[1]付 莉,黄 晶,苗 娜,等.视黄酸相关孤儿受体α对阿霉素诱导心肌损伤的改善作用及机制研究[J].陕西医学杂志,2023,52(12):1754-1758.[doi:DOI:10.3969/j.issn.1000-7377.2023.12.028]
　FU Li,HUANG Jing,MIAO Na,et al.Improvement effect of RORα on adriamycin-induced myocardial injury and its mechanism[J].,2023,52(12):1754-1758.[doi:DOI:10.3969/j.issn.1000-7377.2023.12.028]
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视黄酸相关孤儿受体α对阿霉素诱导心肌损伤的改善作用及机制研究
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《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
52
期数:
2023年12期
页码:
1754-1758
栏目:
临床病理
出版日期:
2023-12-05

文章信息/Info

Title:
Improvement effect of RORα on adriamycin-induced myocardial injury and its mechanism
作者:
付 莉1; 黄 晶1; 苗 娜1; 王志强2
(1.新疆医科大学第一附属医院病理科,新疆 乌鲁木齐 830054; 2.新疆医科大学第二附属医院,新疆 乌鲁木齐 830054)
Author(s):
FU Li; HUANG Jing; MIAO Na; WANG Zhiqiang
(Department of Pathology,First Affiliated Hospital of Xinjiang Medical University,Urumqi 830054,China)
关键词:
心肌损伤;  视黄酸相关孤儿受体α;  阿霉素;  锰超氧化物歧化酶;  改善作用;  机制
Keywords:
Heart injury;  Retinoic acid receptor-related orphan receptor α;  Doxorubicin;  Manganese superoxide dismutase;  Improvement effect;  Mechanism
分类号:
R 542.2
DOI:
DOI:10.3969/j.issn.1000-7377.2023.12.028
文献标志码:
A
摘要:
目的:探讨视黄酸相关孤儿受体α(RORα)对阿霉素(DOX)诱导的心肌损伤的改善作用及机制。方法:采用尾静脉注射RORα过表达慢病毒建立心肌RORα高表达模型。随机将小鼠分为对照组(NC组)、RORα过表达组、DOX组和RORα过表达+DOX组,每组20只。其中,DOX组和RORα过表达+DOX组一次性给予15 mg/(kg·d)DOX腹腔注射,NC组和RORα过表达组给予腹腔注射同等体积0.9%氯化钠溶液。2周后,采用超声检测左心室射血分数(LVEF)和左心室短轴缩短率(LVFS); 采用相应试剂盒检测血浆血浆肌酸激酶(CK)和乳酸脱氢酶(LDH)活性; 采用TUNEL法检测小鼠心肌凋亡情况; 采用电镜观察心肌线粒体形态; 采用比色法检测心肌活性氧簇(ROS)水平; 采用Western blot检测RORα和锰超氧化物歧化酶(MnSOD)蛋白表达水平。结果: 与NC组比较,DOX组LVEF和LVFS降低,CK、LDH活性增加,心肌细胞凋亡增加,心肌ROS水平增加,MnSOD蛋白表达降低(均P<0.05),并且心肌线粒体发生损伤。与DOX组比较,RORα过表达+DOX组LVEF和LVFS 增加,CK、LDH活性下降,心肌细胞凋亡减少,心肌ROS水平降低,MnSOD蛋白表达增加(均P<0.05),并且心肌线粒体损伤有明显改善。结论:在DOX诱导的心肌损伤中,RORα可能通过调控MnSOD表达发挥改善心肌的作用。
Abstract:
Objective:To investigate the improvement effect and mechanism of retinoic acid receptor-related orphan receptor α(RORα)against adriamycin(DOX)-induced myocardial injury.Methods:A cardiac RORα high expression model was established by tail vein injection of RORα overexpression lentivirus.The mice were randomly divided into control group(NC group),RORα overexpression group,DOX group and RORα overexpression+DOX group,with 20 mice in each group.The DOX group and RORα overexpression+DOX group were intraperitoneally injected with DOX at a dose of 15 mg/(kg·d),and the NC group and RORα overexpression group were intraperitoneally injected with the same volume of 0.9% sodium chloride solution.Two weeks later,left ventricular ejection fraction(LVEF)and left ventricular fractional shortening(LVFS)were detected by ultrasound; the activities of creatine kinase(CK)and lactate dehydrogenase(LDH)in plasma were detected by corresponding kits; myocardial apoptosis was detected by TUNEL assay; the morphology of myocardial mitochondria was observed by electron microscopy; the level of reactive oxygen species(ROS)in myocardium was detected by colorimetry; the protein expression levels of RORα and manganese superoxide dismutase(MnSOD)were detected by Western blot.Results:Compared with the NC group,in the DOX group,the LVEF and LVFS were decreased,CK and LDH activities were increased,cardiomyocyte apoptosis was increased,ROS level was increased,MnSOD protein expression was decreased(all P<0.05),and myocardial mitochondria were damaged.Compared with the DOX group,in the RORα overexpression+DOX group,LVEF and LVFS were increased,CK and LDH activities were decreased,cardiomyocyte apoptosis was decreased,ROS level was decreased,MnSOD protein expression was increased(all P<0.05),and myocardial mitochondrial damage was significantly improved.Conclusion:RORα may play a role in DOX-induced myocardial injury by regulating the expression of MnSOD.

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备注/Memo

备注/Memo:
基金项目:新疆维吾尔自治区自然科学基金资助面上项目(2023D01C113)
更新日期/Last Update: 2023-12-05