Atorvastatin Mediates Down Regulation of IFN-λ / Il-1ß /NF-kB on Testicular Inflammation in Experimental Male Rats

Document Type : Original Article

Authors

1 Biochemistry and Molecular Biology Department, Faculty of Veterinary Medicine, New Valley University, New Valley, Egypt.

2 Biochemistry Department, Faculty of Veterinary Medicine, Beni-Suef University, Egypt.

Abstract

Testicular inflammation (TIN) provokes reproductive impairments via endocrine disruption. Atorvastatin (AT) is one of the statins that have a crucial role in attenuating metabolic disorders. In this study, the prospective impacts of AT on TIN generated by a high-fat fructose diet (HFFD) in the testicular tissue were investigated through the oxidative stress-inflammatory pathway.
Male albino rats were employed in the research and split into three groups control (CR), induction (TIN), and treated (TIN-AT). Animals in TIN administrated 3 ml/kg Bwt ghee and coconut oil (3:1) (v/v) along with 25% fructose in daily drinking water, for 3 months, while AT used against TIN in AT-TIN was given for one month at 10 mg/Kg Bwt after TIN induction period.
Indicators of liver and kidney functions in serum, oxidative stress, and inflammation in the testicular tissue were assessed using biochemical and molecular techniques. In addition, a histopathological examination was conducted.
The acquired results evoked that TIN induced by HFFD leads to the reduction of antioxidant enzymes and an increase in the reactive oxygen species and inflammatory parameters. On the other hand, AT exhibited antioxidant influence by improving minimized glutathione levels, and glutathione-S-transferase and glutathione peroxidase enzyme actions, in testicular tissue. AT also attenuated lipid peroxidation and nitric oxide levels. Moreover, gene expressions of interferon-gamma, interleukin-1 beta, and nuclear factor-kappa B were downregulated in TIN-AT rats. AT could counter the pathomorphological alterations of TIN. Further studies are recommended to address other molecular roles of AT versus the TIN.

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