Renoprotective Effects of Antroquinonol in Rats with Nω-Nitro-l-Arginine Methyl Ester-Induced Hypertension.
Jiun-Rong ChenJung KoWan-Ju YehWen-Chih HuangHsin-Yi YangPublished in: Nutrients (2018)
Endothelial dysfunction leads to elevation of blood pressure and vascular remodeling, which may result in tissue injuries. The aim of this study was to investigate the mechanisms and effects of antroquinonol on hypertension and related renal injuries. Rats were fed water containing 25 mg/kg/day Nω-nitro-l-arginine methyl ester (L-NAME) to induce hypertension, and a diet with or without antroquinonol (20 or 40 mg/kg/day) for a 9-week experiment. During the experimental period, antroquinonol reduced the elevation of systolic and diastolic blood pressure. At the end of the study, we found that the antroquinonol groups had lower serum creatinine, renal endothelin-1, angiotensin II, and malondialdehyde levels and arteriole thickening. We found that the 40 mg/kg/day antroquinonol group had lower renal nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activities, greater nuclear factor erythroid-2, and heme oxygenase-1 expressions. Moreover, we also found that antroquinonol decreased proinflammatory cytokine concentrations in the kidney by modulating the nuclear factor-κB pathway. These results suggest that antroquinonol may ameliorate hypertension and improve renal function by reducing oxidative stress and inflammation in rats with endothelial dysfunction.
Keyphrases
- blood pressure
- nuclear factor
- hypertensive patients
- angiotensin ii
- oxidative stress
- toll like receptor
- heart rate
- nitric oxide
- blood glucose
- physical activity
- type diabetes
- signaling pathway
- dna damage
- adipose tissue
- ischemia reperfusion injury
- clinical trial
- vascular smooth muscle cells
- immune response
- amino acid
- uric acid
- randomized controlled trial
- skeletal muscle
- endothelial cells
- stress induced
- endoplasmic reticulum stress
- induced apoptosis
- atrial fibrillation