亚低温对HIBD新生鼠大脑皮质神经元NSE表达及血糖水平影响的研究

Effect of Mild Hypothermia on the Activity of Neuron Specific Enolase in Cortical Neurons and Blood Glucose Level in Neonatal Rats with Hypoxic Ischemic Brain Damage

摘要:

目的：通过亚低温对新生鼠缺氧缺血脑损伤(HIBD)大脑皮质神经元特异性烯醇化酶(NSE)及血糖水平影响的研究，探讨亚低温对HIBD的保护作用机制。方法：建立新生鼠HIBD标准化动物模型，将其随机分为对照组、31℃亚低温和34℃亚低温干预组及假手术组，应用免疫组化染色观察大脑皮质区NSE阳性神经元数目，并利用微量血糖监测仪测定血糖。结果：缺血缺氧后12 h，24 h亚低温干预组大脑皮质NSE阳性神经元数目均显著低于对照组［31℃亚低温组：(54.3±6.5) vs (82.3±6.0)，(34.6±5.6) vs (53.3±5.6)，P<0.05 或 0.01；34℃亚低温组：(56.8±7.1) vs (82.3±6.0)，(32.9±4.9) vs (53.3±5.6)，P<0.05］。缺氧缺血后12 h，24 h 血糖水平［31℃亚低温组：(5.74±1.52)，(5.89±1.62) mmol/L；34℃亚低温组：(5.69±1.48)，(5.91±1.53) mmol/L］亦显著高于对照组［(3.64±1.22)，(4.16±1.54) mmol/L］(P<0.01)。31℃亚低温和34℃亚低温干预两组间各个时期大脑皮质区NSE阳性神经元数目及血糖水平差异无显著性(P>0.05)。结论：亚低温可通过抑制神经元内NSE活性及升高血糖水平，对HIBD新生鼠大脑皮质神经细胞起到保护作用。

Abstract:

OBJECTIVE: To study the neuroprotection of mild hypothermia on hypoxic ischemic brain damage (HIBD). METHODS: The HIBD model rats were randomly assigned into the 31℃ and 34℃ mild hypothermia groups, sham operated group and control group. The number of cortical neuron specific endolase (NSE) positive neurons was assayed using immunohistochemistry and the blood glucose level was detected in the four groups. RESULTS: The number of the cortical NSE positive neurons 12 and 24 h after hypoxic ischemia [( 54.3 ± 6.5 ) and ( 34.6 ± 5.6 ), respectively] in the 31℃ mild hypothermia group was significantly lower compared with the control group [( 82.3 ± 6.0 ) and ( 53.3 ± 5.6 ), respectively] (P< 0.01 or 0.05 ). It was also significantly lower in the 34℃ mild hypothermia group at 12 and 24 h [( 56.8 ± 7.1 ) and ( 32.9 ± 4.9 , respectively] compared with the control group (P< 0.01 or 0.05 ). The blood glucose level 12 and 24 h after hypoxic ischemia [( 5.74 ± 1.52 ), ( 5.89 ± 1.62 ) mmol/L, respectively] in the 31℃ mild hypothermia group was significantly higher than that in the control group [( 3.64 ± 1.22 ) and ( 4.16 ± 1.54 ) mmol/L, respectively] (both P< 0.01 ); and so was the 34℃ mild hypothermia group at 12 and 24 h [( 5.69 ± 1.48 ) mmol/L vs ( 3.64 ± 1.22 ) mmol/L; ( 5.91 ± 1.53 ) mmol/L vs ( 4.16 ± 1.54 ) mmol/L] (both P< 0.01 ). No significant difference was found in the number of cortical NSE positive neurons and blood glucose level between the 31℃ and 34℃ mild hypothermia groups. CONCLUSIONS: Mild hypothermia may have a protective effect on hypoxic ischemic neurons by restraining the NSE activity in cortical neurons and increasing the blood glucose level.