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目的探讨血管紧张素Ⅱ(AngⅡ)及其Ⅰ型受体(Angiotensin Type 1 Receptor,AT1R)拮抗剂洛沙坦(Losartan)对被动致敏人气道平滑肌细胞(human airway smooth muscle cells,HASMCs)合成Ⅰ型胶原的影响。方法体外培养HASMCs,按处理因素将细胞分为4组:①被动致敏组(10%哮喘血清);②被动致敏+AngⅡ组(10%哮喘血清+10-7mol/L AngⅡ);③被动致敏+Losartan组(10%哮喘血清+10-6mol/L Losartan);④被动致敏+AngⅡ+Losartan组(10%哮喘血清+10-7mol/L AngⅡ+10-6mol/L Losartan)。免疫荧光染色法鉴定HASMCs,荧光定量PCR检测Ⅰ型胶原mRNA表达,ELISA检测Ⅰ型胶原蛋白分泌。结果 10-7mol/l AngⅡ作用于被动致敏的HASMCs 24 h后,Ⅰ型胶原mRNA及蛋白的表达较被动致敏组明显增加(P<0.01)。在Losartan存在的情况下,AngⅡ对被动致敏HASMCsⅠ型胶原mRNA及蛋白表达的促进作用明显受到抑制(P<0.01)。结论 AngⅡ能促进被动致敏的HASMCs分泌Ⅰ型胶原,可能是通过与AT1R结合而实现的。
Objective To investigate the effects of angiotensin Ⅱ (AngⅡ) and its antagonist of angiotensin type 1 receptor (Losartan) on the synthesis of passive sensitized human airway smooth muscle cells (HASMCs) Ⅰ Collagen effects. Methods HASMCs were cultured in vitro. The cells were divided into 4 groups according to the treatment factors: ① passive sensitization group (10% asthma serum); ② passive sensitization + AngⅡ group (10% asthma serum + 10-7mol / L AngⅡ); ③ passive Sensitization + Losartan group (10% asthma serum + 10-6mol / L Losartan); ④ Passive sensitization + AngⅡ + Losartan group (10% Asthma serum + 10-7mol / L AngⅡ + 10-6mol / L Losartan). HASMCs were identified by immunofluorescence staining, type Ⅰ collagen mRNA was detected by fluorescence quantitative PCR and type Ⅰ collagen was detected by ELISA. Results The expression of type Ⅰ collagen mRNA and protein in HASMCs sensitized with 10-7mol / L AngⅡ for 24 h was significantly increased (P <0.01). In the presence of Losartan, the effect of AngⅡ on the expression of type Ⅰ collagen mRNA and protein in passively sensitized HASMCs was significantly inhibited (P <0.01). Conclusion Ang Ⅱ can promote the passive sensitization of type I collagen secreted by HASMCs, probably by binding to AT1R.