[1]余娜,徐路晴,沈涤非.L-茶氨酸通过Nrf2/HO-1通路减轻H9c2心肌细胞缺氧再复氧的氧化应激和细胞凋亡[J].心血管病学进展,2025,(10):954.[doi:10.16806/j.cnki.issn.1004-3934.2025.10.017]
　YU Na,XU Luqing,SHEN Difei.Theanine Alleviates Oxidative Stress and Apoptosis in H9c2 Cardiomyocytes Exposed to Hypoxia-Reoxygenation via the Nrf2/HO-1 Pathway[J].Advances in Cardiovascular Diseases,2025,(10):954.[doi:10.16806/j.cnki.issn.1004-3934.2025.10.017]
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L-茶氨酸通过Nrf2/HO-1通路减轻H9c2心肌细胞缺氧再复氧的氧化应激和细胞凋亡()

《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2025年10期
页码:
954
栏目:
论著
出版日期:
2025-10-25

文章信息/Info

Title:
Theanine Alleviates Oxidative Stress and Apoptosis in H9c2 Cardiomyocytes Exposed to Hypoxia-Reoxygenation via the Nrf2/HO-1 Pathway
作者:
余娜; 徐路晴; 沈涤非
（武汉大学人民医院心血管内科 代谢与相关慢病湖北省重点实验室，湖北 武汉 430060）
Author(s):
YU Na; XU Luqing; SHEN Difei
（Department of Cardiology，Renmin Hospital of Wuhan University，Hubei Provincial Key Laboratory of Metabolic and Chronic Diseases，Wuhan 430060，Hubei，China）
关键词:
L-茶氨酸; 心肌细胞; 缺氧再复氧; 氧化应激; 细胞凋亡
Keywords:
L-theanine; Cardiac muscle cell; Hypoxia-reoxygenation; Oxidative stress; Apoptosis
DOI:
10.16806/j.cnki.issn.1004-3934.2025.10.017
文献标志码:
A
摘要:
目的 探讨L-茶氨酸对H9c2心肌细胞缺氧再复氧损伤的影响及作用机制? 方法 构建H9c2心肌细胞缺氧再复氧模型,将H9c2细胞随机分为常氧组?缺氧再复氧组?及缺氧再复氧+L-茶氨酸(2mM?4mM?8mM)组。采用CCK-8法检测细胞活力，生化试剂盒评估氧化应激标志物（MDA、SOD、CAT）及心肌损伤指标（LDH、CK-MB、cTnI），TUNEL染色和caspase-3活性检测分析细胞凋亡，Western blot和qPCR检测Nrf2/HO-1通路相关蛋白及基因表达。 结果 HR刺激显著降低细胞活力，并升高心肌损伤标志物LDH、CK-MB和cTnI水平，而L-茶氨酸预处理可有效恢复细胞活性并减少损伤标志物释放（p＜0.05）。HR处理诱导的氧化应激表现为ROS和MDA水平升高、SOD和CAT活性降低，而L-茶氨酸干预显著逆转上述变化（p＜0.05）。此外，HR组细胞凋亡率（TUNEL阳性细胞比例）及caspase-3活性显著增加，且促凋亡蛋白Bax表达上调、抗凋亡蛋白Bcl-2下调，而L-TH治疗可抑制凋亡并调节Bax/Bcl-2平衡（p＜0.05）。进一步研究发现HR组Nrf2和HO-1蛋白表达及mRNA表达显著降低，而L-TH干预后其表达恢复至接近常氧组水平（p＜0.05）。 结论 L-茶氨酸可以减轻缺氧再复氧的2H9c2心肌细胞的氧化应激损伤及细胞凋亡,可能是通过Ｎｒｆ２／ＨＯ-１通路发挥作用?
Abstract:
Objective To investigate the effects of L-theanine on hypoxia- reoxygenation (HR)-induced injury in H9c2 cardiomyocytes and its underlying mechanisms. Methods An HR injury model was established in H9c2 cardiomyocytes. Cells were randomly divided into the following groups: normoxia group, HR group, and HR + L-theanine (2 mM, 4 mM, 8 mM) groups. Cell viability was measured using the CCK-8 assay. Oxidative stress markers (malondialdehyde, MDA superoxide dismutase, SOD catalase, CAT) and myocardial injury indicators (lactate dehydrogenase, LDH creatine kinase-MB, CK-MB cardiac troponin I, cTnI) were assessed with biochemical kits. Apoptosis was evaluated via TUNEL staining and caspase-3 activity assays. Protein and mRNA expression levels of Nrf2 and HO-1 were detected by Western blot and quantitative real-time PCR (qPCR). Results HR stimulation significantly reduced cell viability and increased the levels of myocardial injury markers (LDH, CK-MB,cTnI p＜0.05). Pretreatment with L-theanine effectively restored cell viability and reduced the release of injury markers (p＜0.05). HR-induced oxidative stress was characterized by elevated ROS and MDA levels and decreased SOD and CAT activity, which were significantly reversed by L-theanine (p＜0.05). Additionally, HR increased the apoptosis rate (TUNEL-positive cells) and caspase-3 activity, upregulated pro-apoptotic Bax expression, and downregulated anti-apoptotic Bcl-2 expression. L-theanine treatment inhibited apoptosis and restored the Bax/Bcl-2 balance (p＜0.05). Mechanistically, HR downregulated both protein and mRNA expression of Nrf2 and HO-1, whereas L-theanine restored their expression to near-normoxia levels (p＜0.05). Conclusion L-theanine mitigates oxidative stress and apoptosis in H9c2 cardiomyocytes exposed to hypoxia-reoxygenation, potentially via activation of the Nrf2/HO-1 pathway

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更新日期/Last Update: 2026-01-16