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目的通过测定大鼠肝细胞内游离钙离子浓度（［Ｃａ２＋］ｉ），观察三七总皂苷（ＰＮＧＳ）对肝细胞Ｃａ２＋浓度的影响，探讨其抑制肝细胞钙超载的机制。方法胶原酶分离大鼠肝细胞，Ｆｕｒａ２／ＡＭ技术测定［Ｃａ２＋］ｉ，研究ＰＮＧＳ对静息和被激动状态下肝细胞［Ｃａ２＋］ｉ的影响。结果１０ｎｍｏｌ·Ｌ－１血管加压素及１０ｎｍｏｌ·Ｌ－１血管紧张素分别使肝细胞［Ｃａ２＋］ｉ增加２００％和９４％，ｖｅｒａｐａｍｉｌ、ｎｉｆｅｄｉｐｉｎｅ和ＰＮＧＳ均能不同程度地抑制血管加压素、血管紧张素激动引起的肝细胞［Ｃａ２＋］ｉ升高，ＰＮＧＳ的抑制作用显著强于ｖｅｒａｐａｍｉｌ、ｎｉｆｅｄｉｐｉｎｅ且呈明显的剂量依赖性。ＰＮＧＳ还能轻度降低静息状态下肝细胞［Ｃａ２＋］ｉ，而ｖｅｒａｐａｍｉｌ、ｎｉｆｅｄｉｐｉｎｅ无此作用。结论ＰＮＧＳ能特异性阻断肝细胞膜上受体依赖性钙通道（ＲＯＣ），抑制肝细胞的钙内流，阻断肝细胞内源性ＩＰ３途径，防止肝细胞内钙超载。ＰＮＧＳ抑制钙超载机制还可能与其本身轻度结合钙离子有关。
Objective To investigate the effect of Panax notoginseng saponins (PNGS) on Ca2+ concentration in hepatocytes by measuring intracellular free calcium concentration ([Ca2+]i) in rat hepatocytes, and to explore the mechanism of inhibition of hepatic calcium overload. METHODS: Collagenase was used to isolate rat hepatocytes. Fura-2/AM technique was used to measure [Ca2+]i. The effects of PNGS on hepatocyte [Ca2+]i in resting and stimulated conditions were studied. Results 10 nmol·L-1 vasopressin and 10 nmol·L-1 angiotensin increased the [Ca2+]i of hepatocytes by 200% and 94%, respectively. Verapamil, nifedipine and PNGS all inhibited vasopressin to varying degrees. The increase of [Ca2+]i in hepatocytes induced by angiotensin agonism, PNGS inhibition was significantly stronger than verapamil, nifedipine and showed significant dose-dependence. PNGS can also slightly reduce [Ca2+]i in hepatocytes at rest, whereas verapamil and nifedipine do not have this effect. Conclusions PNGS can specifically block receptor-dependent calcium channels (ROC) on hepatocyte membrane, inhibit calcium influx in hepatocytes, block endogenous IP3 pathway in hepatocytes, and prevent calcium overload in hepatocytes. The inhibition of calcium overload by PNGS may also be associated with its own mild binding to calcium ions.