Expression Of TNF-α And CD11a In Diabetic Rat Kidney Tissue

Objective: To evaluate the changes of TNF-α and CD11a expression in renal tissue of diabetic and control rats, and explore the clinical significance of the different expression of TNF-α and CD11a in the occurrence of diabetic nephropathy.Methods: Adult (aged 8 weeks) male Wistar rats were divided into nondiabetic (n=8), diabetic (n=9) groups and insulin therapy diabetic groups (n=9) . Diabetic rats were made by a single injection of streptozotocin (STZ) at a dose of 55mg/kg and control rats were injected by citrate buffer (PH4.5) in the same dose. Quantitative immunohistochemistry assay for TNF-α and CD11a was used in control,diabetic and therapy rats at the end of study for 8w, respectively. Values are expressed as means ± SD. Statistical significance was evaluated by one-way analysis of variance followed by the One-Way ANOVA tests for multiple comparisons. All statistical tests were performed on raw data. The quantitative analysis was used to evaluate the positive rate of TNF-α and CD11a expression by SPSS 10.0 process. And correlation analysis was used to evaluate the relationship between TNF-a-positive cell infiltration ,CD11a-positive cell infiltration and GHb,BUN,Cr. P<0.05 was considered significant.Results: 1. TNF-a protein was seldom detectable in renal tissue from nondiabetic rats in the end of study. On the contrary, in diabetic rats,theexpression of TNF-a was observed at 8 weeks(the positive rate was 3.75 ± 1.38%). and it was observed poorly in the therapy group(the positive rate was 1.47±0.35%). A pronounced expression was found in diabetic group compared with therapy and control groups.2. TNF-a was expressed in tubuli from diabetic rats, but undetect from control and therapy rats. It was an increased staining in diabetic versus nondiabetic animals .3. CD1 la was seldom expressed in renal tissue of control rats(the positive rate was 2.05 ± 0.83%). At 8 weeks of induced diabetic rats, the positive rate of diabeic group was 5.77 ± 0.74%, and the positive rate of therapy group was 3.57±1.88%. Moreover, immunostaining for CD11a was weak in diabetic, while higher glucose was controlled.4. The TNF-a-positive cells and CD11a-positive cells in renal tissue of diabetic rats closely correlated with GHb(r=0.876,r=0.823,P<0.05), BUN(r=0.828,r=0.776, P<0.05) ,and Cr (r = 0.796,r=0.808,JP<0.05). The correlation is significant at the 0.01 level (2-tailed) between TNF-a and CD1 la(r=0.868,P<0.05).Conclusion: 1. The hyperglycemia induces or upregulates TNF-a production in renal tissue, and the expression of TNF-a was decreased under the hyperglycemia controlled. Furthermore, the TNF-a-positive cells in renal tissue closely correlated with GHb,BUN,and Cr. These findings suggest that TNF-a-positive cell infiltration may play an important role in the pathogenesis of diabetic nephropathy (DN),and the control of hyperglycemia may postpone the progression of DN , the degree of its expression may be predictive of therapy of DN.2. TNF-a was expressed in tubuli from diabetic rats,and the expression of TNF-a was markly decreased by both nondiaetic and theray diabetes.The detect of ural TNF-a may be a supervised index.3.CD11a was detectable in renal tissue from diabetic rats,it was poorlydetected in therapy and nondiabetic rats, which suggested the leukocyte maybe paticipate in the pathogenesis of diabetic nephropathy.4. In hyperglycemia condition, TNF-α and CD11a may play an important role in the pathogenesis of diabetic nephropathy.5.Inflammatory cytokines may contribute to the occurrence of DN. While hyperglycemia was controlled,inflammatory may be poorly, so to postphone DN.