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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 diabetic lung injury and the preventive and therapeutic effects of α-ALA on diabetic lung injury. Methods The experiment was divided into control (NC) group and diabetic model group for 8 weeks (DM), diabetes + α-lipoic acid for 8 weeks [DM + α-ALA The levels of TGF-β1, Smad2 and Smad7 were detected by immunohistochemical method in the DM + α-ALA (12W) group. The changes of blood glucose, HbA1c and body weight were observed respectively. Results Compared with NC group, the expression of TGF-β1 and Smad2 increased and the expression of Smad7 decreased in DM group. Compared with DM group, the expression of TGF-β1 and Smad2 decreased in DM + -ALA group (8W) Compared with DM + α-ALA (8W) group, the expression of TGF-β1 and Smad2 in DM + α-ALA (12W) group decreased and the expression of Smad7 protein increased. Compared with DM group, α-ALA treatment decreased blood glucose and HbA1 c levels. Conclusion Pulmonary tissue of STZ diabetic rats can cause hyperglycemia in the lung and increase the levels of blood glucose, HbA1c and weight, and activate the TGF-β1 / Smads signaling pathway, which may aggravate the occurrence and development of diabetic pulmonary fibrosis. α-ALA has a preventive and therapeutic effect on diabetic lung injury, and the effect is more significant with the prolongation of treatment time.