葛根素对大鼠颅脑损伤后ICAM-1和NF-κB表达的影响

Influence of kakkonein on ICAM-1 and NF-κB expression in rat after craniocerebral injury

目的观察葛根素对大鼠颅脑损伤后细胞间黏附分子-1(ICAM-1)和核因子(NF-κB)表达的影响。方法雄性SD大鼠,建立大鼠颅脑损伤模型,随机分组,给予葛根素治疗后,测定脑组织中MDA含量和SOD活性;分别通过Western blot方法,分析组织中ICAM-1和NF-κB蛋白表达的变化。同时利用RT-PCR法,观察脑组织中ICAM-1和NF-κB表达水平的变化。结果大鼠颅脑受到损伤后,脑组织中SOD活性显著降低(P<0.05),MDA含量显著增加(P<0.05),经葛根素预先处理的大鼠,可以显著增加脑组织中SOD的活性,并降低MDA的含量。与假手术组相比,模型组大鼠脑组织中ICAM-1和NF-κB表达显著升高(P<0.05),经葛根素处理组的大鼠,与模型组大鼠相比较,脑组织中ICAM-1和NF-κB mRNA表达显著降低。结论葛根素调节大鼠颅脑损伤后ICAM-1和NF-κB的表达,可能是葛根素保护大鼠颅脑损伤的分子机制。

Objective To investigate the influence of kakkonein on ICAM-1 and NF-κB expression in rat after craniocerebral injury. Methods The rat model of craniocerebral injury was established, after treatment with kakkonein the experssion of ICAM-1 and NF-κB by the methods of RT-PCR and Western blot were detected, respectively. Quantification of MDA and SOD in whole brain tissue were also performed. Results After craniocerebral injury,the expression of ICAM-1 and NF-κB increased significantly in model group compared with sham-operation group （P〈O.05）. After treatment with procyanidins, the expression of ICAM-1 and NF-~B decreased significantly compared with model group （P〈0.05）. Conclusion Kakkonein can decrease the expression of ICAM-1 and NF-κB in rat after craniocerebral injury,which could be the mechanism for protecting cramiocerebral injury.