目的：探明线粒体分裂抑制剂(Mdivi-1)在椎间盘炎症微环境下髓核(NP)细胞衰老过程中的作用。方法：体外分离培养SD大鼠NP细胞。首先评估不同浓度的脂多糖(LPS)(0、20、50、100 μg·ml^-1)对NP细胞增殖活力的影响，根据结果选择LPS的干预浓度为100 μg·ml^-1。将实验分为3组，对照组、LPS组和LPS+Mdivi-1组。应用细胞增殖实验、免疫荧光、Western blot、Real time-PCR和β半乳糖苷酶染色评估线粒体功能和NP细胞衰老变化。结果：与对照组相比，LPS降低了NP细胞增殖活力，促进了线粒体自噬、活性氧(ROS)大量产生和线粒体膜电位丢失；Mdivi-1的预处理明显加剧了LPS诱导的ROS产生、线粒体膜电位丢失和ATP合成减少并抑制了线粒体自噬的发生。此外，与LPS组相比，Mdivi-1的预处理明显增加了β半乳糖苷酶染色阳性率，导致LPS诱导的p53，p21，MMP3和MMP13的蛋白表达进一步增高，Aggrecan和Collagen Ⅱ的蛋白表达进一步减少；同时还导致LPS诱导的炎症因子TNF-α和IL-1β明显增多。结论：线粒体分裂抑制剂Mdivi-1通过抑制线粒体自噬进一步加剧LPS炎症微环境下NP细胞的衰老退变。

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