王佳.山姜素下调微小RNA146a-5p表达减轻血管内皮细胞氧化应激损伤[J].内科急危重症杂志,2023,29(4):326-331
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DOI:10.11768/nkjwzzzz20230416 |
中文关键词: 山姜素 血管内皮细胞 氧化应激 凋亡 miR-146a-5p |
英文关键词: |
基金项目:湖北省自然科学基金(No:WJ2015Q037) |
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中文摘要: |
摘要 目的:探讨山姜素调控微小RNA(miR)146a-5p表达对内毒素诱导的血管内皮细胞氧化应激损伤的影响。方法:采用1μg/mL的脂多糖处理人脐静脉血管内皮细胞(HUVEC)构建细胞损伤模型。将HUVEC分为对照组、LPS组、LPS+山姜素低、中、高剂量组、LPS+anti-miR阴性对照组、LPS+anti-miR-146a-5p组、LPS+山姜素+miR-NC阴性对照组、LPS+山姜素+miR-146a-5p组。采用生化法检测超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性以及丙二醛(MDA)水平。采用流式细胞术检测HUVEC的凋亡率。采用实时定量聚合酶链式反应(RT-qPCR)检测miR-146a-5p表达。结果:与Con组比较,LPS组细胞凋亡率、MDA水平、miR-146a-5p表达显著升高,SOD和GSH-Px活性显著降低。与LPS组比较,LPS+山姜素低、中、高剂量组细胞凋亡率、MDA水平、miR-146a-5p表达显著降低,而SOD和GSH-Px活性显著升高(P均<0.05)。与LPS+anti-miR-阴性对照组比较,LPS+anti-miR-146a-5p组细胞凋亡率、MDA水平显著降低,而SOD和GSH-Px活性显著升高(P均<0.05)。与LPS+山姜素+miR-阴性对照组比较,LPS+山姜素+miR-146a-5p组细胞凋亡率、MDA水平显著升高,而SOD和GSH-Px活性显著降低(P均<0.05)。结论:山姜素通过下调miR-146a-5p表达减轻内毒素诱导的血管内皮细胞氧化应激损伤。 |
英文摘要: |
Abstract Objective: To investigate the effect of alpinetin on endotoxin-induced oxidative stress injury in vascular endothelial cells by regulating miR146a5p expression. Methods: Human umbilical vein endothelial cells (HUVECs) were treated with 1μg/mL lipopolysaccharide (LPS) to construct a cell injury model. HUVECs were divided into control (Con) group, LPS group, LPS+alpinetin (low dose) group, LPS+alpinetin (medium dose) group, LPS+alpinetin (high dose) group, LPS+antimiRNC group, LPS+antimiR146a5p group, LPS+alpinetin+miRNC group, LPS+alpinetin+miR146a5p group. Biochemical methods were applied to detect the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSHPx), and the level of malondialdehyde (MDA). Flow cytometry was used to detect the apoptosis rate of HUVECs. Real-time quantitative PCR (RTqPCR) was employed to detect the miR146a5p expression. Results: As compared with the Con group, the apoptosis rate, MDA level, and miR146a5p expression in the LPS group were significantly increased (P<0.05), and the SOD and GSHPx activities were significantly decreased (P<0.05). As compared with the LPS group, the apoptosis rate, MDA level and miR146a5p expression in the LPS+alpinetin (low dose) group, LPS+alpinetin (medium dose) group and LPS+alpinetin (high dose) group were significantly reduced (P<0.05), SOD and GSHPx activities were significantly increased (P<0.05). As compared with the LPS+antimiRNC group, the apoptosis rate and MDA level in the LPS+antimiR146a5p group were significantly reduced (P<0.05), and the activities of SOD and GSHPx were significantly increased (P<0.05). As compared with the LPS+alpinetin+miRNC group, the apoptosis rate and MDA level in the LPS +alpinetin+miR146a5p group were significantly increased (P<0.05), and SOD and GSHPx activities were significantly reduced (P<0.05). Conclusion: Alpinetin could reduce endotoxin-induced oxidative stress damage to vascular endothelial cells by down-regulating the miR146a5p expression. |
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