CAJ | 학술논문

目的观察血管紧张素Ⅱ(AngⅡ)对人正常肝细胞白蛋白表达及Ⅰ型胶原合成的影响.方法常规培养人正常肝细胞系HL-7702细胞并分为对照组、AngⅡ刺激组、AngⅡ十依贝沙坦组(共刺激组).采用免疫荧光法和Western印迹法检测各组肝细胞中白蛋白及胶原改变;免疫荧光法观察各组肝细胞中是否有胶原合成;实时定量PCR法定量检测各组肝细胞中Ⅰ型胶原mR-NA表达水平的变化.结果与对照组相比,经AngⅡ(10-7mol/L)处理72 h后,AngⅡ刺激组肝细胞中白蛋白表达减少(1.41±0.23比0.85±0.11,P=0.000),Ⅰ型胶原mRNA的表达明显升高(1.00±0.08比3.72±0.19,P=0.000),Ⅰ型胶原蛋白合成增加,而经依贝沙坦预处理后,共刺激组肝细胞白蛋白表达较AngⅡ刺激组明显增多(0.85±0.11比1.38±0.32,P=0.000),肝细胞Ⅰ型胶原mRNA表达较AngⅡ刺激组显著下降(3.72±0.19比2.86±0.13,P=0.000),Ⅰ型胶原蛋白合成减少.结论 AngⅡ经Ⅰ型受体诱导人肝细胞表达白蛋白减少,胶原合成增加.
목적 관찰혈관긴장소Ⅱ(AngⅡ)대인정상간세포백단백표체급Ⅰ형효원합성적영향.방법 상규배양인정상간세포계HL-7702세포병분위대조조、AngⅡ자격조、AngⅡ십의패사탄조(공자격조).채용면역형광법화Western인적법검측각조간세포중백단백급효원개변;면역형광법관찰각조간세포중시부유효원합성;실시정량PCR법정량검측각조간세포중Ⅰ형효원mR-NA표체수평적변화.결과 여대조조상비,경AngⅡ(10-7mol/L)처리72 h후,AngⅡ자격조간세포중백단백표체감소(1.41±0.23비0.85±0.11,P=0.000),Ⅰ형효원mRNA적표체명현승고(1.00±0.08비3.72±0.19,P=0.000),Ⅰ형효원단백합성증가,이경의패사탄예처리후,공자격조간세포백단백표체교AngⅡ자격조명현증다(0.85±0.11비1.38±0.32,P=0.000),간세포Ⅰ형효원mRNA표체교AngⅡ자격조현저하강(3.72±0.19비2.86±0.13,P=0.000),Ⅰ형효원단백합성감소.결론 AngⅡ경Ⅰ형수체유도인간세포표체백단백감소,효원합성증가.
Objective To investigate the effects of angiotensin Ⅱ (AngⅡ) on the expression of albumin and the synthesis of type Ⅰ collagen in human normal hepatic cells. Methods HL-7702 cells (human normal hepatocyte) were cultured and divided into control group, Ang Ⅱ treated group, an AngⅡ+irbesartan (co-stimulated) group. The expressions of albumin and type Ⅰ collagen were detected by immunofluorescence and Western blotting, respectively. The mRNA level of type Ⅰ collagen was measured by real time-PCR(qRT-PCR). Results After stimulated with 10-7 mol/L Ang Ⅱ for 72 hours, the expression of albumin significantly decreased in Ang Ⅱ treated group compared with control group (0.85±0.11 vs 1. 41±0.23,P=0.000), while the mRNA expression increased in AngⅡ treated group compared with control group (1.00±0.08 vs 3.72±0.19,P=0.000). In costimulated group, however, the expression of albumin significantly increased (0.85 ± 0.11 vs 1.38 ±0.32,P=0.000),and mRNA expression (3. 72±0.19 vs 2.86±0.13,P=0.000) and synthesis of type Ⅰ collagen were reduced when compared with Ang Ⅱ treated group. Conclusions The reduction of albumin and elevated systhesis of type Ⅰ collagen in HL-7702 cells are induced via Ang Ⅱ AT1 receptor.