2018Chin J Biomed EngRequires access

Mechanisms underlying the protective effect of vitamin D3 on myocardial function in rat model of myocardial ischemia reperfusion

Yunfang Ning, Xiaolin Wang, Yanli Lv

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Abstract

Objective To investigate the protective effect of vitamin D3 (VD3) on myocardial function in rat model of myocardial ischemia reperfusion and its possible mechanism. Methods Twenty male Sprague-Dawley rats were randomly divided into the sham operation group, sham operation + VD3 group, ischemia-reperfusion group, ischemia-reperfusion + VD3 group (n=5 each) . Rats in the sham operation + VD3 group and ischemia reperfusion + VD3 group were given gastric gavage of VD3 daily, while the other two groups were given equal aliquot of normal saline. Modeling of myocardial ischemia-reperfusion performed four weeks later. After reperfusion for 3 h, blood sample was collected from the carotid artery to determine the activities of creatine kinase (CK) and lactate dehydrogenase (LDH) . The size of myocardial infarction was determined by staining. The activity of poly-ADP-ribose polymerase (PARP) in the myocardial tissue was detected by immunohistochemistry. Results After the 3 h reperfusion, the activities of serum CK and LDH in the ischemia-reperfusion group and ischemia-reperfusion+VD3 group were significantly higher than those in the sham operation group and sham operation+VD3 group, with statistically significant differences between groups (all P 0.05) ; the PARP activities in the ischemia-reperfusion group and ischemia-reperfusion+VD3 group were significantly higher than those in the sham operation group and sham operation+VD3 group (all P<0.05) ; however, the PARP activity in the ischemia-reperfusion+VD3 group was significantly lowered compared with the ischemia-perfusion group (P<0.05) . Conclusion Vitamin D3 can alleviate myocardial ischemia-reperfusion injury. Such myocardial protection may be exhibited through reduced myocardial enzymes release and PARP activation in myocardial tissues. Key words: Vitamin D3; Myocardial reperfusion injury; Myocardial function

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Objective To investigate the protective effect of vitamin D3 (VD3) on myocardial function in rat model of myocardial ischemia reperfusion and its possible mechanism. Methods Twenty male Sprague-Dawley rats were randomly divided into the sham operation group, sham operation + VD3 group, ischemia-reperfusion group, ischemia-reperfusion + VD3 group (n=5 each) . Rats in the sham operation + VD3 group and ischemia reperfusion + VD3 group were given gastric gavage of VD3 daily, while the other two groups were given equal aliquot of normal saline. Modeling of myocardial ischemia-reperfusion performed four weeks later. After reperfusion for 3 h, blood sample was collected from the carotid artery to determine the activities of creatine kinase (CK) and lactate dehydrogenase (LDH) . The size of myocardial infarction was determined by staining. The activity of poly-ADP-ribose polymerase (PARP) in the myocardial tissue was detected by immunohistochemistry. Results After the 3 h reperfusion, the activities of serum CK and LDH in the ischemia-reperfusion group and ischemia-reperfusion+VD3 group were significantly higher than those in the sham operation group and sham operation+VD3 group, with statistically significant differences between groups (all P 0.05) ; the PARP activities in the ischemia-reperfusion group and ischemia-reperfusion+VD3 group were significantly higher than those in the sham operation group and sham operation+VD3 group (all P<0.05) ; however, the PARP activity in the ischemia-reperfusion+VD3 group was significantly lowered compared with the ischemia-perfusion group (P<0.05) . Conclusion Vitamin D3 can alleviate myocardial ischemia-reperfusion injury. Such myocardial protection may be exhibited through reduced myocardial enzymes release and PARP activation in myocardial tissues. Key words: Vitamin D3; Myocardial reperfusion injury; Myocardial function

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Available abstract

Objective To investigate the protective effect of vitamin D3 (VD3) on myocardial function in rat model of myocardial ischemia reperfusion and its possible mechanism. Methods Twenty male Sprague-Dawley rats were randomly divided into the sham operation group, sham operation + VD3 group, ischemia-reperfusion group, ischemia-reperfusion + VD3 group (n=5 each) . Rats in the sham operation + VD3 group and ischemia reperfusion + VD3 group were given gastric gavage of VD3 daily, while the other two groups were given equal aliquot of normal saline. Modeling of myocardial ischemia-reperfusion performed four weeks later. After reperfusion for 3 h, blood sample was collected from the carotid artery to determine the activities of creatine kinase (CK) and lactate dehydrogenase (LDH) . The size of myocardial infarction was determined by staining. The activity of poly-ADP-ribose polymerase (PARP) in the myocardial tissue was detected by immunohistochemistry. Results After the 3 h reperfusion, the activities of serum CK and LDH in the ischemia-reperfusion group and ischemia-reperfusion+VD3 group were significantly higher than those in the sham operation group and sham operation+VD3 group, with statistically significant differences between groups (all P 0.05) ; the PARP activities in the ischemia-reperfusion group and ischemia-reperfusion+VD3 group were significantly higher than those in the sham operation group and sham operation+VD3 group (all P<0.05) ; however, the PARP activity in the ischemia-reperfusion+VD3 group was significantly lowered compared with the ischemia-perfusion group (P<0.05) . Conclusion Vitamin D3 can alleviate myocardial ischemia-reperfusion injury. Such myocardial protection may be exhibited through reduced myocardial enzymes release and PARP activation in myocardial tissues. Key words: Vitamin D3; Myocardial reperfusion injury; Myocardial function

Key concepts: Ischemia, Medicine, Creatine kinase, Myocardial infarction, Reperfusion injury, Internal medicine, Lactate dehydrogenase, Perfusion

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