Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cisplatin is a common anticancer drug, but it comes with significant nephrotoxicity. Further cisplatin-induced oxidative stress contributes to the pathogenesis of the nephrotoxicity. A new compound, BiZn, can potentially prevent this complication. We verified our postulation by in vitro and in vivo models. From our findings, BiZn did not affect cisplatin-induced cytotoxicity on neuroblastoma cells under both in vitro and in vivo settings. However, BiZn significantly reduced the blood urea nitrogen and creatinine levels in cisplatin-treated mice. Under the lethal dosage of cisplatin, co-treatment of BiZn significantly increased the survival rate. BiZn stimulated antioxidant proteins metallothionein (MT) and glutathione (GSH) generation from kidney cells and minimized cisplatin-induced apoptosis. Knocking down MT-IIA and inhibiting GSH abolished such protection. In conclusion, pretreatment of BiZn decreased cisplatin-induced renal toxicity without affecting its antitumor activity. BiZn-induced antioxidant proteins MT and GSH may contribute to the renal protection effect.
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PMID:A Novel Synthetic Compound, Bismuth Zinc Citrate, Could Potentially Reduce Cisplatin-Induced Toxicity Without Compromising the Anticancer Effect Through Enhanced Expression of Antioxidant Protein. 3092 49

Emodin is a natural anthraquinone derivative with numerous beneficial effects, including antioxidant properties, anti-tumor activities, and protecting the nerves. Zinc-induced neurotoxicity plays a crucial role in the pathogenesis of vascular dementia (VD) and Parkinson's disease (PD). Here, the protective activity of emodin inhibiting zinc-induced neurotoxicity and its molecular mechanisms such as cellular Zn2+ influx and zinc-induced gene expression were examined using human neuroblastoma cells (SH-SY5Y cells). Our findings showed that emodin obviously enhanced cell viability and reduced cell apoptosis and lactate dehydrogenase release. Bedsides, we detected a decrease of intracellular Zn2+ concentration after SH-SY5Y cells were pretreated with emodin. Simultaneously, the expression of zinc transporter-1, metallothionein-1, and metallothionein-2 were weakened in emodin-pretreated SH-SY5Y cells. In addition, emodin prevented the depletion of NAD+ and ATP induced by zinc. Emodin also reduced intracellular reactive oxygen species and endoplasmic reticulum-stress levels. Strikingly, emodin elevated SH-SY5Y cell viability and inhibited cell apoptosis caused by AMP-activated protein kinase signaling pathway activation. Thus, emodin could protect against neurotoxicity induced by Zn2+ in neuroblastoma SH-SY5Y cells. It is expected to have future therapeutic potential for VD or PD and other neurodegenerative diseases.
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PMID:Emodin inhibits zinc-induced neurotoxicity in neuroblastoma SH-SY5Y cells. 3102 67


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