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The purpose of the incidence of diabetes is increasing year by year, is a major cause of chronic kidney disease. Recent studies have found that the incidence of diabetic nephropathy in addition to glucose, lipid metabolism disorders and hemodynamic abnormalities, immune-mediated inflammatory response also played a key role in the pathogenesis of diabetic nephropathy. Treatment of diabetic nephropathy hypoglycemic, antihypertensive, application ACEI, ARB-based, the use of immunosuppressive therapy of diabetic nephropathy rarely reported. Mycophenolate mofetil as an immunosuppressant has been in clinical use for many years, can strongly inhibit T lymphocyte and B lymphocyte proliferation, inhibition of inflammatory cytokine release. The purpose of this study is to mycophenolate mofetil in diabetic rats treated dry to the page, and observe the changes of renal tissue pathology and TGF-B1, 0PN expression of inflammatory cytokines, explore the renal protective effect of mycophenolate mofetil animal experimental basis for clinical immunosuppressant treatment of diabetic nephropathy. The Methods STz produced in accordance with 40m ∥ K SD rats diabetic rat model, modeling after successful SD rats were divided into diabetic group (DM group) and the mycophenolate mofetil dry I page group (MMF group). Healthy SD rats were used as normal control group (NC). MMF group was given MMF 15mg / (k · d) orally NC group, DM group given normal saline irrigation, sooner or later, for 8 weeks. 24 urinary protein excretion observed after 8 weeks, blood glucose, serum creatinine, blood urea nitrogen, kidney weight / body weight, blood lipids, Hs-CRP, were killed by HE staining to observe pathological changes of glomerular and tubular, using immunohistochemical observed in renal tissue TGF-B1, 0PN expression. Results 1. Of blood glucose, renal function, 24h urine protein, kidney weight / body weight changes, blood lipids: DM and MMF group urine protein quantification, blood glucose, kidney weight / body weight comparison NC group was significantly higher (P lt; 0.01 ) the 2411 urine protein of the MMF group, kidney weight / body weight, serum creatinine, blood urea nitrogen Compare DN group was significantly reduced (P lt; 0.01) DM and MMF group lipids higher than the NC group, serum lipids and blood glucose change positively correlated. 2. Pathological changes: DM group and the MMF group compared with NC group, pathological changes, there glomerular compensatory hypertrophy, glomerulosclerosis and renal interstitial fibrosis, MMF dry to the page after treatment compared with the DN group a significant improvement. 3. High-sensitivity C-reactive protein (Hs-CRP) change: DM and MMF group Hs-CRP was significantly higher than NC group (P lt; 0.01), MMF MMF dry to page treatment group decreased significantly (P lt; .01). 4. Immunohistochemical examination: DM and MMF group compared with NC group TGF-p1 expression of OPN was significantly increased (P lt; 0.01), TGF-p1 in the MMF group, OPN expression compared with DM group was significantly reduced (P lt ; 0.01), and TGF-B1, OPN expression and urinary protein, kidney weight / body weight ratio is proportional to. Conclusion MMF can reduce serum creatinine, blood urea nitrogen level, can reduce proteinuria, reduce glomerular and tubular sclerosis and fibrosis; diabetic nephropathy in renal tissue TGF-B1 expression of OPN significantly increased; MMF TGF- p1, OPN expression was inhibited. Mechanism may be inhibition correlated with MMF on the expression of TGF-p1, OPN has a therapeutic effect on diabetic nephropathy.
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