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

Expression of insulin signal transduction pathway associated protein in lung tissue of emphysema

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.