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Loxoprofen Sodium Alleviates Oxidative Stress and Apoptosis Induced by Angiotensin II in Human Umbilical Vein Endothelial Cells (HUVECs)
Drug Design, Development and Therapy ( IF 4.8 ) Pub Date : 2020-11-18 , DOI: 10.2147/dddt.s266175 Chuanzhao Ji 1 , Yang Yu 2 , Min Zhang 2 , Wenyan Yu 2 , Shuo Dong 1
Drug Design, Development and Therapy ( IF 4.8 ) Pub Date : 2020-11-18 , DOI: 10.2147/dddt.s266175 Chuanzhao Ji 1 , Yang Yu 2 , Min Zhang 2 , Wenyan Yu 2 , Shuo Dong 1
Affiliation
Background and Purpose: Endothelium exerts an important role in releasing vasoactive substances, maintaining the blood flow, regulating the growth of vessels, moderating the process of coagulation, and the balance of fibrinolytic system, the dysfunction of which is reported to result in arterial stiffness. The present study aimed to investigate the effects of loxoprofen sodium against HUVECs injury induced by angiotensin II.
Methods: The injury model on HUVECs was established through incubation with angiotensin II. The expression levels of AT2R, NOX-4, Bax, Bcl-2, and caspase-3 were evaluated using qRT-PCR and Western Blot. DCFH-DA assay was used to detect the production of ROS and ELISA assay was used to evaluate the level of reduced glutathione. Mitochondrial membrane potential (MMP) was measured using dihydrorhodamine 123 assay. MTT and LDH assays were utilized to determine the proliferation ability of HUVECs. The apoptosis rate of HUVECs was evaluated using flow cytometry.
Results: Loxoprofen sodium suppressed endothelial AT2R elevation by angiotensin II. Loxoprofen ameliorated Angiotensin II–induced production of ROS, reduced GSH, and NOX-2 and NOX-4 expression. Furthermore, Loxoprofen mitigated Angiotensin II, reduced mitochondrial membrane potential and improved cell viability, and suppressed LDH release by angiotensin II. Importantly, loxoprofen showed a beneficial role in protecting endothelial apoptosis by mitigating apoptotic machinery including the balanced expression of Bax, Bcl-2, and caspase-3 cleavage.
Conclusion: Loxoprofen sodium might alleviate the high ROS levels and apoptosis induced by angiotensin II in HUVECs.
Keywords: angiotensin II, apoptosis, endothelial cells, ROS
中文翻译：
洛索洛芬钠可减轻血管紧张素 II 在人脐静脉内皮细胞 (HUVEC) 中诱导的氧化应激和细胞凋亡
背景与目的：内皮在释放血管活性物质、维持血流、调节血管生长、调节凝血过程和纤溶系统平衡方面发挥重要作用，据报道其功能障碍会导致动脉僵硬。本研究旨在探讨洛索洛芬钠对血管紧张素 II 诱导的 HUVECs 损伤的影响。
方法：通过与血管紧张素II孵育建立HUVECs损伤模型。使用 qRT-PCR 和蛋白质印迹评估 AT2R、NOX-4、Bax、Bcl-2 和 caspase-3 的表达水平。DCFH-DA测定用于检测ROS的产生，ELISA测定用于评估还原型谷胱甘肽的水平。使用二氢罗丹明 123 测定法测量线粒体膜电位 (MMP)。MTT和LDH测定用于确定HUVEC的增殖能力。使用流式细胞术评估 HUVECs 的凋亡率。
结果：洛索洛芬钠通过血管紧张素 II 抑制内皮 AT2R 升高。洛索洛芬改善了血管紧张素 II 诱导的 ROS 产生，降低了 GSH、NOX-2 和 NOX-4 的表达。此外，洛索洛芬减轻血管紧张素 II、降低线粒体膜电位和提高细胞活力，并抑制血管紧张素 II 释放 LDH。重要的是，洛索洛芬通过减轻包括 Bax、Bcl-2 和 caspase-3 裂解的平衡表达在内的凋亡机制，在保护内皮细胞凋亡方面表现出有益的作用。
结论：洛索洛芬钠可减轻血管紧张素Ⅱ诱导的HUVECs高活性氧水平和细胞凋亡。
关键词：血管紧张素Ⅱ，细胞凋亡，内皮细胞，活性氧
更新日期：2020-11-18
Methods: The injury model on HUVECs was established through incubation with angiotensin II. The expression levels of AT2R, NOX-4, Bax, Bcl-2, and caspase-3 were evaluated using qRT-PCR and Western Blot. DCFH-DA assay was used to detect the production of ROS and ELISA assay was used to evaluate the level of reduced glutathione. Mitochondrial membrane potential (MMP) was measured using dihydrorhodamine 123 assay. MTT and LDH assays were utilized to determine the proliferation ability of HUVECs. The apoptosis rate of HUVECs was evaluated using flow cytometry.
Results: Loxoprofen sodium suppressed endothelial AT2R elevation by angiotensin II. Loxoprofen ameliorated Angiotensin II–induced production of ROS, reduced GSH, and NOX-2 and NOX-4 expression. Furthermore, Loxoprofen mitigated Angiotensin II, reduced mitochondrial membrane potential and improved cell viability, and suppressed LDH release by angiotensin II. Importantly, loxoprofen showed a beneficial role in protecting endothelial apoptosis by mitigating apoptotic machinery including the balanced expression of Bax, Bcl-2, and caspase-3 cleavage.
Conclusion: Loxoprofen sodium might alleviate the high ROS levels and apoptosis induced by angiotensin II in HUVECs.
Keywords: angiotensin II, apoptosis, endothelial cells, ROS
中文翻译：
洛索洛芬钠可减轻血管紧张素 II 在人脐静脉内皮细胞 (HUVEC) 中诱导的氧化应激和细胞凋亡
背景与目的：内皮在释放血管活性物质、维持血流、调节血管生长、调节凝血过程和纤溶系统平衡方面发挥重要作用，据报道其功能障碍会导致动脉僵硬。本研究旨在探讨洛索洛芬钠对血管紧张素 II 诱导的 HUVECs 损伤的影响。
方法：通过与血管紧张素II孵育建立HUVECs损伤模型。使用 qRT-PCR 和蛋白质印迹评估 AT2R、NOX-4、Bax、Bcl-2 和 caspase-3 的表达水平。DCFH-DA测定用于检测ROS的产生，ELISA测定用于评估还原型谷胱甘肽的水平。使用二氢罗丹明 123 测定法测量线粒体膜电位 (MMP)。MTT和LDH测定用于确定HUVEC的增殖能力。使用流式细胞术评估 HUVECs 的凋亡率。
结果：洛索洛芬钠通过血管紧张素 II 抑制内皮 AT2R 升高。洛索洛芬改善了血管紧张素 II 诱导的 ROS 产生，降低了 GSH、NOX-2 和 NOX-4 的表达。此外，洛索洛芬减轻血管紧张素 II、降低线粒体膜电位和提高细胞活力，并抑制血管紧张素 II 释放 LDH。重要的是，洛索洛芬通过减轻包括 Bax、Bcl-2 和 caspase-3 裂解的平衡表达在内的凋亡机制，在保护内皮细胞凋亡方面表现出有益的作用。
结论：洛索洛芬钠可减轻血管紧张素Ⅱ诱导的HUVECs高活性氧水平和细胞凋亡。
关键词：血管紧张素Ⅱ，细胞凋亡，内皮细胞，活性氧
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