1. Rosmarinic Acid Alleviates the Endothelial Dysfunction Induced by Hydrogen Peroxide in Rat Aortic Rings via Activation of AMPK
- Author
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Gang Li, Jianxin Xie, Xiangquan Mi, Hui Zhou, Zhenhua Wang, Baocai Fu, Chengjun Ma, Ji Li, and Bo Xu
- Subjects
0301 basic medicine ,Male ,Aging ,medicine.medical_specialty ,Article Subject ,Endothelium ,Myocytes, Smooth Muscle ,030204 cardiovascular system & hematology ,In Vitro Techniques ,medicine.disease_cause ,Biochemistry ,Depsides ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Downregulation and upregulation ,Enos ,Internal medicine ,medicine ,Animals ,Endothelial dysfunction ,Rats, Wistar ,lcsh:QH573-671 ,Hydrogen peroxide ,Aorta ,biology ,lcsh:Cytology ,Rosmarinic acid ,AMPK ,Cell Biology ,General Medicine ,Hydrogen Peroxide ,medicine.disease ,biology.organism_classification ,Rats ,Oxidative Stress ,030104 developmental biology ,medicine.anatomical_structure ,Endocrinology ,chemistry ,Cinnamates ,Endothelium, Vascular ,Oxidative stress ,Research Article - Abstract
Endothelial dysfunction is the key player in the development and progression of vascular events. Oxidative stress is involved in endothelial injury. Rosmarinic acid (RA) is a natural polyphenol with antioxidative, antiapoptotic, and anti-inflammatory properties. The present study investigates the protective effect of RA on endothelial dysfunction induced by hydrogen peroxide (H2O2). Compared with endothelium-denuded aortic rings, the endothelium significantly alleviated the decrease of vasoconstrictive reactivity to PE and KCl induced by H2O2. H2O2 pretreatment significantly injured the vasodilative reactivity to ACh in endothelium-intact aortic rings in a concentration-dependent manner. RA individual pretreatment had no obvious effect on the vasoconstrictive reaction to PE and KCl, while its cotreatment obviously mitigated the endothelium-dependent relaxation impairments and the oxidative stress induced by H2O2. The RA cotreatment reversed the downregulation of AMPK and eNOS phosphorylation induced by H2O2 in HAEC cells. The pretreatment with the inhibitors of AMPK (compound C) and eNOS (L-NAME) wiped off RA’s beneficial effects. All these results demonstrated that RA attenuated the endothelial dysfunction induced by oxidative stress by activating the AMPK/eNOS pathway.
- Published
- 2017