Baicalein protects rat cardiac myocytes from hypoxia/reoxygenation induced apoptosisviaantioxidant and modulation of intracellular calcium concentration★

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Protective mechanisms of baicalein against myocardial hypoxia/reoxygenation injury are still nuclear.


To investigate the protective role of baicalein in cardiomyocytes against hypoxia/reoxygenation induced apoptosis.


Neonatal rat cardiomyocytes were isolated and cultured in vitro, and the cells were randomly divided into three groups: normal control group with no treatment, hypoxia/reoxygenation group exposed to hypoxia/reoxygenation, and baicalein group pretreated with 10 μmol/L baicalein for 30 minutes followed by hypoxia/reoxygenation. The extent of cellular injury was determined by measuring activity of lactate dehydrogenase released in the supernatant, the number of apoptotic cardiomyocytes was detected by flow cytometry. To further study the mechanism, the myocardial Bcl-2 and Bax protein levels were determined by Western blot, the changes of intracellular calcium concentration was monitored by Fura-2-acetoxymethyl ester.


Compared with the normal control group, the activity of lactate dehydrogenase, the number of apoptotic cardiomyocytes, myocardial Bax protein level, intracellular calcium concentration were increased (P < 0.05), as well as myocardial Bcl-2 protein level was decreased (P < 0.05). However, pretreatment with baicalein could protect rat cardiomyocytes from hypoxia/reoxygenation induced apoptosis, increase anti-apoptotic protein level of Bcl-2, decrease the pro-apoptotic protein level of Bax, and down-regulate intracellular calcium concentration. These findings indicate that baicalein can inhibit the apoptosis of cardiomyocytes induced by hypoxia/reoxygenation injury, and its mechanism may be related to antioxidant and modulation of intracellular calcium concentration.

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