Sex-Dependent Protective Effect of Combined Application of Solubilized Ubiquinol and Selenium on Monocrotaline-Induced Pulmonary Hypertension in Wistar Rats.

Tatyana Kuropatkina,Anastasiya Khutorova,Sergey Stvolinsky,Mikhail Gulyaev,Yury Pirogov,Natalia Medvedeva,Olga Pavlova,Oleg Medvedev

doi:10.3390/antiox11030549

Tatyana Kuropatkina, Anastasiya Khutorova + Show 6 more

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https://doi.org/10.3390/antiox11030549

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Abstract

Ubiquinol exhibits anti-inflammatory and antioxidant properties. Selenium is a part of a number of antioxidant enzymes. The monocrotaline inducible model of pulmonary hypertension used in this study includes pathological links that may act as an application for the use of ubiquinol with high bioavailability and selenium metabolic products. On day 1, male and female rats were subcutaneously injected with a water-alcohol solution of monocrotaline or only water-alcohol solution. On days 7 and 14, some animals were intravenously injected with either ubiquinol’s vehicle or solubilized ubiquinol, or orally with selenium powder daily, starting from day 7, or received both ubiquinol + selenium. Magnetic resonance imaging of the lungs was performed on day 20. Hemodynamic parameters and morphometry were measured on day 22. An increased right ventricle systolic pressure in relation to control was demonstrated in all groups of animals of both sexes, except the group of males receiving the combination of ubiquinol + selenium. The relative mass of the right ventricle did not differ from the control in all groups of males and females receiving either ubiquinol alone or the combination. Magnetic resonance imaging revealed impaired perfusion in almost all animals examined, but pulmonary fibrosis developed in only half of the animals in the ubiquinol group. Intravenous administration of ubiquinol has a protective effect on monocrotaline-induced pulmonary hypertension development resulting in reduced right ventricle hypertrophy, and lung mass. Ubiquinol + selenium administration resulted in a less severe increase in the right ventricle systolic pressure in male rats but not in females 3 weeks after the start of the experiment. This sex-dependent effect was not observed in the influence of ubiquinol alone.

Highlights

Introduction conditions of the Creative CommonsCoenzyme Q10 (CoQ10) is an endogenous electron carrier in the mitochondrial respiratory chain of almost any cell in the body
In the process of the research, we studied the ubiquinol level in the experimental animals after double intravenous administration of 1% ubiquinol at a dose of 30 mg/kg animals after double intravenous administration of 1% ubiquinol at a dose of 30 mg/kg
The acts as an important fat-soluble antioxidant and is characterized by an antiprevious research of the CoQ10 effect on MCT Pulmonary hypertension (PH) development in rats demonstrated that inflammatory effect which explains its protective properties in various cardiovascular the two intravenous injections of ubiquinol contributed to a decrease of right ventricular diseases (CVD) [1,31,32]

Summary

Introduction

Coenzyme Q10 (CoQ10) is an endogenous electron carrier in the mitochondrial respiratory chain of almost any cell in the body. In the process of cellular respiration, it binds and releases electrons and protons and is subsequently converted from ubiquinol to ubiquinone. It has been established that about 95% of CoQ10 in the human body exists as a reduced form, ubiquinol, which has a high redox potential and, as a consequence, more pronounced antioxidant properties [1]. According to the literature reports, three out of four patients with cardiovascular disease show low CoQ10 levels [2]. There are three suggested mechanisms of CoQ10 activity in cardiovascular disease treatment. CoQ10 as ubiquinol can effectively suppress free radical oxidation, i.e., exhibits antioxidant properties [2,3]. It is known that the products of oxidative stress and cytokines can result in cardiomyocyte hypertrophy [2,4]

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