Effect of high-level spinal cord injury on expression of mitochondrial voltage-dependent anion channel 2 in rat cardiomyocytes

Objective To evaluate the effect of high-level spinal cord injury(SCI)on the expression of mitochondrial voltage-dependent anion channel 2(VDAC2)in rat cardiomyocytes. Methods Forty-eight pathogen-free healthy adult male Sprague-Dawley rats, weighing 200-250 g, were divided into 2 groups(n=24 each)using a random number table: sham operation group(group S)and high-level SCI group(group H). The animals were anesthetized with intraperitoneal chloral hydrate and subjected to SCI using the modified Allen weight-drop method in group H. The spinal cord was only exposed in group S. At 6, 12, 24 and 48 h after SCI(T1-4), 6 rats in each group were randomly selected and sacrificed, and myocardial specimens were collected from the cardiac apex for microscopic examination of the cell morphology(with a transmission electron microscope) and for determination of cell apoptosis(by TUNEL assay), expression of Bax, Bcl-2 and VDAC2 protein and mRNA in cardiomyocytes(by Western blot and real-time polymerase chain reaction, respectively). The apoptosis rate and ratios of Bax/Bcl-2 protein and mRNA were calculated. Results Compared with group S, the apoptosis rate and ratios of Bax/Bcl-2 protein and mRNA were significantly increased at T1-4, the expression of VDAC2 protein and mRNA was significantly down-regulated at T2-4(P<0.05 or 0.01), and the pathologic changes of cardiomyocytes were aggravated in group H. Conclusion The mechanism of myocardial damage is related to down-regulation of mitochondrial VDAC2 expression in cardiomyocytes and promotion of cell apoptosis in rats with high-level SCI. Key words: Spinal cord injuries; Myocardium; Voltage-dependent anion channel 2