التفاصيل البيبلوغرافية
| العنوان: |
LncRNA MALAT1 在衰老大鼠心肌缺血后处理自噬水平降低中的作用. (Chinese) |
| العنوان البديل: |
Role of LncRNA MALAT1 in myocardial autophagy reduction in aging rats after ischemic postconditioning. (English) |
| المؤلفون: |
杨慧霞, 揭育祯, 白志刚, 焦 运, 杨 勇, 马天龙, 马胜超, 姜怡邓 |
| المصدر: |
Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; 7/18/2023, Vol. 27 Issue 20, p3173-3179, 7p |
| مصطلحات موضوعية: |
LINCRNA, ISCHEMIC postconditioning, SPRAGUE Dawley rats, REPERFUSION injury, PROTEIN expression |
| الملخص (بالإنجليزية): |
BACKGROUND: Ischemic postconditioning can alleviate myocardial ischemia-reperfusion injury, but the specific mechanism is not clear. OBJECTIVE: To investigate the mechanism of long non-coding RNA (lncRNA) MALAT1 in the reduction of autophagy levels in aging myocardium induced by ischemic postconditioning. METHODS: Twenty-seven Sprague-Dawley rats aged 22-24 months were randomly divided into three groups, with nine rats in each group: sham operation, ischemia-reperfusion, and ischemic postconditioning groups. Morphological changes of myocardial tissue were observed by hematoxylin-eosin staining and Masson staining. Rat myocardial cells (H9C2) were induced in vitro with 8 mg/mL D-galactose for 9 days and then divided into normoxia, hypoxia-reoxygenation, and hypoxia postconditioning groups. Western blot was used to detect the protein expression levels of LC3II/I and p62. Fluorescence quantitative PCR was used to detect the expression of lncRNA MALAT1 in aging myocardium and aging cardiomyocytes. Autophagy double-labeled adenovirus (RFP-GFP-LC3) was used to observe the changes of autophagic flux in aging cardiomyocytes. lncRNA MALAT1 interference fragment and overexpression plasmid were transfected into aging cardiomyocytes and the protein expression levels of LC3II/I and p62 were detected by western blot. RESULTS AND CONCLUSION: Compared with the ischemia-reperfusion group, the myocardial tissue structure of the ischemic postconditioning group was basically clear, the nucleus was intact, and the deposition of blue collagen fibers in the myocardial tissue was reduced. Compared with the ischemia-reperfusion group, the expression of LC3II/I was decreased and the expression of p62 was increased in the ischemic postconditioning group (P < 0.05). Compared with the hypoxia-reperfusion group, the expression of LC3II/I was decreased (P < 0.01) and the expression of p62 was increased (P < 0.05) in the hypoxia postconditioning group, and the number of intracellular autophagosomes and autophagolysosomes was decreased (P < 0.05). Compared with the ischemiareperfusion group, the expression of MALAT1 in the aging myocardial tissue was decreased the ischemic postconditioning group (P < 0.01); compared with the hypoxia-reperfusion group, the expression of MALAT1 in aging cardiomyocytes was decreased in the hypoxic postconditioning group (P < 0.01). Compared with the hypoxia postconditioning+si-NC group, the expression of LC3II/I was decreased and the expression of p62 was increased in the hypoxia postconditioning +si-lncRNA MALAT1 (P < 0.01); compared with the hypoxia postconditioning+ad-NC group, the expression of LC3II/I was increased and the expression of p62 was decreased in the hypoxia postconditioning+ad-lncRNA MALAT1 group (P < 0.01). To conclude, the lncRNA MALAT1 mediated reduction of autophagy levels is an important mechanism underlying the protective effect of ischemic postconditioning in aging myocardium. [ABSTRACT FROM AUTHOR] |
| Abstract (Chinese): |
背景：缺血后处理可缓解心肌缺血再灌注损伤，但是其具体机制尚不清楚。 目的：探讨lncRNA MALAT1在缺血后处理所引起衰老心肌自噬水平降低中的作用。 方法： 27只22-24月龄SD大鼠随机分为3组：假手术组、缺血再灌注组和缺血后处理组，每组9只，采用苏木精-伊红染色和Masson染色 观察心肌组织形态学变化； 体外使用8 mg/mL D-半乳糖诱导大鼠心肌(H9C2)细胞9 d后，分为正常氧组、缺氧复氧组和缺氧后处理组。 Western blot检测衰老心肌组织及衰老心肌细胞中LC3Ⅱ/Ⅰ和p62蛋白的表达；采用qRT-PCR检测衰老心肌组织和衰老心肌细胞中MALAT1相 对表达；转染自噬双标腺病毒(RFP-GFP-LC3)观察衰老心肌细胞自噬流的变化；衰老心肌细胞转染MALAT1干扰片段和过表达质粒，Western blot检测各组细胞中LC3Ⅱ/Ⅰ和p62蛋白的表达。 结果与结论： 与缺血再灌注组比较，缺血后处理组心肌组织结构基本清晰，细胞核完整，心肌组织间蓝色胶原纤维沉积减少； 与缺 血再灌注组比较，缺血后处理组LC3Ⅱ/Ⅰ表达降低且p62表达增高(P < 0.05)； 与缺氧复氧组比较，缺氧后处理组LC3Ⅱ/Ⅰ表达降低(P < 0.01)且p62表达增加(P < 0.05)，细胞内自噬体和自噬溶酶体数量均减少(P < 0.01)； 与缺血再灌注组比较，缺血后处理组衰老心肌组织的 MALAT1表达降低(P < 0.01)；与缺氧复氧组比较，缺氧后处理组衰老心肌细胞的MALAT1表达降低(P < 0.01)； 衰老心肌细胞转染MALAT1 干扰片段和过表达质粒后，与缺氧复氧+si-NC组比较，缺氧复氧+si-MALAT1组LC3Ⅱ/Ⅰ表达降低且p62表达增加(P < 0.01)；与缺氧后处理+ ad-NC组比较，缺氧后处理+ad-MALAT1组LC3Ⅱ/Ⅰ表达增加且p62表达降低(P < 0.01)； 结果表明：lncRNA MALAT1介导的自噬水平降低是 衰老大鼠心肌缺血后处理发挥保护作用的重要机制。 [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
