【摘要】 目的　研究工频磁场抑制细胞缝隙连接通讯（ ＧＪＩＣ） 功能的可能作用机制。方法　中国仓鼠肺成纤维（ ＣＨＬ） 细胞受０ ．８ ｍ Ｔ５０ Ｈｚ 脉冲磁场作用２３ 小时后，加入不同浓度的蛋白激酶Ｃ（ ＰＫＣ）抑制剂———斯特罗斯孢啉（ Ｓｔａｕｒｏｓｐｏｒｉｎｅ，ＳＴＳ） 或十六酰基肉毒硷（ ＰａｌｍｉｔｏｙｌＤＬｃａｒｎｉｔｉａ ，ＰＭＣ） 共同作用１ 小时，中止作用后，用微注射方法检测ＧＪＩＣ 功能。结果　５０ Ｈｚ 脉冲磁场对ＧＪＩＣ 的抑制作用能被ＳＴＳ或ＰＭＣ 所拮抗，拮抗程度与 ＳＴＳ 或ＰＭＣ 的浓度有关，当ＳＴＳ、ＰＭＣ 分别达到１０ ｎｍｏｌ／ Ｌ、１０μｍｏｌ／ Ｌ 时，ＧＪＩＣ 功能恢复至（８ ．７１ ±１ ．０７） 个、（９ ．００ ±１ ．０７） 个，接近于辐照前水平（１０ ．０１ ±２ ．０１） 个。结论　工频磁场抑制ＧＪＩＣ 与ＰＫＣ 激活有关。更多还原

【Abstract】 Objective To explore the mechanism of 50 Hz pulse magnetic fields(PMF) inhibiting gap junctional intercellular communication(GJIC). Methods Chinese hamster lung(CHL) cells were exposed to 50 Hz PMF at 0.8 mT for 24 h,then combined with protein kinase C(PKC) inhibitor Staurosporine(STS) or Palmitoyl DL carnitina(PMC) at different concentrations for another one hour.GJIC was determined by microinjection immediately after exposure. Results The GJIC inhibition induced by PMF could be blocked by PKC inhibitor,STS or PMC.The blocking was dependent on concentration.When STS or PMC was at certain concentration,the function of GJIC basically restored to the level before exposure. Conclusion The inhibition of GJIC might be related to the activation of PKC.更多还原