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Influence of Leflunomide on Nuclear Factor-κB and Tumor Necrosis Factor-α in Diabetic Nephropathy Rats

Author: LiuJunPing
Tutor: YuWeiMin
School: Shanxi Medical
Course: Internal Medicine
Keywords: Leflunomide Diabetic nephropathy Nuclear transcription nuclear factor - kappa B Tumor necrosis factor - alpha
CLC: R587.2
Type: Master's thesis
Year: 2009
Downloads: 76
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Abstract

Objective: through the establishment of diabetic nephropathy (DN) rat model to study the effects of leflunomide on the rat kidney NF-kB and TNF-alpha expression, to further explore the therapeutic effect of leflunomide on DN rats and its possible mechanism . Methods: 30 healthy male Wistar rats were randomly divided into three groups: (1) control group; (2) DN group; group ③ leflunomide. After removal of the left kidney, DN model group with leflunomide group streptozotocin: 35mg/kg intraperitoneal injection of the control group were intraperitoneally injected with citrate buffer. LEF group fed daily into a mold: leflunomide 5mg/kg. Eight weeks, 12 weeks before being killed in each group were measured 24h urine and 24h urinary protein; heart blood test creatinine (Scr), blood urea nitrogen (BUN); electron microscopy and HE staining observed pathological changes of immunohistochemical method to measure renal tissue expression of NF-kappa B protein concentration of the enzyme-linked immunosorbent assay (ELISA) measured serum levels of tumor necrosis factor-alpha. Results: (1) DN model is only a minor mode, rate of 95% into a mold, by the alternate DN model is added to continue the experiment. No one rat into a mold of death, mortality was 0%. (2) DN rats with the duration of the extension, the kidney weight increased endogenous creatinine clearance rate increased, proteinuria, compared with the control group, a significant difference (P <0.05). Leflunomide rats urine protein, serum creatinine, blood urea nitrogen with the same period in DN group significantly reduced, the difference was significant (P <0.05). (3) histopathology LEF group was significantly reduced compared with the DN group glomerular basement membrane thickening, reduced mesangial cell proliferation and extracellular matrix deposition, leflunomide can reduce kidney damage. (4) The results of immunohistochemistry: DN model rats the expression of NF-kappa B 8 weeks, 12 weeks, gradually increase, compared with the same period in the normal control group and the LEF group, the difference was significant (P lt; 0.05 ). After leflunomide treatment, the optical density was significantly reduced compared with DN group (P lt; 0.05), and with the extension of the duration of treatment (P = 0.013). (5) The results of the ELISA method: 8 weeks, 12 weeks DN rats TNF-alpha expression representing a normal control group was significantly higher (P lt; 0.001), and gradually increased with time (P = 0.006) ; leflunomide, TNF-alpha expression decreased compared with the DN group was statistically significant (P lt; 0.001), and with the extension of the duration of treatment (P = 0.003). Conclusion: NF-κB, TNF-α is accompanied by changes in renal pathology and sustained activation may play an important role in the DN rat kidney disease, leflunomide by inhibiting NF-kappaB, TNF-alpha expression play kidney protection.

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