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The Research of the Interfering Effect of Fluvastatin on Diabetic Rats Expression of TNF-a

Author: XiongDi
Tutor: LiZuo
School: Nanchang University
Course: Internal Medicine
Keywords: Diabetic nephropathy Fluvastatin Tumor necrosis factor -α
CLC: R587.1
Type: Master's thesis
Year: 2009
Downloads: 61
Quote: 0
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Abstract


Objective: In this study, through the establishment of diabetic rats, and given fluvastatin intervention therapy, blood and urine of rats tumor necrosis factor (TNF) expression and kidney disease, and to explore the development of diabetic nephropathy TNF's role and statins protect the kidney mechanism for the prevention and treatment of diabetic nephropathy provide a theoretical basis. Methods: Medical College of Nanchang University Experimental Animal Center of male SD rats weighing 180-220g, were randomly divided into normal control group (A), diabetic model group (B group), diabetic model intervention group (C group). Group B and group C streptozotocin (STZ) diabetic rats established by intraperitoneal injection model, C group were given fluvastatin intervention for 8 weeks, rats were observed glucose, blood lipids, urine protein, renal function and kidney and serum TNF-α expression. Results: (1) glucose: diabetes model group B group (26.11 ± 6.53mmol / L) and C group (22.98 ± 4.58 mmol / L) at 8 weeks after the blood sugar is still significantly higher than the model group A group (9.90 ± 2.09 mmol / L) (P lt; 0.01), prompted diabetes model was successfully established, and no spontaneous remission; while group B and group C was no significant difference between the blood glucose (P gt; 0.10). (2) lipid: triglyceride levels in three groups of rats with no significant difference between (P gt; 0.10); total cholesterol among the three groups showed no significant difference (P gt; 0.10). (3) renal function: rat serum creatinine levels between the three groups had no significant difference (P gt; 0.10); but made modules serum urea nitrogen levels in group B (15.46 ± 2.53 mmol / L), C group (12.58 ± 2.01 mmol / L) were significantly higher in group A did not build modules (10.08 ± 2.03 mmol / L) (P lt; 0.05). (4) urine protein / creatinine ratio: B group (0.185 ± 0.048) and group C (0.105 ± 0.021) than in group A (0.031 ± 0.006) was significantly higher (P lt; 0.01), while group C was lower than B group (P lt; 0.01). (5) Serum TNF-α: B group (2.23 ± 0.49) and group C (1.64 ± 0.29) in serum TNF-α levels were significantly higher in group A (1.04 ± 0.21) (P lt; 0.01), while the C group lower than group B (P lt; 0.05). (6) kidney TNF-α expression by immunohistochemistry: A group of rat TNF-α in the glomerular and interstitial little or no expression (3.71 ± 2.430). Compared with group A, B group TNF-α in the glomerular mesangial area there is a strong expression (32.00 ± 5.182) (P lt; 0.01), C group also expressed in mesangial area, but lower than in group B weak (20.62 ± 5.605) (P lt; 0.01). Conclusion: Fluvastatin probably via the inhibition of TNF-α reduce urinary protein excretion in diabetic rats, reducing kidney disease, delaying the development of diabetic nephropathy.

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CLC: > Medicine, health > Internal Medicine > Endocrine diseases and metabolic diseases > Islet disease > Diabetes
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