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Research Of TFA On Inflammation Factors And Fibrosis Factors Of DN Models In Intervention

Posted on:2016-07-25Degree:MasterType:Thesis
Country:ChinaCandidate:C Z TaoFull Text:PDF
GTID:2284330470463791Subject:Integrative Medicine Internal Medicine
Abstract/Summary:PDF Full Text Request
Objective:The observation of male SD rat model of DN in TNF-α, TFR, TGF-β1 and CTGF expression, To investigate the protection mechanism of TFA against diabetic nephropathy in rats by the effect of TFA on TNF-α, TFR, TGF-β1 and CTGF expression, and to investigate the curative effect of TFA in treatment of DN and its possible mechanism.Methods:Fifty male SD rats were randomly divided into normal control group, DN untreated group, positive group, and TFA low- and TFA high-dose group,10 rats in each group. DN-untreated group, resulting in positive group, low dose group and high dose group rats, positive group rats according to the dose of 4ml/kg/d was given to Irbesartan, low dose group and high dose group rats were in accordance with the doses of 4ml/kg/d were given low concentration and high concentration of TFA pigment suspension gavage, normal control group and untreated group before and the 12th week after the induction,24-hour urinary micro-albumin were detected in different groups. At the 12th week, urine was collected, determination of urinary albumin/creatinine and the rats were sacrificed to collect the blood samples and renal tissues. The contents of BUN and Scr were detected and the pathological change in renal tissues was observed by HE Staining; the level of TNF-α、TFR、TGF-β1、CTGF was detected by enzyme-linked immunosorbent assay and the expression of TNF-α、TFR、 TGF-β1、CTGF in renal tissues was measured by real time PCR method.Results:Compared with the normal control group, urinary albumin/creatinine of rats in DN untreated group, Scr, BUN, TNF-α, TGF-β1 level, the expression level in renal tissue of TNF-α、TFR、TGF-β1、CTGF were significantly increased; compared with the DN untreated group, urinary albumin/creatinine of positive group rats, serum BUN, TNF-α, TGF-β1 level, the gene expression in renal tissue of TNF-α, TFR, TGF-β1, CTGF decreased significantly; compared with the DN untreated group, urinary albumin/creatinine of rats in high dose group, serum Scr, BUN, TNF-α, TGF-β1 expression level, the level of TNF-α, TFR, TGF-β1, CTGF in renal tissue decreased significantly. Compared with the DN untreated group, the serum level of BUN in low dose group rats decreased, other indexes were tested were not statistically significant. Pathological changes in glomerular, renal tissue in DN untreated group rats hyperplasia, glomerular capillary plexus obvious hyalinization, sclerosis, mesangial matrix, basement membrane collapse, glomerular capillary lumen occlusion.Conclusion:In the pathogenesis of DN, renal damage were accompanied by TNF-α, TFR, TGF-β1, CTGF expression increased, suggesting the role of inflammatory response in the pathogenesis of renal fibrosis; in the use of TFA on male SD rat model of DN intervention, compared with the rats in the DN untreated group, not only have a certain degree of renal function recovery, at the same time, expression of TNF-α, TFR, TGF-β1, CTGF was also reduced. Therefore TFA, may be through inhibition of the inflammatory reaction and improve renal fibrosis, so as to achieve the protection of renal function, delay the duration of DN.
Keywords/Search Tags:Inflammatory factors, Fibrosis factors, Diabetic nephropathies, SD rats, TFA
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