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

被引:5
作者
Yin, Min [1 ]
Li, Na [1 ]
Makinde, Emmanuel Ayobami [2 ]
Olatunji, Opeyemi Joshua [2 ]
Ni, Ziyuan [1 ]
机构
[1] Jilin Univ, China Japan Union Hosp, Dept Nephrol, Changchun 130033, Jilin, Peoples R China
[2] Prince Songkla Univ, Fac Thai Tradit Med, Hat Yai, Thailand
关键词
Cisplatin; inflammation; nephrotoxicity; n(6)-2-hydroxyethyl-adenosine; oxidative stress; INDUCED NEPHROTOXICITY; OXIDATIVE STRESS; APOPTOSIS; INFLAMMATION; TOXICITY; SUPPRESSION; DYSFUNCTION; MODULATION; INDUCTION; MECHANISM;
D O I
10.1080/26895293.2020.1760149
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
N-6-2-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-alpha), interleukin 1 beta (IL-1 beta) 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-alpha, IL-1 beta 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.
引用
收藏
页码:244 / 251
页数:8
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