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利用间接免疫荧光染色、荧光探针标记、免疫细胞化学染色及免疫印迹等实验方法 ,从细胞增殖转化功能、细胞膜脂质流动性、蛋白酪氨酸激酶 (PTK )活性以及细胞周期调控蛋白表达的变化等方面探讨了胆固醇缺乏对Jurkat细胞的功能影响及其分子机制。结果显示 :经去脂血清培养基培养的Jurkat细胞加洛伐他丁处理 3d后 ,细胞膜脂流动性明显增大 ,细胞生长速度明显下降 ,细胞增殖受抑 ,PTK活性及细胞周期素D1(cyclinD1)、周期素依赖性激酶 4 (CDK4 )蛋白的表达明显降低 ,加入低密度脂蛋白可以部分逆转上述变化。结果提示 ,无论是内源性还是外源性胆固醇的缺乏都能使Jurkat细胞膜脂流动性发生变化 ,细胞PTK活性下降 ,cyclinD1、CDK4蛋白表达降低 ,推测这一变化与细胞增殖受抑有直接关系
Indirect immunofluorescence staining, fluorescent probe labeling, immunocytochemical staining and western blotting were used to investigate the effects of cell proliferation and transformation on cell membrane lipid fluidity, protein tyrosine kinase (PTK) activity and cell cycle regulatory protein expression Changes and other aspects of the lack of cholesterol on Jurkat cell function and its molecular mechanism. The results showed that the cell membrane lipid fluidity was significantly increased, the cell growth rate was significantly decreased, the cell proliferation was inhibited, the PTK activity and the expression of cyclin D1 (superscript +) were decreased in Jurkat cells treated with delavogation serum medium for 3 days. ), Cyclin-dependent kinase 4 (CDK4) protein expression was significantly reduced, adding low-density lipoprotein can partially reverse the above changes. The results suggest that either endogenous or exogenous cholesterol deficiency can change the membrane fluidity of Jurkat cells, PTK activity decreased, cyclinD1, CDK4 protein expression decreased, speculated that this change is directly related to the inhibition of cell proliferation