Introduction
To investigate the effects of crocin on proliferation and migration of endogenous neural stem cells and the Notch1 signalling pathway in rats after cerebral ischemia reperfusion.

Material and methods
SD rats were randomly divided into the sham operation group, model group and administration group (crocin). Middle cerebral artery occlusion (MCAO/R) was used to establish the focal cerebral ischemia reperfusion model in rat. After surgical treatment, the treatment group was treated with crocin. Quantitative polymerase chain reaction (qPCR) was used to detect the changes in the expression of Notch1, Bax and bcl-2 proteins in rat endogenous neural stem cells after cerebral ischemia reperfusion. ELISA was used to detect changes in inflammatory factors. Neural stem cells were cultured in vitro, which were divided into: the normal control group, the hypoglycaemic deprivation/reoxygenation group, hypoglycaemic deprivation/reoxygenation group with a low concentration of crocin, and hypoglycaemic deprivation/reoxygenation group with a high concentration of crocin. The cell proliferation assay detects cell activity. The cell migration assay tests the cell migration ability. And flow cytometry was used to determine cell apoptosis.

Results
Compared with the sham group, the Notch1 signalling pathway was activated in the model group. The expression of Notch1 in the crocin group was increased compared to the model group. Crocin can inhibit the release of inflammatory factors. The results of our experiments showed that crocin could induce the proliferation and migration of neural stem cells and inhibit the apoptosis of neural stem cells in the hypoglycaemic/reoxygenation model group.

Conclusions
Crocin sufficiently promotes the proliferation and migration of neural stem cells and inhibits the apoptosis of these cells in rats after ischemia-reperfusion by manipulating the Notch signalling pathway.



中文翻译：

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Crocin 通过激活 Notch1 通路调节脑缺血后神经干细胞的增殖和迁移

引言
研究藏红花素对大鼠脑缺血再灌注后内源性神经干细胞增殖、迁移及Notch1信号通路的影响。

材料与方法
SD大鼠随机分为假手术组、模型组和给药组（藏红花素）。采用大脑中动脉闭塞术（MCAO/R）建立大鼠局灶性脑缺血再灌注模型。手术治疗后，治疗组给予藏红花素治疗。采用定量聚合酶链反应(qPCR)检测大鼠脑缺血再灌注后内源性神经干细胞中Notch1、Bax和bcl-2蛋白表达的变化。ELISA用于检测炎症因子的变化。体外培养神经干细胞，分为：正常对照组、低血糖剥夺/复氧组、低浓度藏红花素低血糖剥夺/复氧组、和高浓度藏红花素的低血糖剥夺/复氧组。细胞增殖试验检测细胞活性。细胞迁移试验测试细胞迁移能力。并用流式细胞术测定细胞凋亡。

结果
与sham组相比，模型组Notch1信号通路激活。与模型组相比，藏红花素组Notch1的表达增加。藏红花素能抑制炎症因子的释放。我们的实验结果表明，在低血糖/复氧模型组中，藏红花素可以诱导神经干细胞的增殖和迁移，抑制神经干细胞的凋亡。

结论
藏红花素通过调控Notch信号通路，充分促进大鼠缺血再灌注后神经干细胞的增殖和迁移，抑制这些细胞的凋亡。