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

Abstract

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-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.

Quinacrine Ameliorates Cisplatin-Induced Renal Toxicity via Modulation of Sirtuin-1 Pathway

“…Cisplatin is an efficient chemotherapeutic agent in in the treatment of different types of cancers, including non-small cell lung carcinoma, cervical, ovarian, testicular and head and neck cancers [ 1 , 2 , 3 ]. Unfortunately, cisplatin clinical use is accompanied with serious side effects on various normal tissues [ 4 ]. Cisplatin accumulates in renal proximal tubules, causing acute kidney injury [ 5 ].…”

Cisplatin-Induced Kidney Toxicity: Potential Roles of Major NAD+-Dependent Enzymes and Plant-Derived Natural Products

“…In addition to the oxidative stress implicated in the pathogenesis of cisplatin kidney injury [ 28 , 29 , 30 , 31 , 32 , 33 ], inflammation and renal fibrosis have also been postulated to be involved in cisplatin-induced kidney injury [ 34 , 35 , 36 , 37 , 38 , 39 ]. Cisplatin-induced kidney injury may also involve NAD + redox signaling pathways such as sirt3 [ 40 ], poly-ADP ribosylase (PARP) [ 41 ], and mitochondrial dynamics [ 18 ] including mitochondrial fission and fusion [ 42 , 43 , 44 ].…”

Broad Efficacy of Scavenging Free Radicals: Cordyceps sp.

“…In a continuous report, cordycepin is found to direct the motor issues in MPTP-treated Parkinsonism rodents and seemed to apply neuroprotective effects through easing up bothering and oxidative pressing factor response. Likewise, such neuroprotective effects may be connected with the limitation of the TLR/NF-κB hailing pathway in MPTP-started Parkinson's disorder rodents and LPS-incited BV2 cells [101]. Stroke is perhaps the most notable ailments in cerebrovascular affliction and can be clinically isolated into two genuss: ischemic and hemorrhagic.…”

“…The CPZ-prompted demyelination model has been by and large used to assessment MS, especially in investigating de-and re-myelination in the corpus callosum. Cordycepin mitigates CPZ-prompted incidental effects in mice by protecting motor brokenness, propelling re-myelination, stifling glial-cell incitation, lessening the outpouring of the steady of combustible cytokines, IL-1β and IL-6, and growing the levels of the quieting cytokine IL-4 [101,106,110]. All around, cordycepin is useful in Parkinson's infection and applies its possessions generally by reducing oxidative pressing factor and against oxidant bothering through the TLR/NF-κB hailing pathway.…”