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目的探讨Ca2+在高温诱导海马神经元凋亡中的作用,为丹曲林钠在热致脑损伤疾病中的应用提供实验依据。方法通过体外建立高温诱导原代培养的海马神经元凋亡模型,应用Ca2+特异性阻断剂丹曲林钠,观察其对神经元凋亡率、细胞内Ca2+荧光强度及其动态变化的影响。结果丹曲林钠能够明显降低高温处理后海马神经元的凋亡率;42℃处理并加入丹曲林钠组的扫描结果显示,Ca2+荧光强度为107.35±6.0,较正常培养的细胞内Ca2+荧光强度(159.12±33.8)明显降低,加入丹曲林钠20～25s后Ca2+浓度即开始下降,约50s后下降至最低值,然后稳定于低于原来基线的水平。结论丹曲林钠在高温诱导的海马神经细胞凋亡中具有重要的保护作用,在预防热致脑损伤疾病中具有一定的应用价值。
Objective To investigate the role of Ca2 + in hippocampal neuron apoptosis induced by high temperature and provide experimental evidence for the application of dantrulin sodium in the pathogenesis of thermal-induced brain injury. Methods Apoptosis model of hippocampal neurons induced by high temperature was established in vitro. Dantrulin sodium, a Ca2 + -specific blocker, was used to observe the effect on neuronal apoptosis rate, intracellular Ca2 + fluorescence intensity and its dynamic changes. Results Dantrolene sodium significantly decreased the apoptotic rate of hippocampal neurons after hyperthermia treatment. Scanning results of 42 ℃ treatment and addition of dantrolene sodium showed that the fluorescence intensity of Ca2 + was 107.35 ± 6.0, which was significantly lower than that of normal cultured cells The intensity (159.12 ± 33.8) decreased significantly. After adding 20 ~ 25s, the Ca2 + concentration of dantrolene began to decrease, then decreased to the lowest after about 50s, then stabilized at the level below the baseline. Conclusion Dantrolene sodium has an important protective effect on hippocampal neuronal apoptosis induced by hyperthermia and has certain value in the prevention of heat-induced brain injury.