:常氧组(N组),低氧高二氧化碳组(H组),DMSO对照组(HD组),R1干预组(R8、R40、R100组)。采用免疫印迹法测定ERK1/2磷酸化蛋白表达,半定量逆转录-聚合酶链反应技术检测ERK1、ERK2基因表达水平。结果:p-ERK蛋白在N组表达弱,与H、HD组比较,R8、R40、R100组均不同程度下调,以R8组为著,差异有统计学意义(P<0.01);ERK1mRNA、ERK2mRNA在N组弱表达,与H、HD组比较,R8、R40、R100组表达均不同程度降低(P<0.01和P<0.05),以R8组为著。结论:ERK1/2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R1可能通过抑制ERK1/2通路减轻低氧高二氧化碳性肺动脉收缩。AIM:To study the effect of monomer R1 aleviating HHPV via MAPKs signal pathway.METHODS: To culture pulmonary arterial smooth muscle cells(PASMCs) of male SD rats primarily,PASMCs were randomly divided into 6 groups: control group(N),hypoxia hypercapnia group(H),DMSO incubation group(HD),R1 groups(R8,R40,R100).Incubated cells were collected.p-Erk1/2 was investigated through western blot,and ERK1 mRNA and ERK2 mRNA were detected via RT-PCR.RESULTS:The expretion of p-ERK protein was weak in the N group,and in R8,R40 and R100 groups the level of p-ERK was reduced significantly(P0.01),declining mostly in R8 group.The expretion of ERK1 mRNA and ERK2 mRNA was not obvious in N group,and comparing with H and HD groups it markedly down-regulated in R8,R40 and R100 groups(P0.01,P0.05),reaching its lowest point in R8 group.CONCLUSION: ERK1/2 signal pathway may play an important role in HHPV in rat.The effect of R1 on relaxing HHPV may be related to inhibiting expression of ERK1/2.
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