沉默信息调节因子1在结核性气管支气管狭窄中的作用

Role of SIRT-1 in tuberculous tracheobronchial stenosis

目的探讨沉默信息调节因子1(Sirtuin 1,SIRT-1)在结核性气管支气管狭窄中的作用。方法将患者分为正常对照组(A)、增生性狭窄组(B)、瘢痕性狭窄组(C)3组;收集患者术前的血清,运用ELISA检测SIRT-1、转化生长因子-β1(TGF-β1)、白细胞介素(IL)-8的表达水平;收集术中病变气管支气管组织,运用免疫组化检测SIRT-1、TGF-β1、I型胶原蛋白(COL-1)蛋白阳性表达情况,Western印迹法和实时定量逆转录聚合酶链反应(RT-qPCR)检测SIRT-1、TGF-β1、COL-1蛋白表达水平及mRNA的相对表达量。结果1)SIRT-1在血清及气管支气管组织中的表达水平为B<C<A组(P<0.05);2)TGF-β1在血清及气管支气管组织中的表达水平为B>C>A组(P<0.05);3)COL-1在气管支气管组织中的表达水平总趋势为B>A组(P<0.05),但在C组与A组之间比较无统计学意义(P>0.05)。结论结核性气管支气管狭窄的发生发展可能与SIRT-1的表达被抑制,致使炎症反应及纤维化加重相关。

Objective To investigate the role of Sirtuin 1(SIRT-1)in tuberculous tracheobronchial stenosis.Methods The patients were divided into three groups:th normal control group(the group A),the tuberculous proliferative tracheobronchial stenosis group(th group B)and the tuberculous scar tracheobronchial stenosis group(the group C).The serum of patients before surgery was collected and the expression levels of SIRT-1,transforming growth factor-β1(TGF-β1)and interleukin(IL)-8 were detected by ELISA.The tracheobronchial tissues were collected during the operation,and it used immunohistochemistry to detect the positive expression of SIRT-1,TGF-β1,and type I collagen(COL-1)protein.Western blot and real-time quantitative reverse transcription polymerase chain reaction qPCR)was used to detect SIRT-1,TGF-β1,and COL-1 protein expression levels and mRNA relative expression levels.Results 1.The expression level of SIRT-1 in serum and tracheobronchial tissue was the lowest in the group B,followed by the group C and A(P<0.05).2.The expression level of TGF-β1 in serum and tracheobronchial tissue was the highest in the group B,followed by the group C and A(P<0.05).3.The general trend of COL-1 expression level in tracheobronchial tissue was higher in the group B than in the group A(P<0.05),but there was no statistical significance between the group C and the group A(P>0.05).Conclusion The occurrence and development of tuberculous tracheobronchial stenosis may be related to airway inflammation and fibrosis caused by the suppression of SIRT-1 expression.