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目的探讨藻酸双酯钠(polysaccharidesulfate,PSS)对局灶性脑缺血再灌注大鼠脑组织神经细胞凋亡的保护机制。方法经大鼠颈内动脉将一线栓插入右侧大脑中动脉1.5h后再灌注24h制成局灶性脑缺血再灌注大鼠模型;在再灌前30min或再灌后5h经腹腔给予不同剂量的藻酸双酯钠或赋形剂;用流式细胞术测量受损脑组织神经元内钙离子浓度及凋亡率,同时观察大鼠的神经功能缺损评分。结果藻酸双酯钠治疗组神经功能缺损较非治疗组明显减轻,相应的藻酸双酯钠治疗组细胞内钙离子浓度增高受抑、细胞凋亡减少;不同时间点给药组间上述指标亦有显著性差异。结论藻酸双酯钠可以减轻脑组织神经元再灌注损伤和抑制神经元凋亡;抑制受损神经元胞内钙离子浓度增高是其保护作用的可能机制。
Objective To investigate the protective mechanism of sodium polysulfate (PSS) on neuronal apoptosis after focal cerebral ischemia in rats. Methods A rat model of focal cerebral ischemia-reperfusion was established by inserting first-line suppositories into the right middle cerebral artery for 1.5 h and then reperfusion for 24 h in the rat’s internal carotid artery. The rats were given intraperitoneally 30 min before reperfusion or 5 h after reperfusion. Dosage of sodium alginate or excipients; measurement of calcium concentration and apoptotic rate in neurons of injured brain tissue by flow cytometry; and observation of neurological deficit scores in rats. RESULTS: Neurological deficits in the sodium alginate treated group were significantly less than those in the non-treated group. Corresponding to the sodium alginate treatment group, the intracellular calcium concentration was inhibited and the apoptosis was decreased. The above indicators were administered between the groups at different time points. There are also significant differences. Conclusion Sodium alginate can reduce the neuronal reperfusion injury and inhibit neuronal apoptosis in brain tissue, and inhibiting the increase of intracellular calcium concentration in damaged neurons is the possible mechanism of its protective effect.