摘要
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。
he effect of two important
factors,calcium over-load and ROS, of proximal tubule epithelial cell injurywere assessed by
measuring cytosolic free calcium,content of products of lipid peroxidation, activity
ofSOD,CAT,and observating ultrastructure change ofcells.A Chinese medicine, panax
notoginseng(PNS),was also used to vertify the possibility of above mecha-nism.These studies
suggested that calcium overloadand ROS are the factors of proximal tubular cells in-jury and
can influence,and stimulate each other.Panax Notoginseng can affect ROS system by
blockingcalcium passage,and safeguarding proximal tubulecells from injury caused by
cadmium.
出处
《中华肾脏病杂志》
CAS
CSCD
北大核心
1995年第2期72-75,共4页
Chinese Journal of Nephrology
基金
国家自然科学基金
