标题：Dexmedetomidine Promotes SH-SY5Y Cell Resistance Against Impairment of Iron Overload by Inhibiting NF-B Pathways
作者：Hu, Xi-bei; Xi, Zhi-yu; Liu, Lin-qing; Kang, Kai; Li, Wan-hong; Shen, Yu-xian; Kang, Fang; Li, Juan
作者机构：[Hu, Xi-bei; Li, Juan] Shandong Univ, Sch Med, Jinan 250012, Shandong, Peoples R China.; [Hu, Xi-bei; Li, Wan-hong; Kang, Fang; Li, Juan] Univ Sci & 更多
通讯作者：Li, J;Li, J;Li, J
通讯作者地址：[Li, J]Shandong Univ, Sch Med, Jinan 250012, Shandong, Peoples R China;[Li, J]Univ Sci & Technol China, Div Life Sci & Med, Affiliated Hosp USTC 1, De 更多
关键词：Iron overload; Dexmedetomidine; Oxidative stress; Inflammation;; Apoptosis; NF-B
摘要：Iron overload is a common pathophysiological state underlying many diseases that has a detrimental influence on cells. The protective effects of Dexmedetomidine (Dex), a high selective alpha-2-adrenoceptor agonist, have been revealed through many experimental models, whereas no study reports its effects on an iron overload model. To elucidate these effects, we used FeCl2 with or without Dex to treat SH-SY5Y cells for 24h and then detected indicators of oxidative stress, inflammation and apoptosis and investigated possible mechanisms further. After treatment with FeCl2 for 24h, cell viability decreased in a dose dependent manner, and Dex promoted cell survival in FeCl2 incubation, also in a dose-dependent manner. Compared with the FeCl2 group, 20 mu M Dex significantly attenuated ROS accumulation, reduced pro-inflammatory cytokine expression, and inhibited apoptosis. Furthermore, 20 mu M concentration of Dex remarkably downregulated the expression of pro-apoptotic protein and activation of caspase 3 while increasing anti-apoptotic protein expression. Additionally, Dex also effectively suppressed the expression of NF-B and its activation. In conclusion, Dex exerted anti-oxidative stress, anti-inflammation, and anti-apoptosis effects on FeCl2-treated SH-SY5Y cells, possibly by inhibiting NF-B signaling pathway.