Benzbromarone Attenuates Oxidative Stress in Angiotensin II- and Salt-Induced Hypertensive Model Rats.
Nanako MurayaDaisuke KadowakiShigeyuki MiyamuraKenichiro KitamuraKohei UchimuraYuki NaritaYohei MiyamotoVictor Tuan Giam ChuangKazuaki TaguchiToru MaruyamaMasaki OtagiriSumio HirataPublished in: Oxidative medicine and cellular longevity (2018)
Oxidative stress induced by hyperuricemia is closely associated with the renin-angiotensin system, as well as the onset and progression of cardiovascular disease (CVD) and chronic kidney disease (CKD). It is therefore important to reduce oxidative stress to treat hyperuricemia. We previously found that benzbromarone, a uricosuric agent, has a direct free radical scavenging effect in vitro. The antioxidant effects of benzbromarone were evaluated in vivo via oral administration of benzbromarone for 4 weeks to model rats with angiotensin II- and salt-induced hypertension. Benzbromarone did not alter plasma uric acid levels or blood pressure but significantly reduced the levels of advanced oxidation protein products, which are oxidative stress markers. Furthermore, dihydroethidium staining of the kidney revealed a reduction in oxidative stress after benzbromarone administration. These results suggest that benzbromarone has a direct antioxidant effect in vivo and great potential to prevent CVD and CKD.
Keyphrases
- oxidative stress
- angiotensin ii
- diabetic rats
- uric acid
- blood pressure
- chronic kidney disease
- dna damage
- cardiovascular disease
- angiotensin converting enzyme
- ischemia reperfusion injury
- induced apoptosis
- vascular smooth muscle cells
- metabolic syndrome
- end stage renal disease
- high glucose
- type diabetes
- endothelial cells
- single cell
- heart rate
- coronary artery disease
- risk assessment
- adipose tissue
- hydrogen peroxide
- anti inflammatory
- human health
- nitric oxide
- insulin resistance
- cardiovascular events
- stress induced
- protein protein