Volume 8, Number 2 (volume 8, number 2 2016)                   IJDO 2016, 8(2): 77-84 | Back to browse issues page


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Mohammadi M T, Faghihi N, Eidi A. Anti-Inflammatory Effects of Atorvastatin by the Modulation of NF-κB Expression during Hyperglycemia-Induced Nephropathy in Rat. IJDO. 2016; 8 (2) :77-84
URL: http://ijdo.ssu.ac.ir/article-1-291-en.html

Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
Abstract:   (215 Views)

Objective: Atorvastatin has the pleiotropic effects, including anti-inflammation and antioxidant. Therefore, this study considered to examine the effects of atorvastatin on NF-қB expression, as a main transcription factor for expression of inflammatory cytokines, in hyperglycemia-induced nephropathy in rat.

Materials and Methods: Twenty four male Wistar rats were randomly divided into four groups; Normal, Normal treatment, Diabetic, and Diabetic treatment. Rats were made diabetic by an intravenous injection of streptozotocin (40 mg/kg). Treated rats received atorvastatin for 60 days (40 mg/kg/day). At the end of experiment, blood samples were collected for measurement of blood glucose. Moreover, the mRNA expression level of NF-қB in kidney was determined by RT-PCR technique.

Results: Induction of diabetes significantly increased the mean value of blood glucose in diabetic rats (>450 mg/dl) compared with normal rats (P=0.001). Chronic hyperglycemia also increased the mRNA expression level of NF-қB in diabetic kidney. Moreover, the mean value of kidney index was significantly increased in diabetic rats compared to normal group (P=0.001). Treatment with atorvastatin in diabetic rats for 60 days reduced the mRNA expression level of NF-қB and kidney index compared to non-treated diabetic rats (P=0.014).

Conclusion: Our findings revealed that atorvastatin is able to prevent the development of diabetic nephropathy during chronic uncontrolled hyperglycemia possibly by the inhibition of NF-қB expression in the kidneys of diabetic rats.

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Type of Study: Research | Subject: Special
Received: 2017/03/15 | Accepted: 2017/03/15 | Published: 2017/03/15

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