Protective Effect of Dihuang Yinzi on Cerebral Ischemia-reperfusion Injury in Rats and Its Mechanism / 中国实验方剂学杂志

ABSTRACT

Objective: To explore the protective effect and the preliminary mechanism of Dihuang Yinzi on cerebral ischemia-reperfusion injury in rats. Method: The middle cerebral artery occlusion (MCAO) model was established. Totally 90 SD rats were randomly divided into 6 groupssham operation group, model group, nimodipine group (0.01 g·kg-1) and high, medium, low-dose Dihuang Yinzi groups (38.80, 19.40, 9.70 g·kg-1), with 20 rats in each group.The modified neurological severity score (mNSS) was assayed at the 7th, 14th, 28th days after operation, and the volume of cerebral infarction, pathological changes of brain tissue, the BrdU positive cells and mRNA levels of Notch1, Jagged1 and Hes1 in subventricular zone(SVZ)were observed respectively by triphenyl tetrazolium chloride(TTC) stain, htorylin eastin(HE) stain, immunofluorescence technique and reverse transcriphase polymerase chain reaction(Real-time PCR) methods at the 28th day after the operation. Result: The mNSS on the 7th, 14th, 28th days of high, medium-dose Dihuang Yinzi groups and nimodipine group were significantly lower than that of model group(PPth day, the percentage of cerebral infarction volume in brain tissue volume of high, medium-dose Dihuang Yinzi groups and nimodipine group were smaller than that of model group(Pth day, the BrdU positive cells in SVZ of the above 3 groups were significantly higher than model group(PPPth day, the mRNA levels of Notch1, Jagged1 and Hes1 of high, medium-dose Dihuang Yinzi groups and nimodipine group were significantly higher than those of model group(PPPPConclusion: Dihuang Yinzi can improve the nerve function defect of MCAO rat model, and reduce the volume of cerebral infarction and the pathological changes of brain tissue, thus playing a protective role in cerebral ischemia-reperfusion injury rats. Its mechanism may be related to the activation of the Notch signaling pathway, and the up-regulation of expressions of Notch1, Jagged1 and Hes1 mRNA, thus promoting the proliferation of NSCs.