血管紧张素Ⅱ诱导被动致敏人气道平滑肌细胞合成Ⅰ型胶原  

Angiotensin Ⅱ induces collagen Ⅰ synthesis in human passively sensitized airway smooth-muscle cells in vitro

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作  者:沈彬[1] 程远雄[1] 李宁[2] 牛毅[1] 谢浩俊[1] 霍雅婷[1] 

机构地区:[1]南方医科大学南方医院呼吸内科,广州510515 [2]广东省汕头市中心医院呼吸内科,汕头515031

出  处:《第三军医大学学报》2013年第18期1957-1960,共4页Journal of Third Military Medical University

摘  要: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 determine the effects of angiotensin(Ang) Ⅱ and losartan,an antagonist of angiotensin type 1 receptor(AT1R),on the production of collagen type Ⅰ in human passively sensitized airway smooth muscle cells.Methods After human airway smooth muscle cells were isolated from normal bronchial tissue samples,and primarily cultured and identified by immunofluorescence staining of α-actin.The obtained cells were divided into the following 4 groups:① passively sensitized group:10% serum from asth-matic patients;② passively sensitized + AngⅡ group:10% serum from asthmatic patients + AngⅡ(final concentration of 10-7mol / L);③ passively sensitized + losartan group:10% serum from asthmatic patients + losartan(final concentration of 10-6mol / L);④ passively sensitized + AngⅡ + losartan group:10% serum from asthmatic patients + AngⅡ(final concentration of 10-7mol / L) + losartan(final concentration of 10-6mol / L).The effect of AngⅡ and losartan on the collagen type Ⅰ mRNA expression in the passively sensitized HASMCs was detected by real-time RT-PCR,and its protein content was analyzed by ELISA.Results Compared to control group,the mRNA expression and protein release of collagen type Ⅰ in AngⅡ-induced group(10-7mol / L for 24 h) was significantly higher(P 0.01).Losartan treatment produced a significantly inhibitory effect on the expression of mRNA and protein synthesis(P 0.01).Conclusion AngⅡ induces the synthesis of collagen type Ⅰ by human passively sensitized airway smooth muscle cells,which might be through binding with AT1R.

关 键 词:人气道平滑肌细胞 被动致敏 血管紧张素Ⅱ Ⅰ型胶原 

分 类 号:R322.34[医药卫生—人体解剖和组织胚胎学] R562.25[医药卫生—基础医学]

 

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