胰岛素信号转导通路相关蛋白在肺气肿患者肺组织中的表达

摘要

目的:研究胰岛素治疗对慢性阻塞性肺疾病(CO PD)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-M A PK)、核转录因子-κB(N F-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-M A PK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N F-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N F-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 ki-nase(P38-MAPK)and nuclear factor-κB(NF-κB)in lung tissue were detected by Western blotting.Results:The ex-pression of Phosphorylated protein kinase B(pAkt)in lung tissue of patients with emphysema after insulin therapy was higher than that in control group(P<0.05).The expression of pP38-MAPK in lung tissue in patients with em-physema after insulin treatment was not significantly different from that in control group(P>0.05).The expres-sion of NF-κB in lung tissue of patients with emphysema after insulin therapy was higher than that in control group(P<0.05).Conclusion:Insulin may inhibit cell apoptosis by stimulating a variety of stimuli by activating the PI 3K/Akt signaling pathway and activating its downstream transcription factor NF-κB in lung tissue of COPD patients.