黄芩苷对MPTP致帕金森病模型小鼠行为能力影响

IMPACT OF BAICALIN ON BEHAVIORAL CAPACITY IN MOUSE MODEL OF PARKINSON DISEASE CAUSED BY MPTP

目的探讨黄芩苷对1-甲基-4-苯基1,2,3,6-四氢吡啶(MPTP)致帕金森病(PD)模型小鼠行为能力及黑质多巴胺能神经元的影响。方法将45只C57/BL小鼠随机分为模型组、黄芩苷组和对照组。模型组、黄芩苷组小鼠腹腔注射MTPT(60mg/kg)3.5d,对照组小鼠腹腔注射等量生理盐水3.5d,黄芩苷组同时给予黄芩苷(150mg/kg)灌胃14d。观察小鼠在不同转速下的跑步维持时间、黑质多巴胺能神经元细胞的形态及数量变化。结果在25、30r/min较高转速时,黄芩苷组小鼠的跑步维持时间较模型组明显延长(t=4.58、3.88,P<0.01)。黄芩苷治疗使PD模型小鼠黑质区的酪氨酸羟化酶阳性细胞丢失明显减少(F=38.76,q=8.99,P<0.01)。结论黄芩苷可以部分对抗MPTP对多巴胺能神经元的损害,并对PD模型小鼠的转棒跑步行为能力有一定的保护作用。

Objective To observe the impact of baicalin on behavior and dopaminergic neurons of substantia nigra （SN） in mouse models of Parkinson disease （PD） caused by MPTP. Methods Forty-five C57/BL mice were divided into three group- sin random as model group, baicalin group and normal control group. The mice in the model group and baicalin group were given intraperitoneal injection of MPTP, 60 mg/kg, for 3.5 d, and at the same time, those in the baicalin group were given intragastric administration of baicalin （150 mg/kg）, once a day for 14 days. The mice in the normal control group were given intraperitoneal in jection of equal volume of normal saline for 3.5 d. Running time of the mice at different rotation speeds, and the changes of form and number of dopaminergic neurons of substantia nigra were observed. Results At high rotation speed of 25 and 30 r/min, the hold time of running in mice in the baicalin group was extended versus those in the control group （t=4.58,3.88 ;P〈0.01）. Treated with baicalin notably reduced the loss of TH-positive neurons in SN of PD （F=38.76,q=8.99,P〈0.01）. Conclusion Baicalin can partly fight against MPTP damage to dopaminergic neurons and protect the behavioral capability of rotarod test in mouse model of Parkinson disease.