摘要
目的探讨神经节苷脂(GM1)对新生缺氧缺血性损伤(HIBD)大鼠脑细胞凋亡的影响。方法采用拴线法建立新生大鼠的大脑中动脉缺血再灌注损伤模型。腹腔注射GM1,采用原位缺口末端标记法(TUNEL)进行细胞凋亡染色,测定血清内皮素水平和NO水平。结果假手术组偶见神经细胞凋亡,缺血再灌注组可见大量的神经细胞凋亡现象,GM1治疗组新生大鼠与缺血再灌注组相比,凋亡细胞数明显减少;假手术组、缺血再灌注组和GM1治疗组新生大鼠血浆的内皮素含量(ng/L)分别为41.6±4.06、63.45±6.91、50.67±5.20;NO2-/NO3-分别是44.67±8.6、63.65±9.9、47.7±9.8。结论GM1对新生大鼠脑缺氧缺血的保护作用可能通过抑制缺血缺氧性脑损伤后血浆内皮素和NO的生成,而抑制神经细胞的凋亡过程。
Objective To investigate the impact of GM1 on nerve-cell apoptosis in neonatal rots of hypoxic-ischemic brain damage. Method The model of neonatal rats was set with ischemic reperfusion damage of arteria cerebral anterior. GM1 was injected into the models, the endothelin (ET) and nitric oxide (No) were measured and the effect on apoptosis of nerve-cells was observed. Result In the sham operation group a little nerve-cell apoptosis was found. In the ischemic reperfusion damage group a lot of nerve-cell apoptosis could be found, and compared with these, the GM1 group nerve-cell apoptosis decreased obviously. In the sham operation group/the isehemie reperfusion damage group and the GM1 group the ET level of neonatal rats were: 41.6± 4.06,63.45±6.91, 30.67±5.20 (ng/L), the content of NO2^-/NO3^-were: 44.67±8.6, 63.65±9.9 and 47.7 ±9.8: (ng/L) Conclusion The protective effect of GM1 on neonatal rats' brain cells might be the decrease of ET and NO production in ischemic reperfusion damage rats, accordingly to restrain the course of nerve-cell apoptosis.
出处
《实用医药杂志》
2010年第2期152-153,156,157,共4页
Practical Journal of Medicine & Pharmacy
关键词
脑缺血
再灌注
内皮素
凋亡
Cerebral isehemic
Reoperfusion
Endothelin
Apoptosis