Background: Ecdysteroids, a group of steroid hormones found in insects and many plants, have been shown to prevent various changes in mammalian tissues after female sex hormone deprivation. Purpose: To… Click to show full abstract
Background: Ecdysteroids, a group of steroid hormones found in insects and many plants, have been shown to prevent various changes in mammalian tissues after female sex hormone deprivation. Purpose: To examine whether an ecdysteroid, 20‐hydroxyecdysone (20‐HE), exhibits regulatory or protective roles in the cardiovascular system. Study design/method: Blood pressure and cardiac function were evaluated in spontaneously hypertensive rats (SHR) during and after daily treatment with 20‐HE for six weeks. Results: The progressive increase in systolic blood pressure with age in SHR rats was significantly lower in animals treated with either 5 or 10 mg/kg body weight of 20‐HE. However, treatment with 20‐HE did not diminish the increase in diastolic pressure. Echocardiography after six weeks of treatment demonstrated that the left ventricular chamber of SHR rats treated with 20‐HE was smaller than that of SHR controls, while contractility was not affected by 20‐HE. Histological images also demonstrated a decrease in cardiomyocyte cross‐sectional area in 20‐HE treated groups. Interestingly, treatment with 20‐HE caused a shift in cardiac myosin heavy chain towards more &bgr;‐isoforms. SHR rats treated with 20‐HE also exhibited a decrease in seminal vesicular weight and an increase in testicular weight, especially at a dose of 10 mg/kg body weight. This finding suggests a possible anti‐androgenic effect of 20‐HE. Conclusion: Our finding reveal that 20‐HE has a beneficial effect on reducing blood pressure and consequently preventing dilated cardiac hypertrophy in SHR rats. Graphical abstract Figure. No caption available. Highlights20‐HE significantly reduces systolic blood pressure in SHR rats.20‐HE significantly attenuates dilated cardiac hypertrophy in SHR rats.20‐HE significantly upregulates the expression of cardiac &bgr;‐MHC isoform in SHR rats.
               
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