Xidant enzymes GPx, GST, SOD and CAT were associated to the impaired glomerular filtration. The degree of those alterations was diminished in animals treated with curcumin. Additionally, curcumin modulated the inflammatory response in gentamicin-treated rats by means of NF-B expression within a time-dependent manner [50]. Cyclosporin A (CsA) CsA is widely utilized as immunosuppressant drug in organ transplantation to prevent rejection. This therapeutic agent induces renal harm as side effect. Tirkey et al. [81] showed that curcumin was helpful by safeguarding CsA-induced harm, due to the fact animals that received the phenolic compound plus CsA did not show renal function deterioration or depletion of antioxidant enzymes. CsA increased the thiobarbituric acid reactive substances (TBARS), decreased renal endogenous antioxidant enzymes and deteriorated the renal function as assessed by increased serum creatinine, BUN and decreased creatinine and urea clearance. Curcumin reducedRenal injury induced by drugs Cisplatin and oxaliplatin Cisplatin is an productive anticancer drug applied against lung, ovarian cancer and a few lymphomas, however renal harm hasJ. Trujillo et al. / Redox Biology 1 (2013) 448?elevated levels of TBARS, attenuated renal dysfunction, enhanced the levels of antioxidant enzymes and normalized the altered renal morphology in CsA treated rats.Adriamycin (doxorubicin) Adriamycin is a chemotherapeutic drug that may perhaps induce nephrotoxicity as a side impact. Therapy with curcumin (200 mg/kg/day in 1 gum acacia for 30 days) markedly protected against adriamycininduced proteinuria, albuminuria, hypoalbuminaemia and hyperlipidemia. In addition, curcumin also lowered urinary levels in the enzyme N-acetyl–D-glucosaminidase (NAG), a marker of tubular harm [83].Chloroquine Chloroquine is a drug utilised in the malaria treatment and induces renal injury and oxidant tension as secondary effect. It was identified that THU (80 mg/kg/day for 15 days) and curcumin remedy prevents chloroquine-induced nephrotoxicity and lipid peroxidation as well as the decrease within the antioxidants vitamin C, vitamin E, SOD, CAT and GPx in kidneys of those rats [60].Fig. 3. Curcumin is able to stop mitochondrial dysfunction associated to renal injury. Curcumin is capable to prevent lipid peroxidation along with the decrease inside the following mitochondrial determinations: oxygen consumption, activity of complexes I, II, II-III and V, activity of aconitase and antioxidant enzymes, GSH content material, membrane prospective, calcium retention and ATP content material [51]. GSH (Glutathione), SOD (superoxide dismutase), CAT (catalase), GPx (glutathione peroxidase), GST (glutathione-S-transferase), GR (glutathione reductase), NAD ?(nicotinamide adenine dinucleotide), NADH (nicotinamide adenine dinucleotide, decreased type), FAD ?(flavin adenine dinucleotide), FADH2 (flavin adenine dinucleotide, reduced type), ATP (adenosine triphosphate), ADP (adenosine diphosphate).(S,R,S)-AHPC-amido-C5-acid site Renal injury induced by chemical compounds Sodium fluoride (NaF) Renal harm induced by chemical compounds also has drawn interest.2-Bromo-5-methylthiazole-4-carbonitrile custom synthesis Nabavi et al.PMID:32926338 [54] reported the renoprotective effect of curcumin (ten and 20 mg/kg) in rats with nephrotoxicity induced by NaF. Renal damage in these rats relies on an impairment of renal function evidenced by increased serum creatinine and BUN and structural impairment as a consequence of interstitial edema, inflammation and fibrosis which was related with increased nitric oxide, peroxides, ROS and MDA. However, curcumin treated animals showed.
