中文摘要：

目的：观察体外培养的大鼠肝细胞在促炎细胞因子IL-1β刺激下一氧化氮（NO）的产生和线粒体膜电位的变化，探讨两者之间的关系。方法：原位胶原酶灌注法分离和培养原代大鼠肝细胞后，分别用生理盐水、脂多糖（LPS）（10mg·L-1）、IL-1β（1nmol·L-1）及LPS（10mg·L-1）联合IL-1β（1nmol·L-1）刺激肝细胞，并分别在刺激后6、12、24、48h留取细胞和上清液，采用分光光度法测定上清液NO的含量，采用荧光探针Jc-1结合流式细胞仪检测肝细胞线粒体膜电位的变化。结果：IL-1β刺激后肝细胞产生NO增加而线粒体膜电位降低，两者均呈时间依赖性，并在24h达峰值；LPS对肝细胞NO的合成没有直接诱导作用，与IL-1β联合刺激也没有协同作用。结论：IL-1β诱导肝细胞过度产生NO从而抑制线粒体呼吸功能可能是炎症应激下肝损伤的潜在机制之一。

英文摘要：

Objective To observe the variation of nitric oxide （NO） production and mitochondrial membrane po- tential in cultured rat hepatocytes stimulated by IL-1β. The correlation between NO production and mitochondrial mem- brane potential alteration was investigated. Methods Primary cultured rat hepatocytes were isolated by an in situ colla- genase perfusion method. The cultured hepatocytes were stimulated by saline, LPS（ 10 mg · L-1） ,IL-1β（ 1 nmol · L-1） and LPS（10 mg· L-1） combined with IL-1β（ 1 nmol · L-1） respectively. The culture medium and hepatocytes were collected at 6,12,24 and 48 hours after stimulation. The concentration of NO in the medium was detected by spectropho- tometry and the mitochondrial membrane potential of the hepatocytes was detected with flow cytometry after incubated with fluorescent probe JC-1. Results IL-1β promoted NO production and decreased mitochondrial membrane potential in cultured rat hepatocytes. Both effects were time-dependent and peaked at 24 hours. LPS did not induce NO produc- tion in rat hepatocytes and no synergistic effect was observed when co-stimulated by IL-1β stimulating simultaneously. Conclusion Excessive nitric oxide production induced by IL-1β results in an inhibition of mitochondrial function, which may be involved in the pathology of hepatic injury during inflammatory stress.