Fisetin prevents fluoride- and dexamethasone-induced oxidative damage in osteoblast and hippocampal cells

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• 作者：Iwona Inkielewicz-Stepniak^a ; ^{iinkiel@gumed.edu.pl} ; Marek W. Radomski^b ; Michal Wozniak^a
• 关键词：Fluoride and dexamethasone ; Osteoblast cells ; Hippocampal cells ; Oxidative/nitrosative stress ; Apoptosis ; Fisetin
• 刊名：Food and Chemical Toxicology
• 出版年：2012
• 期刊代码：20_02786915
• 类别：pha
• 出版时间：March-April, 2012
• 卷：50
• 期：3-4
• 页码：583-589
• 文件大小：1064 K

摘要

Fluoride intoxication and dexamethasone treatment produce deleterious effects in bone and brain. The aim of this study was to evaluate the effect of fluoride (F) and dexamethasone (Dex) co-exposure on oxidative stress and apoptosis in osteoblast-like MC3T3-E1 and hippocampal HT22 cell lines. Co-exposure to F and Dex resulted in a concentration-dependent decrease in cell viability, induction of apoptosis and increased generation of reactive oxygen species (ROS) and nitric oxide (NO) following 72 h of incubation. Fluoride-induced apoptosis in MC3T3-E1 and HT22 cells was attenuated by catalase and L-NNMA, indicating a role for H₂O₂ and NO as mediators of cytotoxicity. Dexamethasone-induced apoptosis was associated with H₂O₂ generation in both cell lines and it was attenuated during co-incubation with catalase. These data indicate that co-exposure to F and Dex amplifies their respective cytotoxicity in H₂O₂- and NO-dependent manner. As flavonoid fisetin prevented F- and Dex-induced cytotoxicity the potential role of this product in pharmacology and diet may be considered.