中文摘要：

目的观察烟酰胺（Nia）对白细胞介素-1β（IL-1β）诱导的体外培养的退变兔椎间盘组织内细胞凋亡及能量代谢相关基因表达的影响。方法构建兔椎间盘组织凝胶培养模型,分为正常对照组（不加入药物）,烟酰胺组（加入0.5 mg/ml烟酰胺）,退变组（加入10 ng/ml IL-1β）和治疗组（加入10 ng/ml IL-1β及0.5 mg/ml烟酰胺）。培养2周后对各组标本分别行TUNEL染色,Fas、Caspase 3、Bcl-2、HIF-1α、GLUT-1及VEGF免疫组化染色。结果TUNEL染色示治疗组阳性细胞染色率较退变组有所下降。Fas、Bcl-2染色示治疗组阳性细胞率均与退变组接近（均P〉0.05）。Caspase 3染色示治疗组阳性细胞率较退变组明显降低（P〈0.05）。HIF-1α、VEGF染色示治疗组阳性细胞率较退变组均明显降低（均P〈0.01）。GLUT-1染色示治疗组阳性细胞率较退变组轻微下降（P〉0.05）。结论烟酰胺可以抑制IL-1β诱导的椎间盘细胞凋亡,改善IL-1β导致的椎间盘能量代谢障碍。

英文摘要：

Objective To investigate the regulatory effect of niacinamide on IL-1β-induced cell apoptosis and energy metabolism related genes in intervertebral disc（IVD） in vitro. Methods Chiba＇s IVD degeneration model was established. IVDs from adult Japanese white rabbits were randomly divided in to 4 groups： negative control group, niacinamide group, degeneration group,and treatment group. After culture for 2 weeks, TUNEL staining and immunohistochernical staining for Fas, Bcl-2, Caspase 3, HIF-1α,GLUT-1 and VEGF were used to detect apoptosis and the expression of energy metabolism related genes. Results The rate of TUNEL positive-staining cells in treatment group was lower than in degeneration group. The rate of Fas positive-staining cells was lower, and that of Bel-2 was higher in treatment group than in degeneration group. The rate of Caspase 3 positive-staining cells in treatment group was significantly lower than in degeneration group（P〈0.05）. The rate of HIF-1α positive-staining cells in niacinamide group was lower than in negative control group signifieantly（P〈0.01） ,and that in treatment group was lower than in degeneration group significantly（P〈0.01）. The rate of GLUT-1 positive-staining cells in treatment group was lower than in degeneration group（P〈0.05）. The rate of VEGF positive-staining cells in treatment group was lower than in degeneration group significantly（P〈0. 01）. Conclusion Niacinamide can inhibit IL-1β-induced IVD cell apoptosis,improve energy metabolism of cultured IVD tissue,and alleviate IL-1β-induced disturbance of energy metabolism.