الفهرس 
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Abstract
Background:Testicular cancer (TC) is a rare disease that mainly affects young and middle-aged men. Chemical exposure is one of the main causes of testicular damage and carcinoma. Cadmium (Cd) is an environmental and occupational toxin that represents a serious health hazard to humans and other animals. One of the negative consequences of cadmium exposure is testicular damage.This study aimed to investigate the therapeutic effect of etanercept against Cadmium Chloride-induced testicular damage and the probable underlying mechanisms of its action.
Methods:A total of sixty rats were divided into six groups: control, Cadmium Chloride (CdCl2) (7 mg/ kg i.p.), and CdCl2 treated with etanercept (5,10 and 15 mg/kg s.c.) and etanercept only (15 mg/kg s.c.). CdCl2 was administrated as a single dose while, etanercept was administered every 3 days for 3 weeks.
Results:CdCl2 reduced serum testosterone, testicular Glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). However, it elevated the levels of Malondialdehyde (MDA) and microtubule-associated protein light chain 3B (LC3B) in the testes. Cd caused pathogenic alterations as well as increased levels of inflammatory biomarkers such as tumor necrosis factor- alpha (TNF-α) and nuclear factor-kappa B (NF-κB). Besides, the gene expressions of caspase-3 and inducible nitric oxide synthase (i-NOS) and Beclin-1 protein increased with CdCl2 exposure. Interestingly, etanercept relieved the previous toxic effects induced by CdCl2in a dose-dependent manner as evidenced by inhibition of oxidative stress, inflammatory markers, Beclin-1, LC3B, and caspase-3 accompanied by improvement in histopathological changes.
Conclusion:Current data demonstrate that etanercept provides a potential therapeutic approach to treat testicular tissue against the damaging effects of Cd by reducing oxidative stress, inflammation, apoptosis, and autophagy.