Edaravone inhibits pressure overload-induced cardiac fibrosis and dysfunction by reducing expression of angiotensin II AT1 receptor
Autor: | Zhi-Qing Zhao, Erskine A. James, Liwang Yang, Wei-Wei Zhang, Jing Wang, Rong-Hua Zheng, Feng Bai |
---|---|
Jazyk: | angličtina |
Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Angiotensin receptor Cardiac fibrosis cardiac fibrosis heart failure Pharmaceutical Science 030204 cardiovascular system & hematology Benzoates Ventricular Function Left Rats Sprague-Dawley chemistry.chemical_compound 0302 clinical medicine Edaravone Drug Discovery Telmisartan Myofibroblasts Aorta Original Research Angiotensin II Free Radical Scavengers Angiotensin-converting enzyme 2 Cardiology cardiovascular system Angiotensin-Converting Enzyme 2 medicine.drug angiotensin II receptor medicine.medical_specialty Peptidyl-Dipeptidase A Receptor Angiotensin Type 1 03 medical and health sciences Internal medicine medicine Animals Pharmacology Pressure overload Angiotensin II receptor type 1 Drug Design Development and Therapy business.industry Macrophages Myocardium medicine.disease Fibrosis Rats Disease Models Animal 030104 developmental biology Endocrinology chemistry Benzimidazoles cardiac function business Angiotensin II Type 1 Receptor Blockers Antipyrine |
Zdroj: | Drug Design, Development and Therapy |
ISSN: | 1177-8881 |
Popis: | Wei-Wei Zhang,1,2 Feng Bai,1 Jin Wang,1 Rong-Hua Zheng,1 Li-Wang Yang,1 Erskine A James,3 Zhi-Qing Zhao1,4 1Department of Physiology, Shanxi Medical University, 2Department of Anesthesiology, Shanxi Provincial People’s Hospital, Taiyuan, Shanxi, China; 3Department of Internal Medicine, Navicent Health, Macon, 4Department of Basic Biomedical Sciences, Mercer University School of Medicine, Savannah, GA, USA Abstract: Angiotensin II (Ang II) is known to be involved in the progression of ventricular dysfunction and heart failure by eliciting cardiac fibrosis. The purpose of this study was to demonstrate whether treatment with an antioxidant compound, edaravone, reduces cardiac fibrosis and improves ventricular function by inhibiting Ang II AT1 receptor. The study was conducted in a rat model of transverse aortic constriction (TAC). In control, rats were subjected to 8 weeks of TAC. In treated rats, edaravone (10 mg/kg/day) or Ang II AT1 receptor blocker, telmisartan (10 mg/kg/day) was administered by intraperitoneal injection or gastric gavage, respectively, during TAC. Relative to the animals with TAC, edaravone reduced myocardial malonaldehyde level and increased superoxide dismutase activity. Protein level of the AT1 receptor was reduced and the AT2 receptor was upregulated, as evidenced by the reduced ratio of AT1 over AT2 receptor (0.57±0.2 vs 3.16±0.39, p |
Databáze: | OpenAIRE |
Externí odkaz: |