Epigallocatechin-3-gallate exerts antihypertensive effects and improves endothelial function in spontaneously hypertensive rats

Abstract

Objective: To investigate the effect of epigallocatechin-3-gallate (EGCG) on endothelial dysfunction in spontaneously hypertensive rats (SHR). Methods: Wistar-Kyoto (WKY) rats and SHR were divided into four groups; WKY control, SHR control and SHR treated with EGCG (50 mg/kg/day) or losartan (10 mg/kg/day). 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 endothelium-dependent relaxations were assessed in isolated phenylephrine-precontracted aortic rings at the end of treatment. The vascular levels of reactive oxygen species, nitric oxide, tetrahydrobiopterin, and cyclic guanosine monophosphate were also measured. Moreover, the expression of angiotensin Ⅱ type 1 (AT₁) receptor protein was determined. Results: The systolic blood pressure was significantly decreased in SHR treated with EGCG. The impaired endothelium-dependent relaxation was significantly improved in aortic ring isolated from the EGCG-treated SHR group. EGCG also significantly increased the levels of nitric oxide, tetrahydrobiopterin, and cyclic guanosine monophosphate, while decreasing the level of reactive oxygen species and the protein expression of AT₁ receptor in SHR. Conclusions: EGCG attenuates endothelial dysfunction in SHR by decreasing oxidative stress and increasing vascular nitric oxide bioavailability, which may be modulated partly by inhibition of vascular AT₁ receptors. An increase in endothelium-dependent relaxation may contribute to a decrease in blood pressure in hypertensive animals.

Keywords

Epigallocatechin-3-gallate / Vascular protection / Antihypertension / Tetrahydrobiopterin / Cyclic guanosine monophosphate / Angiotensin type Ⅰ receptor / Spontaneously hypertensive rats

Acknowledgments

The authors thank Universiti Tunku Abdul Rahman and Universiti Malaya for financial and material support.

Conflict of interest statement

The authors declare no conflict of interest.

Funding

This study was funded by the Universiti Tunku Abdul Rahman Research fund (IPSR/RMC/UTARRF/2019-C2/L08).

Authors’ contributions

YYYK and WCL performed the research and analyzed the data. WCL, SKL, and DDM designed the research study. WCL, SKL, and DDM contributed to essential reagents and tools. All authors wrote and reviewed the manuscript.

Publisher’s note

The Publisher of the Journal remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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