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钙超载与氧自由基机制是细胞发生损伤的两大重要分子学机制。本文以离体肾小管上皮细胞为研究对象，重金属镉为损伤因素，着重探讨了镉致肾小管损伤中钙超载及氧自由基双重损伤机制的各自作用及联系，此外，尚观察了中药三七皂甙对上述机制的可能影响。结果发现，当镉与肾小管上皮细胞共同孵育后，［Ｃａ］ｉ及脂质过氧化代谢产物明显升高，氧自由基清除酶活力下降，提示钙超载机制及氧自由基机制共同参与了镉致肾小管上皮细胞的损伤，两者之间可能相互影响、相互促进，形成恶性循环。三七皂甙可通过阻滞钙通道，间接影响氧自由基系统而对肾小管上皮细胞起保护作用。
The mechanisms of calcium overload and oxygen free radical are two important molecular mechanisms of cell injury. In this paper, isolated renal tubular epithelial cells as the research object, cadmium as the injury factor, focusing on cadmium induced renal tubular injury in calcium overload and oxygen free radicals double damage mechanisms of their respective roles and links, in addition, we observed the Chinese medicine 37 Possible effects of saponins on these mechanisms. The results showed that when cadmium was incubated with renal tubular epithelial cells, [Ca] i and lipid peroxidation metabolites were significantly increased, the activity of oxygen free radical scavenger decreased, suggesting that calcium overload mechanism and oxygen free radical mechanism participate in cadmium Injury to renal tubular epithelial cells, the two may affect each other and promote each other, forming a vicious circle. Panax notoginseng saponins can protect renal tubular epithelial cells by blocking the calcium channel and indirectly affecting the oxygen free radical system.