Background
the primary function of the kidney is to eliminate metabolic waste products and xenobiotics from the circulation. During this process, the kidney may become vulnerable to toxicity.
Conclusion
TQ showed protective effects against HgCl2-induced nephrotoxicity through modifications of various constitutive and inducible protein and enzyme levels in renal tissues.
Material and methods
HgCl2 (0.4 mg/kg) was administered to all groups (n = 5) except for the normal control. Three treatment groups received TQ (5, 10, and 15 mg/kg) 60 min before HgCl2 administration. The protective effect of TQ was evaluated from renal and liver function biomarkers, urine examination, glomerulus filtration rate (GFR), histopathological features, oxidative stress biomarkers, Hsp-70, apoptosis biomarkers, and gene expression.
Methods
HgCl2 (0.4 mg/kg) was administered to all groups (n = 5) except for the normal control. Three treatment groups received TQ (5, 10, and 15 mg/kg) 60 min before HgCl2 administration. The protective effect of TQ was evaluated from renal and liver function biomarkers, urine examination, glomerulus filtration rate (GFR), histopathological features, oxidative stress biomarkers, Hsp-70, apoptosis biomarkers, and gene expression.
Objective
it was aimed to investigate the impact of thymoquinone (TQ) in mercuric chloride (HgCl2)-induced nephrotoxicity through estimation of various proteins involved in natural defense mechanisms. Material and
Results
TQ significantly attenuated hazardous effects of HgCl2 on renal and hepatic tissues. Urine albumin and glucose were considerably low in the treated groups in comparison with the HgCl2 group. TQ treatment also enhanced % GFR in rats. TQ-enhanced superoxide dismutase, catalase, and glutathione levels by enhancing the expression level of nuclear factor erythroid 2-related factor 2 (Nrf2). TQ increased Hsp-70 and Bcl-2 levels and reduced caspase-3 activity. TQ also protected cells against HgCl2-induced cell death and decreased % DNA fragmentation. TQ increased the expression of protective proteins metallothionein I and II and reduced the expression of kidney injury molecule-1 (Kim-1).