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目的探讨蛋白激酶C(proteinkinaseC,PKC)在K562/A02细胞多药耐药的产生及其逆转中的作用。方法用放射免疫法检测了耐药细胞株K562/A02及其敏感株K562的静息PKC活性水平,并观察了柔红霉素(daunomycin,DNR)以及耐药调节剂粉防己碱(tetrandrine,Tet)、屈洛昔芬(droloxifene,Drol)单独或联合应用后细胞PKC活性的变化。结果静息状态下耐药细胞株K562/A02的PKC活性显著高于敏感株K562,有效调节浓度的Tet、Drol单独作用于K562、K562/A02细胞均可显著下调其PKC活性,联合应用有显著协同性。1μg/mLDNR可显著下调K562细胞的PKC活性,部分下调K562/A02细胞的PKC活性,有效调节浓度的Tet、Drol单独或联合应用均可加强其作用。结论PKC参与K562/A02细胞多药耐药(multidrugresistance,MDR)的形成,Tet、Drol逆转K562/A02细胞的MDR可能与下调其PKC活性有关。
Objective To investigate the role of protein kinase C (PKC) in the generation and reversal of multidrug resistance in K562 / A02 cells. Methods The resting PKC activity of drug-resistant cell line K562 / A02 and its sensitive strain K562 was detected by radioimmunoassay. The effects of daunomycin (DNR) and the drug resistance regulator tetrandrine (Tet ), Changes in PKC activity of cells after droloxifene (Drol) alone or in combination. Results The PKC activity of K562 / A02 cell line was significantly higher than that of K562 cell line at rest. The effective concentration of Tet and Drol alone significantly decreased the PKC activity in K562 and K562 / A02 cells Synergy. 1μg / mL DNR could significantly down-regulate the PKC activity of K562 cells, partially down-regulate the PKC activity of K562 / A02 cells, and effectively regulate the concentrations of Tet and Drol alone or in combination. Conclusions PKC is involved in the formation of multidrug resistance (MDR) in K562 / A02 cells. The reversal of MDR by Tet and Drol in K562 / A02 cells may be related to its down-regulation of PKC activity.