岭南现代临床外科
嶺南現代臨床外科
령남현대림상외과
LINGNAN MODERN CLINICS IN SURGERY
2014年
2期
136-139
,共4页
陈伟强%刘付宁%刘玲%何惠燕%曹铭辉
陳偉彊%劉付寧%劉玲%何惠燕%曹銘輝
진위강%류부저%류령%하혜연%조명휘
吗啡%PC12 细胞%增殖抑制%p38MAPK
嗎啡%PC12 細胞%增殖抑製%p38MAPK
마배%PC12 세포%증식억제%p38MAPK
Morphine%PC12 cells%Proliferation%p38MAPK
目的:探讨吗啡对大鼠嗜铬细胞瘤 PC12细胞增殖的抑制作用及其分子机制。方法 PC12细胞体外培养,将吗啡加入细胞培养液中使吗啡浓度分别稀释至10、20、30μmol/L ,然后分别与 PC12细胞一同孵育,四甲基偶氮噻唑蓝法(MTT)观察吗啡对细胞增殖的抑制作用;免疫印迹法检测PC12细胞p38MAPK 表达及磷酸化水平。结果不同浓度吗啡对PC12细胞增殖有明显的抑制作用,抑制率为17.66%~31.05%;并且吗啡可以诱导PC12细胞p38MAPK 磷酸化水平升高,而p38MAPK 通路阻断剂SB203580可以抑制吗啡诱导 PC12细胞 p38MAPK 磷酸化水平升高,减轻吗啡对 PC12细胞增殖的抑制。结论吗啡可以明显抑制 PC12细胞的增殖,升高p38MAPK 的磷酸化水平可能是其重要分子机制之一。
目的:探討嗎啡對大鼠嗜鉻細胞瘤 PC12細胞增殖的抑製作用及其分子機製。方法 PC12細胞體外培養,將嗎啡加入細胞培養液中使嗎啡濃度分彆稀釋至10、20、30μmol/L ,然後分彆與 PC12細胞一同孵育,四甲基偶氮噻唑藍法(MTT)觀察嗎啡對細胞增殖的抑製作用;免疫印跡法檢測PC12細胞p38MAPK 錶達及燐痠化水平。結果不同濃度嗎啡對PC12細胞增殖有明顯的抑製作用,抑製率為17.66%~31.05%;併且嗎啡可以誘導PC12細胞p38MAPK 燐痠化水平升高,而p38MAPK 通路阻斷劑SB203580可以抑製嗎啡誘導 PC12細胞 p38MAPK 燐痠化水平升高,減輕嗎啡對 PC12細胞增殖的抑製。結論嗎啡可以明顯抑製 PC12細胞的增殖,升高p38MAPK 的燐痠化水平可能是其重要分子機製之一。
목적:탐토마배대대서기락세포류 PC12세포증식적억제작용급기분자궤제。방법 PC12세포체외배양,장마배가입세포배양액중사마배농도분별희석지10、20、30μmol/L ,연후분별여 PC12세포일동부육,사갑기우담새서람법(MTT)관찰마배대세포증식적억제작용;면역인적법검측PC12세포p38MAPK 표체급린산화수평。결과불동농도마배대PC12세포증식유명현적억제작용,억제솔위17.66%~31.05%;병차마배가이유도PC12세포p38MAPK 린산화수평승고,이p38MAPK 통로조단제SB203580가이억제마배유도 PC12세포 p38MAPK 린산화수평승고,감경마배대 PC12세포증식적억제。결론마배가이명현억제 PC12세포적증식,승고p38MAPK 적린산화수평가능시기중요분자궤제지일。
Objective To investigate the effects of morphine on roliferation of pheochromocytoma cell and its mechanism. Methods PC12 cell cultures were exposed to 10,20,30 μmol/L morphine. The inhibition of the cell proliferation was determined by MTT assay. The level of p38MAPK was detected by immunoblotting. Results The proliferation of PC12 cells were inhibited after morphine exposure for 48 h.Immunoblotting showed that morphine increased the phosphorylation of p38MAPK was increased in stimulation of monphine. SB203580 , the inhibitor of p38MAPK , reduced inhibition the proliferation of PC12 cells by morphine. Conclusion These results suggest that morphine can significantly inhibits the proliferation of PC12 cells by an increase in p38MAPK phosphorylation.