» Articles » PMID: 35268072

(-)-Epicatechin Improves Vasoreactivity and Mitochondrial Respiration in Thermoneutral-Housed Wistar Rat Vasculature

Overview
Journal Nutrients
Date 2022 Mar 10
PMID 35268072
Authors
Affiliations
Soon will be listed here.
Abstract

Cardiovascular disease (CVD) is a global health concern. Vascular dysfunction is an aspect of CVD, and novel treatments targeting vascular physiology are necessary. In the endothelium, eNOS regulates vasodilation and mitochondrial function; both are disrupted in CVD. (−)-Epicatechin, a botanical compound known for its vasodilatory, eNOS, and mitochondrial-stimulating properties, is a potential therapy in those with CVD. We hypothesized that (−)-epicatechin would support eNOS activity and mitochondrial respiration, leading to improved vasoreactivity in a thermoneutral-derived rat model of vascular dysfunction. We housed Wistar rats at room temperature or in thermoneutral conditions for a total of 16 week and treated them with 1mg/kg body weight (−)-epicatechin for 15 day. Vasoreactivity, eNOS activity, and mitochondrial respiration were measured, in addition to the protein expression of upstream cellular signaling molecules including AMPK and CaMKII. We observed a significant improvement of vasodilation in those housed in thermoneutrality and treated with (−)-epicatechin (p < 0.05), as well as dampened mitochondrial respiration (p < 0.05). AMPK and CaMKIIα and β expression were lessened with (−)-epicatechin treatment in those housed at thermoneutrality (p < 0.05). The opposite was observed with animals housed at room temperature supplemented with (−)-epicatechin. These data illustrate a context-dependent vascular response to (−)-epicatechin, a candidate for CVD therapeutic development.

Citing Articles

Cocoa flavanols, Nrf2 activation, and oxidative stress in peripheral artery disease: mechanistic findings in muscle based on outcomes from a randomized trial.

Ismaeel A, McDermott M, Joshi J, Sturgis J, Zhang D, Ho K Am J Physiol Cell Physiol. 2024; 326(2):C589-C605.

PMID: 38189132 PMC: 11193455. DOI: 10.1152/ajpcell.00573.2023.


(-)-Epicatechin Inhibits Metastatic-Associated Proliferation, Migration, and Invasion of Murine Breast Cancer Cells In Vitro.

Perez-Duran J, Luna A, Portilla A, Martinez P, Ceballos G, Ortiz-Flores M Molecules. 2023; 28(17).

PMID: 37687058 PMC: 10488497. DOI: 10.3390/molecules28176229.


The Content of Phenolic Compounds and Mineral Elements in Edible Nuts.

Wozniak M, Waskiewicz A, Ratajczak I Molecules. 2022; 27(14).

PMID: 35889199 PMC: 9316459. DOI: 10.3390/molecules27144326.

References
1.
Kingma B, Frijns A, Schellen L, van Marken Lichtenbelt W . Beyond the classic thermoneutral zone: Including thermal comfort. Temperature (Austin). 2016; 1(2):142-9. PMC: 4977175. DOI: 10.4161/temp.29702. View

2.
Yamazaki K, Andreyev A, Ortiz-Vilchis P, Petrosyan S, Divakaruni A, Wiley S . Intravenous (-)-epicatechin reduces myocardial ischemic injury by protecting mitochondrial function. Int J Cardiol. 2014; 175(2):297-306. PMC: 4506135. DOI: 10.1016/j.ijcard.2014.05.009. View

3.
Kizhakekuttu T, Wang J, Dharmashankar K, Ying R, Gutterman D, Vita J . Adverse alterations in mitochondrial function contribute to type 2 diabetes mellitus-related endothelial dysfunction in humans. Arterioscler Thromb Vasc Biol. 2012; 32(10):2531-9. PMC: 3570053. DOI: 10.1161/ATVBAHA.112.256024. View

4.
Li C, Reif M, Craige S, Kant S, Keaney Jr J . Endothelial AMPK activation induces mitochondrial biogenesis and stress adaptation via eNOS-dependent mTORC1 signaling. Nitric Oxide. 2016; 55-56:45-53. PMC: 4860108. DOI: 10.1016/j.niox.2016.03.003. View

5.
Garate-Carrillo A, Navarrete-Yanez V, Ortiz-Vilchis P, Guevara G, Castillo C, Mendoza-Lorenzo P . Arginase inhibition by (-)-Epicatechin reverses endothelial cell aging. Eur J Pharmacol. 2020; 885:173442. PMC: 7418791. DOI: 10.1016/j.ejphar.2020.173442. View