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出 处:《药学实践杂志》2016年第4期354-356,共3页Journal of Pharmaceutical Practice
摘 要:目的探讨姜黄素抗癫的作用机制。方法取健康成年雄性SD大鼠,连续腹腔注射戊四氮,诱发大鼠点燃致癫模型。空白组和模型组灌予生理盐水5ml,1次/d,连续28d。低剂量和高剂量姜黄素组分别灌予姜黄素100mg/kg和200mg/kg,1次/d,连续28d;丙戊酸钠组灌予丙戊酸钠400mg/kg,1次/d,连续28d。治疗结束后,按照Racine的6级评分标准,观察癫大鼠发作等级变化,用酶联免疫法(ELISA)检测海马区IL-2和IL-6表达水平的变化。结果姜黄素组的癫大鼠惊厥发作等级降低。模型组IL-2和IL-6高表达,比空白组呈显著升高(P<0.05)。与模型组比较,姜黄素组大鼠海马区IL-2和IL-6的表达明显降低(P<0.05);与低剂量姜黄素组相比,高剂量姜黄素组IL-2和IL-6水平降低更为明显(P<0.05)。高剂量姜黄素组与丙戊酸钠组比较,无显著差异(P>0.05)。结论姜黄素能降低癫大鼠惊厥发作级别,具有一定的抗癫作用,并且呈剂量依赖性,其可能机制是通过降低海马区IL-2和IL-6的表达发挥作用。DONG Wei;YAN Jianwei;TAN Qiaoling;YE Sen;Yuyao People′s Hospital; Objective To investigate the mechanism of anti-epileptic effect of the curcumin.Methods The SD rats were injected intraperitoneally with pentylenetetrazol kindling 25.0mg/kg to induce a rat epilepsy model.All of the treatments were performed once a day continuously for 28 days.The rats in blank group and model group received 5ml of normal saline.The rats in the high and low curcumin group were given 200mg/kg and 100mg/kg of curcumin once a day,respectively.The rats in the sodium valproate(VPA)group were given 400mg/kg of VPA once a day by gavage.After treatment,the seizures level was recorded by using the Racine′s six point grading scale,and the expression of IL-2and IL-6of hippocampus were detected by the enzyme linked immunoassay(ELISA).Results The seizures level was reduced by curcumin in epileptic rats.The expressions of IL-2and IL-6of the model group were significantly higher than those of the blank group(P〈0.05),while those rats of the anti-epileptic groups,including high dose group and low dose group,were lower than those rats of the model group(P〈0.05).When compared with the curcumin low dose group,the expression of IL-2and IL-6of curcumin high dose group is lower(P〈0.05).There was no significant difference between the high dose curcumin group and VPA group(P〉0.05).Conclusion The curcumin can reduce the seizure level in rats,it shows some anti-epileptic effets and dose-dependently,which may be through down-regulating the expression of IL-2and IL-6in hippocampus.
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