氯化钴对小鼠海马神经元细胞缺氧损伤的影响

Effects of cobalt chloride on hypoxic injury of hippocampal neurons in mice

目的:研究氯化钴(CoCl2)对小鼠海马神经元细胞系HT22细胞缺氧损伤的影响。方法:实验分为3组,分别为低浓度氯化钴组(CoCl2-L)、中浓度氯化钴组(CoCl2-M)和高浓度氯化钴组(CoCl2-H)。利用不同浓度CoCl2处理HT22细胞建立细胞缺氧损伤模型,通过HE染色观察HT22细胞轴突损伤情况,CCK-8法检测HT22细胞体外增殖活性,Western Blot检测HT22细胞中低氧诱导因子-1α(HIF-1α)和tau蛋白的表达情况。结果:HE染色显示CoCl2可致HT22细胞轴突断裂,CCK8检测显示CoCl2对HT22细胞的增殖有明显抑制作用。Western Blot结果显示CoCl2-H组细胞中HIF-1α表达显著上调,tau蛋白表达显著降低。结论:CoCl2可致轴突损伤,并且上调HT22细胞的HIF-1α表达、降低tau的表达。

Objective: To investigate the effects of cobalt chloride(CoCl2) on hypoxic injury of mouse hippocampal neuron cell line HT22.Methods: The experiment was divided into three groups: low concentration CoCl2 group(CoCl2-L),medium concentration CoCl2 group(CoCl2-M) and high concentration CoCl2 group(CoCl2-H).HT22 cells were treated with different concentrations of CoCl2 to establish cell hypoxia damage model.The growth characteristics of axons in HT22 cells were observed by HE staining.The changes in the proliferation activity of HT22 cells were detected by Cell Counting Kit-8(CCK-8).The expressions of hypoxia inducible factor-1α(HIF-1α) and tau protein in HT22 cells were detected by Western Blot.Results: HE staining showed that CoCl2 could cause axonal fracture in HT22 cells.The proliferation of HT22 cells was significantly inhibited by CoCl2.The expression of HIF-1α protein was significantly up-regulated and the expression of tau5 protein was significantly decreased in CoCl2-H group cells.Conclusion: CoCl2 can cause axonal injury,up-regulate HIF-1α expression,and down-regulate tau expression in HT22 cells.