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目的探讨长托宁对急性全脑缺血再灌注损伤的保护作用机制。方法建立大鼠全脑缺血再灌注损伤模型。大鼠全脑缺血10min 后于再灌注的同时分别给予山茛菪碱和长托宁腹腔注射,于再灌注2h、6h、12h 和24h 通过 ELISA 方法检测大鼠脑组织 TNF-α的表达情况,用 HE 染色法检查脑组织受损情况。结果全脑缺血再灌注损伤后脑组织 TNF-α在再灌注2h 表达升高,于再灌注12h 达到高峰,再灌注24h 仍有较高表达;HE 染色光镜下神经细胞变性坏死随再灌注时间延长逐渐加重。长托宁组和山莨菪碱组除再灌注2h 组外,TNF-α表达均较盐水组明显下降,神经细胞受损减轻,且再灌注12h 和再灌注24h 组中,长托宁组与山莨菪碱组 TNF-α表达比较亦明显下降。结论长托宁可以明显抑制全脑缺血再灌注损伤时脑组织 TNF-α的表达,从而减轻缺血再灌注时脑组织损伤,起到脑保护作用,且较山莨菪碱效果明显。
Objective To investigate the protective effect of changning on acute global cerebral ischemia-reperfusion injury. Methods The rat model of global cerebral ischemia-reperfusion injury was established. Rats were injected intraperitoneally with anisodamine and penehyclidine for 10 minutes after reperfusion. The expression of TNF-α in rat brain tissue was detected by ELISA at 2h, 6h, 12h and 24h after reperfusion , HE staining method to check the damage of brain tissue. Results The expression of TNF-α in brain tissue increased after reperfusion for 2h and reached the peak at 12h after reperfusion in cerebral ischemia-reperfusion injury group, and remained high at 24h after reperfusion. The number of necrotic neurons in reperfusion group was higher than that in reperfusion group Extended gradually increased. In addition to the reperfusion 2h group, the long-tonic group and the anisodamine group showed a significant decrease in TNF-α expression compared with the saline group, and reduced neuronal damage. In the reperfusion 12h and reperfusion 24h groups, Scopolamine group TNF-α expression also significantly decreased. Conclusions Penehyclidine can significantly inhibit the expression of TNF-α in brain tissue during global cerebral ischemia-reperfusion injury, and thus reduce the damage of brain tissue during ischemia-reperfusion, and play a neuroprotective effect, which is more effective than anisodamine.