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The Effect of Hydro-alcoholic Extract of Rheum Turkestanicum Roots against Oxidative Stress in Endothelial Cells

INTRODUCTION: Cardiovascular disorders (CVD) are a common cause of mortality worldwide. Oxidative stress is thought to be a major factor leading to CVD. Anti-oxidants such as medicinal plants may have a role in the mitigation of vascular problems through free radicals scavenging. In this study, we e...

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Detalles Bibliográficos
Autores principales: Hosseini, Azar, Sheikh, Sahar, Soukhtanloo, Mohammad, Malaekeh-Nikouei, Bizhan, Rajabian, Arezoo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer - Medknow 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7554444/
https://www.ncbi.nlm.nih.gov/pubmed/33088450
http://dx.doi.org/10.4103/ijpvm.IJPVM_386_19
Descripción
Sumario:INTRODUCTION: Cardiovascular disorders (CVD) are a common cause of mortality worldwide. Oxidative stress is thought to be a major factor leading to CVD. Anti-oxidants such as medicinal plants may have a role in the mitigation of vascular problems through free radicals scavenging. In this study, we evaluated the protective effects of Rheum turkestanicum against hydrogen peroxide (H(2)O(2))-induced toxicity in endothelial cells (BAE-1). METHODS: To evaluate the protective effect of R. turkestanicum against H(2)O(2) toxicity, four groups comprised of control group (the cells without any treatment), H(2)O(2) group (the cells incubated with H(2)O(2 ()200 μM)), and treatment groups (the cells treated with R. turkestanicum (12200 μg/ml) alone or 24h before exposure to H(2)O(2)). Quercetin (30.23 μg/ml) was used as a bioactive ingredient of the extract. Then the cell viability, reactive oxygen species, lipid peroxidation, and apoptosis were evaluated. RESULTS: H(2)O(2) exposure reduced cell viability to 13.6 ± 1.6%, enhanced ROS generation to 1445 ± 80.7%, lipid peroxidation (LPO, 290 ± 13% of control), and apoptotic cells (P < 0.001). In contrast, compared with H(2)O(2) group, R. turkestanicum and quercetin significantly restored the cell viability to 80.3 ± 1.6 and 87.2 ± 2.1%, ROS formation to 186 ± 10 and 129 ± 1%, as well as LPO to 130.7 ± 7.7 and 116 ± 2.5 of control, respectively (P < 0.001). Therefore, the extract reduced H(2)O(2)-induced toxicity in BAE-1 cells by scavenging of free radicals. CONCLUSION: Our findings demonstrated that the extract might reduce toxicity of endothelial cells by attenuation of oxidative stress, which can be related to the presence of active ingredients including quercetin.