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作 者:豆亚伟[1] 王宏涛[1] 田伟[1] 朱建飞[1] 戴云[1] 罗向晖[1] 陈耀华[1]
机构地区:[1]陕西省人民医院,西安710068
出 处:《陕西医学杂志》2017年第10期1386-1388,共3页Shaanxi Medical Journal
基 金:陕西省自然科学基金资助项目(2013JC2-23)
摘 要:目的:研究胰岛素治疗对慢性阻塞性肺疾病(COPD)患者肺组织的作用机制。方法:择期行肺减容手术患者99例,术前2周开始即给予极化液(含胰岛素液)治疗。术中取肺减容切除肺组织,Western blot印迹法检测肺组织蛋白激酶B(Akt)、p38丝裂原活化蛋白激酶(P38-MAPK)、核转录因子-κB(NF-κB)表达的变化。结果:胰岛素治疗后肺气肿患者肺组织内磷酸化蛋白激酶B(pAkt)表达水平较其对照组增加(P<0.05)。胰岛素治疗后肺气肿患者肺组织内P38-MAPK表达与其对照组比较无统计学差异(P>0.05)。胰岛素治疗后肺气肿患者肺组织内NF-κB表达较其对照组增加(P<0.05)。结论:胰岛素可能通过在COPD患者的肺组织中激活PI3/Akt信号转导途径并激活其下游的转录因子NF-κB抑制多种刺激所诱发的细胞凋亡。Objective:To study the mechanism of insulin therapy on lung tissue in COPD patients.Methods:Select 99 patients underwent elective lung volume reduction surgery,2 weeks before surgery to give polarized solution(including insulin solution)treatment.The expression of Protein kinase B(Akt),p38 mitogen-activated protein kinase(P38-MAPK)and nuclear factor-κB(NF-κB)in lung tissue were detected by Western blotting.Results:The expression of Phosphorylated protein kinase B(pAkt)in lung tissue of patients with emphysema after insulin therapy was higher than that in control group(P0.05).The expression of pP38-MAPK in lung tissue in patients with emphysema after insulin treatment was not significantly different from that in control group(P0.05).The expression of NF-κB in lung tissue of patients with emphysema after insulin therapy was higher than that in control group(P0.05).Conclusion:Insulin may inhibit cell apoptosis by stimulating a variety of stimuli by activating the PI3 K/Akt signaling pathway and activating its downstream transcription factor NF-κB in lung tissue of COPD patients.
关 键 词:肺气肿 胰岛素 细胞凋亡 丝裂原活化蛋白激酶磷酸酶 NF-ΚB
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