Abstract
Currently, there is no doubt surrounding a theory that the cardiotropic effects of sex hormones can be due to their direct effect on the cardiovascular system. In recent years, interest in the study of steroid glycosides has increased. We studied the effects of furostanol glycosides (protodioscin and deltozid) from the cell culture of the Dioscorea deltoidea (laboratory code DM-05) on the physiological and biochemical parameters of vascular endothelial function in hypoestrogen-induced endothelial dysfunction after bilateral ovariectomy. It was shown that the use of DM-05 at a dose of 1 mg/kg makes it possible to prevent the development of arterial hypertension (the level of systolic blood pressure (SBP) decreases by 9.7% (p < 0.05) and diastolic blood pressure (DBP) by 8.2%), to achieve a decrease in the coefficient of endothelial dysfunction by 1.75 times against the background of a hypoestrogenic state. With DM-05, an increase in the concentration of stable nitric oxide metabolites (NOx) by 45.6% (p < 0.05) and an increase in mRNA endothelial nitric oxide synthase (eNOS) expression by 34.8% (p < 0.05) was established, which indicates a positive effect of furostanol glycosides on the metabolism of nitric oxide after ovariectomy. Positive dynamics in the histological structure of the heart and the abdominal aorta indicate the pronounced endothelio- and atheroprotective effects of DM-05.
Highlights
Atherosclerotic cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the world
Intraperitoneal administration of DM-05 at a dose of 1 mg/kg prevents the development of arterial hypertension; the level of systolic blood pressure (SBP) decreases by 9.7% (p < 0.05), and diastolic blood pressure (DBP) decreases by 8.2% (Table 1)
The concentration of stable nitric oxide metabolites in endothelial dysfunction simulation by bilateral ovariectomy was statistically significantly reduced by 38.9% (p < 0.05), which reflects the development of endothelial dysfunction and change in the ratio of endothelium-dependent to endothelium-independent vasodilation
Summary
Atherosclerotic cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the world. According to the World Health Organization, there were 56.9 million deaths worldwide in. 2016, and more than half of these (54%) were due to the top 10 causes of death. Ischemic heart disease and stroke are the world’s most significant killers, accounting for a combined 15.2 million deaths in 2016. These diseases have remained the leading causes of death globally in the last 15 years. Endothelial activation, and endothelial dysfunction have been largely identified as the main alterations involved in the pathogenesis of macrovascular diseases [1]. The endothelium plays important roles in modulating vascular tone by synthesizing and releasing an array of endothelium-derived
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