摘要
目的观察启膈散及其活血和化痰两个拆方对原代培养的食管癌细胞磷脂酶C-γ1（PLC-γ1）介导的细胞信号转导的影响，以探讨启膈散治疗食管癌的作用机制。方法从外科切除的原发性食管癌组织采集食管上皮细胞进行原代培养，加入启膈散及其活血和化痰两个拆方的水提物，测定细胞生长活性、PLC-γ1、EGFR、PDGFR、PKCα、磷酸化蛋白PY99和MARCKS（Ser152／156）表达水平、细胞内游离钙离子浓度（[Ca^2＋]I）及PLC-γ1和PKC活性。结果启膈散及其拆方对原代培养的食管癌细胞生长、PLC-γ1、EGFR、PDGFR、PKCα、磷酸化蛋白PY99和磷酸化MARCKS（Ser152／156）表达、[Ca^2＋]1i及PLC-γ1和PKC活性有不同程度的抑制作用，以活血组作用最强。结论启膈散及其拆方通过不同程度的抑制食管痛细胞PLC-γ1介导的信号转导而抑制肿瘤细胞的生长。
Objective To explore the mechanism of Qigesan for treating esophageal cancer, the effects of Qigesan （W） and its separated prescriptions （promoting blood circulation group P, and removing phlegm group R） on the cell growth and phospholipase C-γ1（PLC-γ1）-mediated signaling in primary cultured esophageal carcinoma cells were studied. Methods The cells from surgical human esophageal carcinoma specimens are primary cultured and treated with the water extrects from Qigesan and its separated prescriptions. The cell growth, the expressions of PLC-γ1, EGFR, PDGFR, PKCα, phosphorylated protein PY99 and MARCKS （Ser152/156）, intracellular [Ca^2＋]i concentration, PLC-γ1and PKC activity are measured.. Results The increased protein expression level of PLC-γ1, EGFR, PDGFR, and PKCα, the tyrosine phosphorylation level of EGFR, PDGFR and PLC-γ1, the activity of PLC-γ1 and PKC, intracellular [Ca^2＋]i concentration in the primary cultured esophageal cancer cells are inhibited by Qigesan and its separated prescriptions in different degrees, and with the best effects in group P. Conclusions To our knowledge, it is first reported that PLC-γ1-mediated signaling in esophageal cancer is increased, and Qigesan and its separated prescriptions inhibit the carcinoma growth through inhibiting PLC-γ1- mediated signal transduction.
出处
《国际中医中药杂志》
2007年第1期3-10,共8页
International Journal of Traditional Chinese Medicine
基金
国家自然科学基金（30171160,30371716）
关键词
启膈散
食管癌
磷脂酶C-Γ1
细胞信号转导
拆方研究
Qigesan prescription
Esophageal carcinoma
Phospholipase C-γ1
Signal transduction
Separated prescription research
