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目的研究肝脏老化时枯否细胞（ＫＣ）在肝细胞（ＨＣ）功能损害中的地位和机制．方法应用ＨＣＫＣ共同培养技术研究６，１２，１８和２４月龄大鼠（每组５只）ＫＣ对ＨＣ蛋白质合成和线粒体代谢水平的影响，并探讨了这种影响与老化ＫＣ分泌功能改变的关系．结果单独培养的２４月龄组ＨＣ蛋白质合成能力和线粒体代谢水平较６月龄组明显降低；各月龄组ＨＣ与６月龄组ＫＣ共同培养时，两指标较单独培养者均有明显增加，与２４月龄组ＫＣ共同培养时则显著降低．ＬＰＳ（１０ｎｇ／Ｌ）对单独培养的ＨＣ蛋白质合成和线粒体能量代谢无明显影响，但对共同培养系统中６月龄ＫＣ的增强作用和２４月龄ＫＣ的抑制作用具有明显的放大作用．２４月龄组ＫＣＴＮＦ、ＩＬ８、ＮＯ的分泌水平较６月龄组ＫＣ明显升高，ＰＧＥ２明显降低．各组ＫＣ受ＬＰＳ刺激后ＴＮＦ和ＮＯ水平较未刺激组均有明显升高，其增值以高月龄组为显著；６和１２月龄组ＫＣ受刺激后ＩＬ８水平明显升高，１８和２４月龄组无明显变化；ＰＧＥ２的变化规律与ＩＬ８相反．结论ＫＣ在鼠肝老化时ＨＣ受损过程中起重要作用，这可能与老化ＫＣ分泌细胞因子谱有改变，导致ＨＣ分子微生态环境变化有关．
Objective To investigate the status and mechanism of Kupffer cell (KC) in the functional impairment of hepatocytes (HC) during liver aging. Methods The HC-KC co-culture technique was used to study the effects of KC on protein synthesis and mitochondrial metabolism in HC rats at 6, 12, 18 and 24 months old (5 in each group), and to explore the effect of this effect on the changes of secretion of aging KC Relationship. Results HC synthesis and mitochondrial metabolism in 24-month-old mice were significantly lower than those in 6-month-old mice. HC and 6-month-old KCs in each age group were significantly higher than those in single-culture, Significantly decreased when co-cultured with 24-month-old KC. LPS (10ng / L) had no significant effect on HC protein synthesis and mitochondrial energy metabolism cultured alone, but significantly enhanced the potentiation of 6-month-old KC and 24-month-old KC in the co-culture system. 24-month-old group KCTNF, IL 8, NO secretion was significantly higher than the 6-month-old KC, PGE2 was significantly lower. The levels of TNF and NO in KC of LPS-treated group were significantly higher than those in LPS-stimulated group, and their added value was significant in high-month-old group. The levels of IL-8 in KC of 6 and 12-month-old group were significantly increased Month-old group no significant change; PGE2 changes in the law and IL 8 the opposite. Conclusion KC plays an important role in the process of HC damage in aging rat liver, which may be related to the changes of the cytokine profile of the aging KC secretion and the changes of HC microenvironment.