TRPC1 基因敲除小鼠心肌梗死组织 纤维化指标表达变化.

Objective To investigate the changes in the myocardial fibrosis indexes of myocardial infarction mice with transient receptor potential channel C1(TRPC1） knockout. Methods Twenty wild type mice and 20 TRPC1-/- mice were divided into four groups: the wild control group, wild experimental group, TRPC1-/-control group, and TRPC1-/- experimental group, with 10 mice in each. In the wild experimental group and TRPC1-/- experimental group, the left anterior descending coronary artery was lapped and sutured to establish the myocardial infarction models. In the the wild control group and TRPC1-/- control group, mice were only threaded without ligature. Twenty-four hours later, the mice were sacrificed to obtain the hearts. Normal tissues from the left ventricle were taken from the mice in the two control groups, and infarcted tissues from the anterior wall of the left ventricle were taken from the mice in the two experimental groups. RT-PCR was used to detect the expression of TRPC1 mRNA, and Western blotting was used to detect the TRPC1 protein and Collagen Ⅰ(Col-Ⅰ） and α-smooth muscle actin(α-SMA). ResultsThe mRNA expression of TRPC1 in the wild experimental group was higher than that in the TRPC1-/- experimental group, and that in the wild control group was higher than that in the TRPC1-/- control group（ both P<0. 05). The expression of TRPC1 protein in the wild experimental group was higher than that in the wild control group and the TRPC1-/- experimental group, and the expression of TRPC1 protein in the TRPC1-/-experimental group was higher than that in the TRPC1-/- control group(all P<0. 05). Col-Ⅰ and α -SMA protein expression levels in the wild experimental group were higher than those in the wild control group and TRPC1-/- experimental group, and Col-Ⅰ and α-SMA protein expression levels in the wild control group were higher than those in the TRPC1-/- control group； the expression levels of Col-Ⅰ and α-SMA in the TRPC1-/- experimental group were higher than those in the TRPC1-/- control group（all P<0. 05). Conclusion Knocking down TRPC1 gene expression can down-regulate the expression of myocardial fibrosis indexes of myocardial infarction mice. [ABSTRACT FROM AUTHOR]