Abstract
Context: 3,4-Dihydroxyacetophenone (DHAP) has been reported to possess cardiovascular pharmacological effects.
Objective: This study was designed to determine whether DHAP could improve endothelial function in obese rats.
Materials and methods: Wistar rats were randomly divided into control, obesity, and DHAP groups and fed a normal, high-fat, and high-fat plus DHAP (10 mg kg−1 d−1) diet, respectively, for 8 weeks. Endothelial-dependent vasodilatation was assessed. Endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO) production in endothelial cells were determined. Nuclear transcription factor kappa B (NF-κB) expression and superoxide production in aorta were evaluated.
Results: DHAP treatment significantly decreased plasma triglycerides (0.94 ± 0.31 mmol/l versus 1.36 ± 0.29 mmol/l, p < 0.05) and free fatty acids (0.53 ± 0.15 mmol/l versus 0.99 ± 0.24 mmol/l, p < 0.05), reduced serum tumor necrosis factor α (35.56 ± 9.28 pg/ml versus 68.3 ± 10.24 pg/ml, p < 0.05) and malondialdehyde (2.94 ± 0.58 pg/ml versus 6.45 ± 0.70 pg/ml, p < 0.05), and increased serum adiponectin levels (164.5 ± 34.5 μg/l versus 84.5 ± 20.4 μg/l, p < 0.05). DHAP enhanced endothelial-dependent vasodilatation and improved endothelial function in obese rats (p < 0.05). eNOS activity and NO production in endothelial cells significantly decreased and NF-κB activation and superoxide production in aorta significantly increased in obese rats compared with the control group (p < 0.05). However, DHAP treatment significantly up-regulated the eNOS–NO pathway and decreased NF-κB activation and superoxide production (p < 0.05).
Conclusion: DHAP improved endothelial function in obese rats. This beneficial effect may be associated with up-regulation of the eNOS–NO pathway by improving lipid metabolism and reducing oxidative stress and inflammation activity.
Declaration of interest
All authors declare that there are no known conflicts of interests related to this publication.