[1]范 芮,马玉龙,赖红梅,等.lncRNA GAS5对人心脏微血管内皮细胞缺血再灌注损伤的影响及机制实验研究[J].陕西医学杂志,2026,(5):605-610.[doi:DOI:10.3969/j.issn.1000-7377.2026.05.005]
　FAN Rui,MA Yulong,LAI Hongmei,et al.Effect and mechanism of lncRNA GAS5 on ischemia-reperfusion injury in human cardiac microvascular endothelial cells[J].,2026,(5):605-610.[doi:DOI:10.3969/j.issn.1000-7377.2026.05.005]
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lncRNA GAS5对人心脏微血管内皮细胞缺血再灌注损伤的影响及机制实验研究

《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
期数:
2026年5期
页码:
605-610
栏目:
基础研究
出版日期:
2026-05-05

文章信息/Info

Title:
Effect and mechanism of lncRNA GAS5 on ischemia-reperfusion injury in human cardiac microvascular endothelial cells
作者:
范 芮1; 马玉龙1; 赖红梅2; 向 阳3
（1.昌吉州人民医院心血管内科，新疆 昌吉 831100；2.新疆维吾尔自治区人民医院心内科，新疆 乌鲁木齐 830001；3.新疆医科大学第一附属医院心血管内科，新疆 乌鲁木齐 830013）
Author(s):
FAN Rui1; MA Yulong1; LAI Hongmei2; XIANG Yang3
(1.Department of Cardiology,Changji People’s Hospital,Changji 831100,China;2.Department of Cardiology,People’s Hospital of Xinjiang Uygur Autonomous Region,Urumqi 830001,China;3.Department of Cardiology,the First Affiliated Hospital of Xinjiang Medical University,Urumqi 830013,China)
关键词:
长链非编码RNA生长阻滞特异性转录因子5; 缺血再灌注; 人心脏微血管内皮细胞; 细胞增殖; 细胞凋亡; 自噬
Keywords:
Long non-coding RNA growth arrest-specific transcript 5; Ischemia-reperfusion; Human cardiac microvascular endothelial cells; Cell proliferation; Apoptosis; Autophagy
分类号:
R36
DOI:
DOI:10.3969/j.issn.1000-7377.2026.05.005
文献标志码:
A
摘要:
目的：探讨长链非编码RNA（lncRNA）生长阻滞特异性转录因子5（GAS5）对人心脏微血管内皮细胞（HCMEC）缺血再灌注（IR）损伤的影响及其可能的机制。方法：选取HCMEC，分为正常对照组（常规培养，无干预）、模型组（建立细胞IR损伤模型）、阴性对照组（IR+转染阴性对照慢病毒）、GAS5过表达组（IR+转染lncRNA GAS5过表达慢病毒）、GAS5干扰组（IR+转染lncRNA GAS5干扰慢病毒）。观察各组细胞形态学特征；RT-qPCR检测各组细胞GAS5 mRNA水平；ELISA法检测各组细胞炎症因子水平；MTT法检测各组细胞增殖能力；TUNEL法检测各组细胞凋亡能力；Western blot检测各组细胞微管相关蛋白1轻链3（LC3）、Beclin1蛋白表达。结果：正常对照组HCMEC贴壁紧密、形态规则、胞质均匀，无细胞脱落现象；模型组细胞贴壁能力显著下降、细胞皱缩变圆、胞质颗粒增多，且可见部分细胞从培养皿壁脱落；阴性对照组细胞形态与模型组无明显差异；GAS5过表达组上述细胞损伤相关形态学改变明显改善；GAS5干扰组细胞损伤形态较阴性对照组进一步加重。与正常对照组比较，模型组细胞凋亡率、白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）水平升高，细胞增殖率、GAS5 mRNA及LC3、Beclin1蛋白表达水平降低（均P<0.05）。模型组与阴性对照组上述指标比较差异无统计学意义（均P>0.05）。GAS5过表达组上述指标变化较阴性对照组改善，而GAS5干扰组较阴性对照组加重（均P<0.05）。结论：上调lncRNA GAS5表达可减轻IR造成的HCMEC损伤，其机制可能与激活细胞自噬有关。
Abstract:
Objective:To investigate the effect of long non-coding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5) on ischemia-reperfusion (IR) injury in human cardiac microvascular endothelial cells (HCMEC) and its possible mechanism.Methods：HCMECs were divided into the following groups：normal control group (routine culture without intervention),model group (IR injury model established),negative control group (IR+transfection with negative control lentivirus),GAS5 overexpression group (IR+transfection with lncRNA GAS5 overexpression lentivirus),and GAS5 knockdown group (IR+transfection with lncRNA GAS5 interference lentivirus).Morphological characteristics of cells in each group were observed.RT-qPCR was performed to detect GAS5 mRNA levels.ELISA was used to measure inflammatory cytokine levels.MTT assay was conducted to evaluate cell proliferation.TUNEL assay was employed to assess apoptosis.Western blot was used to detect the protein expression of LC3 and Beclin1.Results:HCMECs in the normal control group exhibited tight adherence,regular morphology,uniform cytoplasm,and no cell detachment.In contrast,cells in the model group demonstrated significantly reduced adherence,shrinkage and rounding,increased cytoplasmic granularity,and partial detachment from the culture dish.No obvious morphological differences were observed between the negative control group and the model group.These IR-related morphological alterations were markedly ameliorated in the GAS5 overexpression group,whereas the GAS5 knockdown group exhibited further aggravated cellular damage compared with the negative control group.Compared with the normal control group,the model group showed increased apoptosis rate and elevated levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α),along with decreased cell proliferation rate,GAS5 mRNA expression,and protein expression of LC3 and Beclin1 (all P<0.05).No statistically significant differences were observed between the model group and the negative control group in these parameters (all P>0.05).The GAS5 overexpression group demonstrated improved changes in the above indicators compared with the negative control group,while the GAS5 knockdown group showed aggravated changes (all P<0.05).Conclusion:Upregulation of lncRNA GAS5 expression can attenuate IR-induced HCMEC injury,and the mechanism may be associated with the activation of autophagy.

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备注/Memo

备注/Memo:
省部共建中亚高发病成因与防治国家重点实验室开放课题（SKL-HIDCA-2023-CJ5）
更新日期/Last Update: 2026-05-05