Thymoquinone alleviates cisplatin-induced kidney damage by reducing apoptosis in a rat model

The aim of the study was to compare the ameliorating effects of thymoquinone at various dosages on cisplatin-induced renal toxicity, and to investigate its effects on cisplatin-induced nephrocyte apoptosis via the mitochondrial pathway in a rat model. A rat model of cisplatin-induced renal damage was established, with thymoquinone treatment groups (receiving 1, 3, 5, 10, or 20 mg/kg of thymoquinone). We determined serum creatinine (Cr) and blood urea nitrogen (BUN), measured the expression of the anti-apoptotic protein Bcl-2, the pro-apoptotic protein Bax, caspase-3, kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) in renal tissue. Additionally, we observed pathological changes in renal tissue and performed paller score for renal tubule injury. Relative to the control, the cisplatin group exhibited significantly elevated Bax, caspase-3, NGAL and KIM-1 expression, elevated serum Cr and BUN concentrations and significantly reduced Bcl-2 expression ( P  < 0.05). Histopathological examination of cisplatin-treated group revealed vacuolar degeneration, tubular epithelial cell swelling, and an absence of brush margins on renal tubules. Paller score was significantly elevated in the cisplatin group relative to the normal control group. Thymoquinone dose-dependently ameliorated these effects. Thymoquinone at 1–20 mg/kg improved cisplatin-induced renal dysfunction in rats. This protective effect is related to the inhibition of mitochondria-mediated apoptosis.