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目的研究氯化钴预处理对脑缺血大鼠基质细胞衍生因子(SDF-1)、CXC家族趋化因子受体4(CXCR4)蛋白表达的影响。方法 45只SD大鼠,随机分为假手术组、模型组、实验组,每组均15只。模型组及实验组,用线栓法制作脑缺血模型;在造模前2天与前1天,实验组腹腔注射氯化钴30 mg·kg~(-1)。用蛋白质印迹法检测各组大鼠脑组织SDF-1、CXCR4蛋白表达,原位末端标记法(TUNEL)检测各组大鼠脑细胞凋亡率,用氯化三苯基四氮唑(TTC)染色并计算2 d后脑组织缺血坏死面积。结果在各时间点,与假手术组(脑组织SDF-1、CXCR4蛋白表达极低)比较,实验组与模型组SDF-1、CXCR4蛋白表达均明显增高(P<0.05),提示氯化钴可上调SDF-1、CXCR4的表达;2 d后,实验组的脑细胞凋亡率明显低于模型组[(9.31±0.79)%vs(18.99±1.13)%,P<0.05];实验组脑组织梗死灶面积也明显低于模型组(P<0.05)。结论氯化钴可上调SDF-1、CXCR4蛋白表达,减少脑细胞凋亡率,缩小脑细胞缺血坏死灶面积,对缺血脑组织具有保护作用。
Objective To investigate the effects of cobalt chloride preconditioning on the expression of stromal cell-derived factor (SDF-1) and CXC family of chemokine receptor 4 (CXCR4) in rats with cerebral ischemia. Methods Forty-five Sprague-Dawley rats were randomly divided into sham operation group, model group and experimental group, with 15 rats in each group. Model group and experimental group, cerebral ischemia model was made by thread method. In the experimental group, intraperitoneal injection of 30 mg · kg ~ (-1) cobalt chloride 2 days before and 1 day before modeling. The expression of SDF-1 and CXCR4 protein in brain tissue of each group was detected by Western blotting. The apoptosis rate of brain cells in each group was detected by TUNEL. Staining and calculating 2 days after cerebral ischemia and necrosis area. Results Compared with the sham operation group (SDF-1 and CXCR4 protein expression was very low) at each time point, the expression of SDF-1 and CXCR4 in experimental group and model group were significantly increased (P <0.05), suggesting that cobalt chloride The expression of SDF-1 and CXCR4 was up-regulated after 2 days, and the apoptosis rate of the experimental group was significantly lower than that of the model group [(9.31 ± 0.79)% vs (18.99 ± 1.13)%, P <0.05] Tissue infarct size was also significantly lower than the model group (P <0.05). Conclusion Cobalt chloride can up-regulate the expression of SDF-1 and CXCR4 protein, reduce the apoptosis rate of brain cells and reduce the area of ischemic necrosis of brain cells, which has a protective effect on ischemic brain tissue.