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目的:研究黄连解毒汤有效部位(HLJDTAF)对神经细胞内钙超载的影响及相关机制。方法:低糖低氧损伤胎鼠皮层神经细胞模拟脑缺血,双波长荧光分光光度法测定神经细胞内钙含量,观察HLJDTAF对细胞内钙超载的抑制作用。并分别采用谷氨酸(Glu),KCl,A23187,乙酰甲胆碱(MCh)和咖啡因(CAF)处理神经细胞,以分析药物的作用环节。结果:HLJD-TAF对低糖低氧处理所致神经细胞钙超载有明显的抑制作用(P<0.05);对200μmol.L-1谷氨酸,50 mmol.L-1剂量的K+,0.05μmol.L-1钙离子载体A23187处理细胞引起神经细胞内钙超载有明显的抑制作用(P<0.05,P<0.01);正常外钙情况下和零外钙情况下,HLJDTAF对5 mmol.L-1CAF和Mch诱导神经细胞内钙超载有明显的抑制作用(P<0.01,P<0.05)。结论:HLJDTAF可显著抑制神经细胞拟缺血损伤后的钙超载,其机制可能是通过多途径抑制缺血缺氧后神经细胞内钙超载,从而拮抗脑缺血损伤。
Objective: To investigate the effect of HLJDTAF on intracellular calcium overload in neurons and related mechanisms. Methods: Mice hypodermis hypoxia injury simulated cerebral ischemia in rat cortical neurons, dual-wavelength fluorescence spectrophotometry determination of intracellular calcium content observed HLJDTAF on intracellular calcium overload inhibition. Nerve cells were treated with glutamic acid (Glu), KCl, A23187, MCh and caffeine respectively to analyze the effect of drugs. Results: HLJD-TAF significantly inhibited the calcium overload induced by low glucose and hypoxia (P <0.05). For 200 μmol.L-1 glutamate and 50 mmol.L-1 K +, 0.05 μmol. L-1 calcium ionophore A23187 treatment cells caused a significant inhibition of intracellular calcium overload (P <0.05, P <0.01); in the case of normal external calcium and the case of zero calcium, HLJDTAF 5 mmol.L-1CAF And Mch induced neuronal intracellular calcium overload significantly inhibited (P <0.01, P <0.05). CONCLUSION: HLJDTAF can significantly inhibit the calcium overload of nerve cells after ischemia-reperfusion injury. The possible mechanism is that HLJDTAF can inhibit cerebral ischemia-reperfusion injury through multi-pathway inhibition of calcium overload in nerve cells after ischemia and hypoxia.