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目的探讨ＯＸ－ＬＤＬ及ＨＭＧ－ＣｏＡ还原酶抑制剂辛伐他汀对人单核细胞（Ｍｏ）表达蛋白激酶Ｃ（ＰＫＣ）活性和胞浆内游离钙（［Ｃａ２＋］ｉ）浓度的影响。方法Ｍｏ ＰＫＣ活性采用 γ－３２Ｐ－ＡＴＰ磷酸转移法，细胞内游离钙采用 Ｆｌｕｏ－３／Ａｍ荧光负载，流式细胞术检测。结果ＯＸ－ＬＤＬ呈剂量依赖方式促进人 Ｍｏ ＰＫＣ活性增加，１２ ｍｉｎ时达峰值，然后缓慢下降，２０ ｍｉｎ后仍维持较高水平，胞浆内［Ｃａ２＋］ｉ升高分２个时相，即快速相和持续相。移去细胞外液钙，ＯＸ－ＬＤＬ仍引起快速相，但持续相消失，而辛伐他汀能明显抑制ＯＸ－ＬＤＬ．引起的Ｍｏ ＰＫＣ活性增加，并降低持续相胞浆内钙水平，而对快速相无明显影响。结论ＯＸ－ＬＤＬ能激活人单核细胞ＰＫＣ活性与升高［Ｃａ２＋］ｉ。ＯＸ－ ＬＤＬ刺激Ｍｏ［Ｃａ２＋］ｉ升高的快速相是有胞浆钙池释放引起，持续相升高主要有胞外钙内流引起。辛伐他汀抑制Ｍｏ ＰＫＣ活性可能是通过胞内钙水平变化起作用。
Objective To investigate the effect of simvastatin, an inhibitor of OX-LDL and HMG-CoA reductase, on the activity of PKC and the concentration of [Ca2 +] i in human monocytes. Methods The activity of Mo PKC was determined by γ-32P-ATP phosphate transfer method. The intracellular free calcium was detected by Fluo-3 / Am fluorescence flow cytometry. Results OX-LDL increased the activity of human PKCK in a dose-dependent manner, reached a peak at 12 min, then decreased slowly and maintained a high level after 20 min. The intracellular [Ca 2+] i increased in two phases, ie Fast and sustained phase. Removing extracellular calcium, OX-LDL still caused a rapid phase, but continued to disappear, while simvastatin significantly inhibited OX-LDL. Caused by increased activity of Mo PKC, and reduce the sustained phase of intracellular calcium levels, but no significant impact on the fast phase. Conclusion OX-LDL can activate PKC activity of human monocytes and increase [Ca2 +] i. OX-LDL stimulated Mo [Ca2 +] i increased fast phase is caused by the release of cytoplasmic calcium pool, sustained phase increase mainly caused by extracellular calcium influx. Inhibition of Mo PKC activity by simvastatin may play a role by intracellular calcium level changes.