دورية أكاديمية

Ameliorative Effect of Rhoifolin in Cisplatin-Induced Nephrotoxicity via Regulating Nuclear Factor-κB Pathway.

التفاصيل البيبلوغرافية
العنوان: Ameliorative Effect of Rhoifolin in Cisplatin-Induced Nephrotoxicity via Regulating Nuclear Factor-κB Pathway.
المؤلفون: Yanfang Song1 ShufangYandhj@163.com, Shufang Yan2, Hong Zhang1, Rui Liu1, Xin An1, Qifeng Zhang1
المصدر: Current Topics in Nutraceutical Research. Aug2020, Vol. 18 Issue 3, p266-272. 7p.
مصطلحات موضوعية: INFLAMMATION prevention, ANIMAL experimentation, ANTIOXIDANTS, BIOLOGICAL models, CELLULAR signal transduction, FLAVONOIDS, GLUTATHIONE, INTERLEUKINS, NEPHROTOXICOLOGY, PHOSPHORYLATION, RATS, SUPEROXIDE dismutase, TUMOR necrosis factors, DNA-binding proteins, MALONDIALDEHYDE, PLANT extracts, OXIDATIVE stress, TREATMENT effectiveness
مستخلص: Dose-dependent nephrotoxicity limits the therapeutic use of cisplatin in tumor chemotherapy. Natural compounds show a protective effect against cisplatin-induced nephrotoxicity. Rhoifolin is a flavone glycoside that demonstrates antioxidant and antiproliferative effects. The influence and mechanism of rhoifolin on cisplatin-induced nephrotoxicity were investigated in this study. First, a rat model of cisplatin-induced nephrotoxicity was established. Intraperitoneal administration of cisplatin induced renal damage in rats as demonstrated by a decrease in body weight, increase in blood urea, nitrogen and creatinine, and destruction of histological integrity. However, treatment with rhoifolin attenuated cisplatin-induced nephrotoxicity. Second, cisplatin induced oxidative stress and inflammatory response in rats as demonstrated by a decrease in superoxide dismutase, glutathione, glutathione S-transferase and catalase, and an increase in malondialdehyde, tumor necrosis factor-α, and interleukin-6. Also, the administration of rhoifolin led to alleviation of cisplatin-induced oxidative stress and inflammatory response. Finally, cisplatin activated the nuclear factor-kappa B signaling pathway via degradation and phosphorylation of IκBα (inhibitor of kappa B). Administration of rhoifolin inhibited nuclear translocation of NF-κB via downregulation of phospho-IκBα and phospho-p65, as well as up-regulation of IκBα. In conclusion, the administration of rhoifolin attenuated cisplatin-induced renal damage, oxidative stress and inflammatory response through inhibition of the NF-κB signaling pathway, suggesting a potential adjunct candidate for cisplatin in tumor treatment. [ABSTRACT FROM AUTHOR]
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قاعدة البيانات: Business Source Index
الوصف
تدمد:15407535
DOI:10.37290/ctnr2641-452X.18:266-272