首页|TRPC1基因敲除小鼠心肌梗死组织纤维化指标表达变化

TRPC1基因敲除小鼠心肌梗死组织纤维化指标表达变化

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目的 观察瞬时受体电位通道C1(TRPC1)敲除的心肌梗死小鼠心肌纤维化指标变化。方法 野生型小鼠与TRPC1基因缺陷(TRPC1-/-)小鼠各20只,分为野生对照组、野生实验组、TRPC1-/-对照组、TRPC1-/-实验组,每组10只。野生实验组和TRPC1-/-实验组结扎冠状动脉左前降支并缝合,制作心肌梗死模型;野生对照组和TRPC1-/-对照组只穿线,不结扎。24 h后处死小鼠,获取心脏,对照组小鼠取左心室正常组织,实验组取左心室前壁梗死组织,采用RT-PCR法检测TRPC1 mRNA,采用Western blotting法检测TRPC1 蛋白及纤维化指标Ⅰ型胶原蛋白(Col-Ⅰ)、α平滑肌肌动蛋白(α-SMA)。结果 野生实验组TRPC1 mRNA表达高于TRPC1-/-实验组,野生对照组TRPC1 mRNA表达高于TRPC1-/-对照组(P均<0。05);野生实验组TRPC1蛋白表达高于野生对照组和TRPC1-/-实验组,TRPC1-/-实验组TRPC1蛋白表达高于TRPC1-/-对照组(P均<0。05)。野生实验组Col-Ⅰ、α-SMA蛋白表达高于野生对照组和TRPC1-/-实验组,野生对照组Col-Ⅰ、α-SMA蛋白表达高于TRPC1-/-对照组,TRPC1-/-实验组Col-Ⅰ、α-SMA表达高于TRPC1-/-对照组(P均<0。05)。结论 敲低TRPC1 基因表达可下调心肌梗死小鼠心肌纤维化指标的表达。
Expression changes of fibrosis indexes in myocardial infarction tissues of TRPC1 gene knockout mice
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).Results The 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 experimen-tal 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 andα-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.

transient receptor potential channel C1myocardial fibrosismyocardial infarctiongene knockout

陈天苗、王联发、童全秀、侯勇、张现格、黄猛珣

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中国人民解放军联勤保障部队第901医院疾病预防控制科,合肥 230031

中国人民解放军联勤保障部队第901医院心内二科

安徽医科大学卫生管理学院

瞬时受体电位通道C1 心肌纤维化 心肌梗死 基因敲除

安徽医科大学青年基金项目安徽医科大学临床科学基金项目

2022xkj1272023xkj245

2024

山东医药
山东卫生报刊社

山东医药

CSTPCD
影响因子:1.225
ISSN:1002-266X
年,卷(期):2024.64(20)
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