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作 者:张琳[1] 袁城栋 曹嵩[1] 周雯静 邓胜利[1] Zhang Lin Yuan Chengdong Cao Song Zhou Wenjing Deng Shengli(Guizhou Provincial Key Laboratory of A nesthesia and Organ Protection Basic Research, Zunyi Medicial University, Zunyi, Guizhou 563003, Chin)
机构地区:[1]贵州省麻醉与器官保护基础研究重点实验室/遵义医学院,贵州遵义563003
出 处:《现代医药卫生》2017年第17期2596-2598,2602,共4页Journal of Modern Medicine & Health
基 金:贵州省科学技术基金资助项目(黔科合J字[2008]2196);遵义医学院科研启动基金资助项目([2010]448)
摘 要:目的观察UrocortinⅠ(UCNⅠ)调控成年大鼠缺氧/复氧心肌细胞钙离子敏感性受体(Ca SR)表达的变化。方法离体成年大鼠心肌细胞分离、培养,随机分为正常组(NOR组,37℃95%O2+5%CO2培养箱中持续培养7 h)、UCNⅠ组、缺氧/复氧组[I/R组,正常培养0.5 h+UCNⅠ(1×10-8 mol/L)0.5 h、缺氧4.0 h、复氧2.0 h]、5-羟葵酸(5-HD)+UrocortinⅠ组[5-HD+UCNⅠ组,5-HD(5×10-9 mol/L)和UCNⅠ(1×10-8 mol/L)依次处理0.5 h后缺氧4 h、复氧2 h]。复氧结束即刻收集细胞运用实时荧光定量PCR(q PCR)检测Ca SR的表达。结果 UCNⅠ组和I/R组Ca SR表达量较NOR组明显增加,I/R组较UCNⅠ组表达量增加,差异均有统计学意义(P<0.01),5-HD+UCNⅠ组Ca SR表达量高于NOR组,但低于UCNⅠ组,差异均有统计学意义(P<0.01)。结论大鼠离体缺氧/复氧心肌细胞中Ca SR表达可受UCNⅠ调控减低,UCNⅠ升高Ca SR效应可部分被5-HD逆转,表明了UCNⅠ抗缺血再灌注损伤过程中可导致腺苷三磷酸(ATP)敏感性钾通道的开放。Objective To observe the changes of calcium sensitive receptors expression regulated by Urocortin Ⅰ(UCNⅠ) in hypoxia/reoxgenation(I/R) cardiomyocytes of adult rats. Methods The cardiomyocytes of adult rat were isolated and cultured,then randomly divided intothe normal group(NOR group,continuous culture in 95% O2+5% CO2 incubator for 7 h at 37 ℃),UCNⅠgroup,I/R group [ normal culture 0.5 h + UCN Ⅰ(1×10^-8 mol/L) 0.5 h,hypoxia for 4.0 h and reoxygenation 2.0 h],5-hydroxydecanote(5-HD) +UCNⅠgroup[in turn treating by 5-HD(5×10^-9 mol/L)and UCNⅠ(1×10^-8 mol/L) for 0.5 h,then hypoxia for 4 h and reoxygenation for 2 h]. The cells were collected immediately after the end of reoxgenation. Then q PCR was performed to detect the expression of Ca SR. Results The expression levels of Ca SR in the UCN I group and I/R group were significantly increased compared with the NOR group(P〈0.01). In addition,the Ca SR expression level in the I/R group was much higher than that in the UCN Ⅰ group,the differences were statistically significant(P〈0.01). The expression level of Ca SR in the 5-HD +UCNⅠgroup was higher than that of the NOR group,but lower than that in the UCN Ⅰ group,the differences were statistically significant(P〈0.01). Conclusion The Ca SR expression in I/R rat cardiomyocytes can be decreased by UCN Ⅰregulation. The effect of UCN increasing Ca SR can be partially reversed by 5-HD,indicating the ATP sensitive potassium channel can be opened during the UCNⅠanti-ischemia/reperfusion injury process.
关 键 词:UrocortinⅠ 缺氧/复氧 心肌细胞 钙离子敏感性受体
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