N⁶-2-hydroxyethyl-adenosine ameliorate cisplatin induced acute kidney injury in mice

Abstract

N⁶-2-hydroxyethyl-adenosine (HEA) is one of the main bioactive components found in Cordyceps cicadae and it has been reported to display antioxidant and anti-inflammatory activities. Cisplatin (CP) is one of the most commonly used chemotherapeutic drug for treating various cancers and tumors, but the use is widely curtailed due to its toxicity of various organs including the kidney. This study was aimed at investigating the protective effect of HEA on cisplatin-induced kidney injury. Mice were pretreated with HEA for 7 days and administered with cisplatin. Kidney function index including blood urea nitrogen (BUN), creatinine, renal oxidative stress and pro-inflammatory indices such as malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), tumor necrosis factor (TNF-α), interleukin 1 beta (IL-1β) and interleukin 6 (IL-6) were measured. Histopathological assessment of the kidney was also performed. The results indicated that HEA noticeably modulated the levels of BUN and creatinine as well as decreased the expression of MDA, TNF-α, IL-1β and IL-6 in the kidney. In addition, HEA up regulated the activities of antioxidant enzymes SOD, CAT and GSH-Px. Therefore, we concluded that HEA could effectively alleviate cisplatin-induced nephrotoxicity by counteracting oxidative stress and inflammation.

KEYWORDS:

• Cisplatin
• inflammation
• nephrotoxicity
• n⁶-2-hydroxyethyl-adenosine
• oxidative stress

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability

The authors confirm that the data supporting the findings of this study are available within the article [and/or] its supplementary materials.