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Objective: To investigate the tumor necrosis factor-α (TNF-α) and adiponectin (ADN) occurred in diabetic skeletal muscle lesions, development, and the relationships between them, and provide a new approach for the prevention and treatment of diabetic skeletal muscle lesions . Methods: 64 male wistar rats were randomly divided into a control group and the experimental group (divided into 8, 12 weeks, respectively, for a total of 8 groups): 32 experimental rats, one-time fasting by intraperitoneal injection of streptozotocin Zuo bacteria the prime (of streptozotocin, STZ) 50mg/kg.wt, induced diabetic rat model: 32 control rats, intraperitoneal injection of an equal volume of citrate buffer. Mode 1,4,8,12 two groups each of eight measured body weight, fasting blood glucose in diabetic rats, respectively; heart blood was collected and centrifuged to obtain serum, serum TNF-α, ADN, C, peptides; take Pathology, the biceps femoris conventional production and electron microscopy sections using image analysis system for determination of muscle fiber cross-section, in light microscopy, electron microscopy skeletal muscle histopathological changes, immunohistochemical SABC method skeletal muscle TNF-α, ADN expression area, capillary basement membrane thickness and muscle tissue of TNF-α, ADN the optical density values, statistical analysis, and analysis of the expression of TNF-α, ADN, the muscle tissue of the experimental group. Results: The experimental rats with the duration of the extension, the muscle fiber generalized contraction, muscle fiber cross-sectional area less than the control group (p <0.01). Myofibrils toward disorder, myofilament presented multifocal dissolved: disordered arrangement of mitochondrial cristae matrilysin vacuolization even: microvascular endothelial thickening, stenosis, vascular basement membrane thickening (with the control group at 12 weeks difference, p <0.05). The experimental rats serum TNF-α levels than those in the control group increased, the difference was significant (p <0.01), the level of serum ADN differences with the control group (p <0.01) at 4, 8 and 12 weeks. Both continued to rise with the progression of each period were different (p <0.05) in each time period, the control group, there were no differences. Semi-quantitative immunohistochemical analysis showed that the muscle tissue of the experimental group, TNF-α, ADN positive expression gradually increased, and with the course of development of the expression of each period, the difference compared with the control group (p <0.01). And the experimental group at various time intervals between different (p <0.01). No difference between the control group at various time intervals. Diabetic rat skeletal muscle tissue TNF-α, ADN's expression of positive correlation (r = 0.794, p <0.01). Conclusion: experimental serum, muscle tissue TNF-α, ADN elevated significantly associated with the development of diabetic skeletal muscle lesions, and a positive correlation between the expression of both muscle tissue, suggesting that TNF-α, ADN involved in diabetes bones development of muscle lesions occurred in the course of interaction, including TNF-α play the role of the injury, while ADN protective role. Inhibition of TNF-α production and increased expression of ADN may provide a new approach for the prevention and treatment of diabetic skeletal muscle lesions.
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