摘要
目的探讨糖尿病肺损伤的机制及α-硫辛酸(α-ALA)对糖尿病肺损伤的防治作用。方法实验分为对照(NC)组和糖尿病模型8周(DM)组、糖尿病+α-硫辛酸治疗8周[DM+α-ALA(8W)]组、糖尿病+α-硫辛酸治疗12周[DM+α-ALA(12W)]组,并分别观察血糖、HbA1c、体重改变,采用免疫组织化学方法测定转化生长因子β1(TGF-β1)、Smad2及Smad7在糖尿病大鼠肺组织表达变化。结果与NC组比较,DM组肺组织中TGF-β1、Smad2蛋白的表达增多,Smad7蛋白表达水平下降;与DM组比较,DM+-ALA(8W)组TGF-β1、Smad2蛋白的表达减少,Smad7蛋白表达水平升高;与DM+α-ALA(8W)组比较,DM+α-ALA(12W)组TGF-β1、Smad2蛋白的表达减少,Smad7蛋白表达水平升高。与DM组比较,α-ALA治疗后血糖及HbA1 c水平下降。结论 STZ糖尿病大鼠肺组织高糖环境下引起血糖、HbA1c升高及体重减轻并激活TGF-β1/Smads信号通路,从而加重糖尿病肺纤维化的发生发展。α-ALA对糖尿病肺损伤有防治作用,并随治疗时间延长而效果更为显著。
Objective To investigate the mechanism of lung injury in diabetic rats and to evaluate the effect of alpha lipoic acid （alpha -ALA） on the prevention and treatment Of diabetic lung injury. Methods The experiment rats were divided into control group （NC）,8-week diabetic model group（DM）, 8-week alpha lipoic acid treated diabetic group[DM＋α-ALA（8W）], 12-week alpha lipoic acid treated diabetic group[DM＋α-ALA（12W）]. Blood glucose, HbA1 c and body weight changes were recorded. Immunohistochemical method was used to measure the expression of transforming growth factor beta （TGF- beta 1） ,Smad2 and Smad7 in the lung tissue of diabetic rats. Results compared with NC group, the expressions of TGF- beta 1 and Srnad2 protein in the lung tissue of DM group were increased, but the expression level of Smad7 protein decreased. Compared with DM group, 8-week alpha -ALA treatment increased the expression of TGF beta 1 and Smad2, and decreased Smad7. This trend was more obvious in 12-week treatment group. Blood glucose and glycosylated hemoglobin （HbA1 c）levels decreased in groups treated with alpha-ALA. Conclusion Lung injury can be induced by TGF beta 1/Smads signaling pathway activation in high glucose environment, alpha-ALA has certain effect on preventing and improving lung injury in diabetic rats.
出处
《中国糖尿病杂志》
CAS
CSCD
北大核心
2016年第11期1021-1025,共5页
Chinese Journal of Diabetes
