Loxoprofen Sodium Alleviates Oxidative Stress and Apoptosis Induced by Angiotensin II in Human Umbilical Vein Endothelial Cells (HUVECs)
| Autor: | Shuo Dong, Chuanzhao Ji, Yang Yu, Min Zhang, Wenyan Yu |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Pharmacology Endothelium Chemistry Pharmaceutical Science Loxoprofen medicine.disease_cause Angiotensin II Umbilical vein 03 medical and health sciences 030104 developmental biology 0302 clinical medicine medicine.anatomical_structure Apoptosis 030220 oncology & carcinogenesis Drug Discovery Renin–angiotensin system medicine Viability assay Oxidative stress medicine.drug |
| Zdroj: | Drug Design, Development and Therapy. 14:5087-5096 |
| ISSN: | 1177-8881 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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