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1.
Article in Chinese | WPRIM | ID: wpr-755648

ABSTRACT

Objective To evaluate the changes in myocardial glucose transporter 4 ( GLUT4 ) membrane translocation in the rats with high-level spinal cord injury ( SCI ) . Methods Thirty-six clean-grade healthy adult male Sprague-Dawley rats, weighing 250-300 g, were divided into 3 groups using a random number table method: control group (group C, n=6), sham operation group (group S, n=6) and high-level SCI group (group SCI, n=24). The model of SCI was established by a modified Allen's method in anesthetized rats. The spinal cord was only exposed in group S. Six rats were selected in C and S groups and at 4, 12, 24 and 48 h after SCI ( T1-4 ) in group SCI, and blood samples were taken from the abdominal aorta to measure the activities of serum creatine kinase and creatine kinase isoenzyme-MB. The rats were then sacrificed, and myocardial specimens were collected for microscopic examination of the ultra-structure ( with a transmission electron microscope) and for determination of ATP weight ratio, phosphoryla-tion of insulin receptor substrate-1 tyrosine and expression of GLUT4 in cell membrane ( by Western blot) . Results Compared with C and S groups, the serum creatine kinase and creatine kinase isoenzyme-MB ac-tivities were significantly increased at T1-4 , the ATP weight ratio was decreased, the expression of GLUT4 in myocardial cell membrane was down-regulated, the expression of phosphorylated insulin receptor sub-strate-1 tyrosine in myocaradium was down-regulated at T2,3 (P<0. 05), and the pathological changes of myocardial tissues were found in group SCI. There was no significant difference in the indexes mentioned a-bove between group C and group S ( P>0. 05) . Conclusion The mechanism of myocardial energy metabo-lism disorder may be related to the reduced membrane translocation of GLUT4 in the rats with high-level SCI.

2.
Article in Chinese | WPRIM | ID: wpr-608259

ABSTRACT

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.

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