摘要
目的利用次氮基三乙酸铁（ferricnitrilotriacetate，FeNTA）引起肝细胞的铁过载，诱导培养的大鼠正常肝细胞凋亡，观察低浓度姜黄素对铁过量诱导的肝细胞凋亡的影响及其机制。方法FeNTA加姜黄素与培养的肝细胞孵育，检测肝细胞凋亡，凋亡相关蛋白的表达，caspase-3活性，自由基的产生，核转录因子KB（NF．KB）活性。结果10μmo1／L的姜黄素使FeNTA诱导的肝细胞凋亡数下降46．65％，下调Bcl-2及Bcl-XL表达，而对Bax及Bad无影响，使FeNTA诱导的自由基及caspase．3分别下降45．01％和59．71％，抑制NF．KB活性。结论低浓度姜黄素能减低铁过量所致的肝细胞凋亡及转录因子NF—KB活性。
Objective Iron is an essential micronutrient for human beings but its overload induces various diseases of liver, the main body storage site for iron, such as liver fibrosis. Curcumin is a natural polyphenol derived from turmeric and has been used widely. Its pharmacological action has attracted great attention in recent years. The apoptosis of rat cultured hepatocytes was induced by FeNTA （ferric nitrilotriacetate）-induced Iron overload. The present study was to examine the effect of eureumin at low concentrations on FeNTA-induced apoptosis of hepatocytes and elucidate the underlying mechanisms. Methods After the incubation of hepatocytes with 100 μmol/L FeNTA in the presence or absence of 1 -10 μmmol/L of curcumin, a series of analyses were performed, including the analyses of hepatocytic apoptosis, the expressions of proteins relating with the regulations of cell apoptosis, caspase-3 activity, the production of reactive oxygen species （ROS） and nuclear factor NF-KB activity. Results Curcumin reduced the FeNTA-induced hepatocytic apoptosis by 46. 65% and significantly down-regulated the protein levels of Bcl-2 and Bcl-XL In contrast, it had no effect on the protein levels of Bax and Bad. The curcumin treatment reduced FeNTA-caused production of ROS and caspase-3 activity by 45.01% and 59. 71% respectively. And the NF-KB activity was also inhibited. Conclusion Curcumin at low concentrations reduces iron overload-caused hepatocytic apoptosis and NF-KB activity, the key regulatory transcription factor for the inflammation-related gene expression in cultured hepatocyte.
出处
《中华医学杂志》
CAS
CSCD
北大核心
2012年第28期1997-2001,共5页
National Medical Journal of China
基金
国家自然科学基金（30971117）
江苏高校优势学科建设工程资助项目
