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Treatment with catalpol protects against cisplatininduced renal injury through Nrf2 and NFκB signaling pathways

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Cisplatin (CP) is one of the most widely used chemotherapy drugs for cancer treatment, but it often leads to nephrotoxicity. It is well known that catalpol exhibits antioxidant and antiinflammatory functions, thus the present study aimed to investigate the potential protective effects of catalpol on CPinduced kidney injury in rats, in addition to determining the underlying mechanisms. SpragueDawley rats were treated with 25, 50 or 100 mg/kg catalpol for two days, injected with 20 mg/kg cisplatin and catalpol on day 3 and sacrificed on day 4. The histological analysis of isolated kidney tissues was performed using hematoxylin and eosin staining, cleaved caspase3 expression levels were analyzed using western blotting and the expression levels of inflammatory cytokines in the tissues, including tumor necrosis factor α (TNFα), interleukin (IL)1β, IL6, IL8, IL10 and inducible nitric oxide synthase (iNOS) were evaluated using ELISAs. Furthermore, the mRNA and protein expression levels of nuclear factor erythroid 2related factor 2 (Nrf2), heme oxygenase 1 (HO1), kelchlike ECHassociated protein 1 (Keap1), NFκB and inhibitory κB (IκB) were determined using reverse transcriptionquantitative PCR and western blotting, respectively. The results revealed that the treatment with catalpol prevented the histopathological injury and renal dysfunction caused by CP. In addition, catalpol significantly suppressed the CPinduced apoptosis of tubular cells, inhibited the CPinduced upregulation of TNFα, IL1β, IL6, IL8 and iNOS and promoted the production of the antiinflammatory cytokine IL10. Additionally, the mRNA and protein expression levels of Nrf2, HO1 and IκB in the kidney tissues were increased, whereas the expression levels of Keap1 and NFκB were significantly decreased following the treatment with catalpol. In conclusion, these results suggested that catalpol may inhibit CPinduced renal injury and suppress the associated inflammatory response through activating the Nrf2 and inhibiting the NFκB signaling pathways, respectively.
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Document Type: Research Article

Affiliations: Department of Nephrology, The key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing 400037, P.R. China

Publication date: October 1, 2020

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  • Experimental and Therapeutic Medicine aims to ensure the expedient publication, in both print and electronic format, of studies relating to biology, gene therapy, infectious disease, microbiology, molecular cardiology and molecular surgery. The journal welcomes studies pertaining to all aspects of molecular medicine, and studies relating to in vitro or in vivo experimental model systems relevant to the mechanisms of disease are also included.

    All materials submitted to this journal undergo the appropriate review via referees who are experts in this field. All materials submitted follow international guidelines with regard to approval of experiments on humans and animals.
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