Investigation of renal and testicular pro-inflammatory cytokine levels in experimental hyperthyroidism: Effects of selenium supplementation

Cytokines play important roles in diseases. Pro-inflammatory cytokines may responsible for thyroid dysfunction. Selenium (Se) regulates pro-inflammatory status in the body. Kidney and testicular functions change in hyperthyroidism. The aim of this study was to investigate the effects of Se supplementation on pro-inflammatory cytokines in renal and testicular tissue in hyperthyroid rats. This study was carried out with 6 experimental groups (G). G-1 consisted of controls receiving standard rat fodder. Other experimental groups were fed with; G-2: 0.5 mg/kg Na2SeO3; G-3: 1 mg/kg Na2SeO3; G-4: 4 mg/kg L-thyroxine; G-5: 0.5 mg/kg Na2SeO3 and 4 mg/kg L-thyroxine; G-6: 1 mg/kg Na2SeO3 and 4 mg/kg L-thyroxine added standard fodder. Interleukin (IL)-1β, IL-6, IL-18, and TNF-α levels were studied in renal and testicular tissues by ELISA. All cytokines levels of kidney samples were measured in tissue homogenates. Kidney values of IL-1β, IL-18, IL-6 and TNF-α were increased in G-4 compared to G-1 (p=0.024, p=0.010, p=0.003, and p=0.011, respectively). Also, these cytokine levels were decreased in G-6 compared to G-4 (p=0.042, p=0.048, p=0.009, and p=0.021, respectively). The IL-1β, IL-18, IL-6 and TNF-α values of G-4 were higher than G-1 in testes samples (p=0.027, p=0.010, p=0.008, and p=0.009, respectively). In addition, G-6 levels of IL-18 and TNF-α were lower than G-4 (p=0.047, and p=0.032 respectively), but IL-1β and IL-6 changes were not significant. As a result, our findings showed that in hyperthyroidism IL-1β, IL-18, IL-6, and TNF-α levels increased in kidney and testis tissues. Also, supplementation of 1 mg/kg Na2SeO3 was more effective for decreasing levels of these pro-inflammatory cytokine levels in the hyperthyroid group than supplementation of 0.5 mg/kg Na2SeO.

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Medicine Science-Cover
  • ISSN: 2147-0634
  • Yayın Aralığı: Yılda 4 Sayı
  • Başlangıç: 2012
  • Yayıncı: Effect Publishing Agency ( EPA )
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