BACKGROUND: Calcitriol (CAL), an active form of vitamin D, plays a vital role in controlling cardiac hypertrophy and heart failure. The aim of the present study is to explore the effects of CAL and to elucidate its underlying mechanisms on myocardial injury induced by isoproterenol (ISO). METHODS: Myocardial impairment was induced by the subcutaneous injection of ISO in adult male Sprague-Dawley rats, and the therapeutic effect of CAL was assessed. Biometric and echocardiographic parameters, interstitial fibrosis, oxidant-antioxidant status, and protein expression relevant to the mitochondrial apoptosis pathway were then measured. RESULTS: Calcitriol treatment improved the cardiac injury resulting from excessive ISO stimulation, as supported by the suppression of the development of myocardial hypertrophy, interstitial fibrosis, and H2O2 level in heart tissue. The decreased superoxide dismutase and catalase activities induced by ISO were also improved by CAL. Finally, the administration of CAL downregulated the protein expression of Bax and caspase-9. CONCLUSIONS: This study provides evidence that CAL ameliorated cardiac hypertrophy, interstitial fibrosis, and oxidative stress in ISO-induced cardiac injury and might play a vital cardioprotective role in such injuries.
BACKGROUND:Calcitriol (CAL), an active form of vitamin D, plays a vital role in controlling cardiac hypertrophy and heart failure. The aim of the present study is to explore the effects of CAL and to elucidate its underlying mechanisms on myocardial injury induced by isoproterenol (ISO). METHODS: Myocardial impairment was induced by the subcutaneous injection of ISO in adult male Sprague-Dawley rats, and the therapeutic effect of CAL was assessed. Biometric and echocardiographic parameters, interstitial fibrosis, oxidant-antioxidant status, and protein expression relevant to the mitochondrial apoptosis pathway were then measured. RESULTS:Calcitriol treatment improved the cardiac injury resulting from excessive ISO stimulation, as supported by the suppression of the development of myocardial hypertrophy, interstitial fibrosis, and H2O2 level in heart tissue. The decreased superoxide dismutase and catalase activities induced by ISO were also improved by CAL. Finally, the administration of CAL downregulated the protein expression of Bax and caspase-9. CONCLUSIONS: This study provides evidence that CAL ameliorated cardiac hypertrophy, interstitial fibrosis, and oxidative stress in ISO-induced cardiac injury and might play a vital cardioprotective role in such injuries.