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作 者:朱述阳[1] 郭茂清[1] 卞宏[1] 段存玲 闫明华[1] 稽桂娟[1] 陈亮[1] 何军[1] 高峰[1]
出 处:《国际呼吸杂志》2010年第16期969-972,F0003,共5页International Journal of Respiration
摘 要:目的 探讨脂联素对气道平滑肌细胞凋亡的影响及相关机制的研究.方法 体外培养大鼠气道平滑肌细胞株,逆转录-聚合酶链反应法检测气道平滑肌细胞脂联素受体的表达.将体外培养的大鼠气道平滑肌细胞于不间浓度的脂联素中孵育48 h,流式细胞仪测定细胞的凋亡率;Western blot法检测活性的一磷酸腺苷激活蛋白激酶(pho-AMPK)蛋白的表达.结果 脂联素能够促进气道平滑肌细胞凋亡,并存在浓度依赖性(r=0.952,P〈0.01);Western blot显示随着脂联素浓度的升高pho-AMPK的表达增加(r=0.907,P〈0.01).结论 脂联素可能通过激活一磷酸腺苷激活蛋白激酶进一步激活凋亡信号通路诱导气道平滑肌细胞凋亡.Objective To investigate the effects of adiponectin on apoptosis of airway smooth muscle cells (ASMC) and the related mechanism. Methods ASMC of rats were cultured in vitro. The expression of adiponectin receptors in ASMC was detected by reverse transcription-polymerase chain reaction. The rat ASMC cultured was incubated with different concentrations of adiponectin for 48 hours. Apoptosis rate was detected by flow cytometry. The protein expression of phosphorylated adenosine monophosphate-activated protein kinase (AMPK) was detected by Western blot. Results Adiponectin could promote apoptosis of ASMC, and there was concentration-dependent ( r =0.952, P 〈0. 01). Western blot indicated that the expression of phosphorylated AMPK increased with the incremental concentrations of adiponectin(r =0. 907, P 〈0. 01). Conclusions Adiponectin may further activate the apoptotic signaling pathway and induce the apoptosis of ASMC by activating AMPK.
关 键 词:脂联素 气道平滑肌细胞 细胞凋亡 一磷酸腺苷激活蛋白激酶
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