[血管紧张素II调节大鼠心脏中胶原蛋白的表达]

[Angiotensin II regulates the expression of collagens in rat heart].

作者信息

Cui Z, Chen X, Chen L, Wang M, Liu L

机构信息

Biochemistry Division, Fu Wai Hospital, CAMS and PUMC, Beijing 100037.

出版信息

Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 1999 Dec;21(6):483-7.

PMID:12567498

Abstract

OBJECTIVE

To testify the effect of angiotensin (Agn) II on the regulation and expression of collagen I, III genes in rat heart as well as the influence of DMP811 (a novel nonpeptide selective angiotension type 1 antagonist) on the effect of Ang II.

METHODS

Six-week-old male SD rats with osmotic minipump subcutaneously containing either Ang II or saline were used. (1) Saline-infused(control) group (n = 6), (2) Ang II-infused group (n = 6). (3) Ang II-infused and DMP811-treated (3 mg.kg-1.d-1, by gavage) group (n = 6). Ang II (200 ng.kg-1.min-1) or saline was continuously infused for 1 week. After extraction of cardiac total RNA, the levels of collagen I, III mRNA and proteins were measured with RT-PCR and Sirius red staining respectively.

RESULTS

Cardiac weight, cardiac weight/body weight radio, the mRNA levels of collagen I, III were increased by (4.7 +/- 0.4)%, (4.9 +/- 0.9)%, (22.0 +/- 4.7)% and (20.6 +/- 4.9)% respectively, in group 2 compared with those in group 1. The analysis of collagen on Sirius red-stained sections showed that Ang II increased the deposits of both collagen I and III. The above changes caused by Ang II could be inhibited fully by DMP811.

CONCLUSIONS

Ang II up-regulated the expressions of collagen I, III via angiotension type 1 receptor.

摘要

目的

验证血管紧张素（Agn）II对大鼠心脏中I、III型胶原蛋白基因调控与表达的作用，以及新型非肽类选择性血管紧张素1受体拮抗剂DMP811对血管紧张素II作用的影响。

方法

选用6周龄雄性SD大鼠，皮下植入含血管紧张素II或生理盐水的渗透微型泵。（1）生理盐水注入（对照）组（n = 6），（2）血管紧张素II注入组（n = 6），（3）血管紧张素II注入及DMP811处理（3mg·kg-1·d-1，灌胃）组（n = 6）。持续注入血管紧张素II（200ng·kg-1·min-1）或生理盐水1周。提取心脏总RNA后，分别用逆转录聚合酶链反应（RT-PCR）和天狼星红染色法检测I、III型胶原蛋白的mRNA水平和蛋白水平。

结果

与第1组相比，第2组心脏重量、心脏重量/体重比值、I、III型胶原蛋白的mRNA水平分别增加了（4.7±0.4）%、（4.9±0.9）%、（22.0±4.7）%和（20.6±4.9）%。天狼星红染色切片上胶原蛋白分析显示，血管紧张素II增加了I、III型胶原蛋白的沉积。血管紧张素II引起的上述变化可被DMP811完全抑制。