Nephroprotective efficacy of chrysin against cisplatin-induced toxicity via attenuation of oxidative stress

Abstract

Objectives Cisplatin‐induced nephrotoxicity is the main cause for its dose‐limited use in the treatment of various cancers and results in acute renal cell injury through generation of reactive oxygen species. Chrysin possess antioxidant, anti‐inflammatory and anti‐cancer properties. The aim of this study was to investigate the protective efficacy of chrysin against cisplatin‐induced nephrotoxicity. Methods Thirty male Wistar rats were divided into five groups with six rats in each group. Group I served as control and received corn oil (vehicle of chrysin) for 14 days and 0.9% saline (vehicle of cisplatin) on day 14 only. Group II received a single intraperitoneal injection of cisplatin on day 14. Group III and IV were pretreated with two different doses of chrysin in addition to cisplatin and group V received chrysin only. Rats were examined for the effect of chrysin on cisplatin induced depletion of antioxidant enzymes, induction of lipid peroxidation and DNA damage in the kidney, utilizing a well‐established model of cisplatin‐induced nephropathy. Key findings Pretreatment with chrysin significantly attenuated cisplatin‐induced renal oxidative damage by diminishing the DNA damage and toxicity markers, such as creatinine and blood urea nitrogen, lipid peroxidation and xanthine oxidase activity, accompanied by increase in enzymatic (catalase, glutathione peroxidase, glutathione reductase and glutathione‐S‐transferase) and non‐enzymatic (reduced glutathione) antioxidant status. Histological findings further substantiated the protective efficacy of chrysin, which reduced cisplatin‐induced renal damage. Conclusions The data of the present study suggest that chrysin effectively suppress cisplatin‐induced renal injury by ameliorating oxidative stress.

The Protective Effect of Chrysin Against Cisplatin İnduced Ototoxicity in Rats

“…It was also reported to increase the enzymatic and nonenzymatic antioxidant status, thereby conferring protection against ototoxicity. Previous experimental studies demonstrated that chrysin shows protective efficacy against cisplatin-induced toxicity of various tissues, such as kidney, colon, and jejunum, by attenuating oxidative stress and apoptotic tissue damage [38][39][40]. Sultana et al [38] examined the nephroprotective efficacy of chrysin against cisplatin toxicity, administering cisplatin and various concentrations of chrysin to Wistar rats for 14 days.…”

“…Previous experimental studies demonstrated that chrysin shows protective efficacy against cisplatin-induced toxicity of various tissues, such as kidney, colon, and jejunum, by attenuating oxidative stress and apoptotic tissue damage [38][39][40]. Sultana et al [38] examined the nephroprotective efficacy of chrysin against cisplatin toxicity, administering cisplatin and various concentrations of chrysin to Wistar rats for 14 days. They reported that pretreatment with chrysin attenuated cisplatin-induced renal oxidative damage by diminishing DNA damage and increasing the enzymatic (catalase, glutathione reductase, glutathione-S-transferase, and glutathione peroxidase) and nonenzymatic (reduced glutathione) antioxidant status [38].…”

“…Sultana et al [38] examined the nephroprotective efficacy of chrysin against cisplatin toxicity, administering cisplatin and various concentrations of chrysin to Wistar rats for 14 days. They reported that pretreatment with chrysin attenuated cisplatin-induced renal oxidative damage by diminishing DNA damage and increasing the enzymatic (catalase, glutathione reductase, glutathione-S-transferase, and glutathione peroxidase) and nonenzymatic (reduced glutathione) antioxidant status [38].…”

Vitamin C pretreatment protects from nickel-induced acute nephrotoxicity in mice

“…This increases the risk of renal failure (26). The measurements of creatinine, urea, and uric acid are considered a tool in the clinical diagnosis of renal dysfunction following acute and chronic oxidative kidney injury (27,28). The increased level of Ni in the kidney that was observed after Ni treatment could be explained by high affinity of metallothionein, a metal binding protein for Ni (29).…”

Chrysin inhibits foam cell formation through promoting cholesterol efflux from RAW264.7 macrophages

“…A bulk of studies have shown that chrysin possesses diverse pharmacological activities including antivirus (Wang et al, 2014), antioxidant (Sultana et al, 2012), anti-tumor (Yu et al, 2013b), anxiolytic (Zanoli et al, 2000), neuroprotection (Kandhare et al, 2014), and anti-diabetes (Ahad et al, 2014;Li et al, 2014). Various mechanisms are involved in chrysinmediated health benefits such as attenuation of inflammation (Rehman et al, 2013), alleviation of oxidative stress (Mantawy et al, 2014), and induction of cell cycle arrest and apoptosis (Rashid et al, 2014).…”