Antihypertensive and vasoprotective effects of epigallocatechin-3-gallate(EGCG) in spontaneously hypertensive rats

Khor, Yucinda Yee Yan (2024) Antihypertensive and vasoprotective effects of epigallocatechin-3-gallate(EGCG) in spontaneously hypertensive rats. Master dissertation/thesis, UTAR.

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Abstract

Epigallocatechin-3-gallate (EGCG), a catechin found in green tea is demonstrated to exert blood pressure-lowering effect in hypertensive subjects with elevated oxidative stress. However, the exact underlying mechanism remains unknown. The current study investigated whether the decrease in ROS production via the modulation of angiotensin type I receptor (AT1) contributes to the vasoprotective action of EGCG observed in an animal model with primary hypertension. Wistar-Kyoto (WKY) rats and Spontaneously Hypertensive Rats (SHR) were grouped into WKY Control, SHR Control, SHR treated with EGCG (50mg/kg/day) and SHR treated with losartan (10mg/kg/day) respectively. The treatment was given daily for 4 weeks by oral gavage and the blood pressure was monitored by tail-cuff method every 3 days. Acetylcholine-induced vascular relaxation was assessed in isolated aortic rings contracted with phenylephrine at the end of treatment. The vascular levels of nitric oxide (NO), reactive oxygen species (ROS), tetrahydrobiopterin (BH4) and cyclic guanosine monophosphate (cGMP) were also measured. Lastly, expression of AT1 receptor protein was analysed. After 4 weeks of treatment, the was a significant decrease in systolic blood pressure of the SHR treated with EGCG and losartan. In line with this, there was significant improvement in endothelium-dependent relaxation in aortic ring isolated from EGCG and losartan-treated SHR groups. The ROS level was also decreased in these groups. Besides that, the levels of NO, BH4 and cGMP were also significantly increased in SHR treated with EGCG or losartan. It was also observed that there was a decreasing trend in the protein expression of AT1 receptor in SHR treated with EGCG and losartan. In conclusion, this study shows that EGCG improves endothelial function in SHR by attenuating oxidative stress and elevating the bioavailability of vascular NO, which may be modulated partly by downregulation of vascular AT1 receptors. The increase in endothelium-dependent relaxation in part may have contributed to the blood pressure lowering effect of EGCG in the hypertensive animals.

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