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目的对泼尼松与促皮质素导致脑损伤的机制进行初步探讨。方法婴幼大鼠(7日龄)和成年大鼠(2月龄)各192只,分为泼尼松婴幼组、泼尼松成年组、促皮质素婴幼组和促皮质素成年组共4个大组(n=96),每大组再分为长、短程治疗剂量组以及相应用药后停药4周组,长、短程小剂量组以及相应用药后停药4周组,及对照组等共计12个观察组(n=8)。对各组血清中NSE水平、脑内Bax与Bcl-2蛋白表达以及神经细胞进行检测。结果短、长程治疗剂量给予婴幼鼠泼尼松或促皮质素后,血清神经元特异性烯醇化酶(Neuro-specific Enolase,NSE)水平较对照组显著升高,其幅度达50.6%～103.2%;长程小剂量给药后其增高幅度为38.3%～60.3%(P>0.05),但这些NSE升高的组同时伴有Bax蛋白表达显著增强(P<0.01)、Bax/Bcl-2比值增高(1.91～2.40倍之间)和TUNEL阳性细胞表达的增多。而成年鼠仅在治疗剂量泼尼松或促皮质素长程给药后见血清NSE及免疫组化、TUNEL等各项指标有显著异常。停药4周后,婴幼鼠或成年鼠各组的各项指标与对照组相比均不再有显著差异。结论过度凋亡与坏死过程的激活是导致婴幼期激素脑损伤的重要机制。
Objective To investigate the mechanism of prednisone and corticotropin-induced brain injury. Methods A total of 192 infants (7 days old) and adult rats (2 months old) were divided into two groups: prednisolone group, prednisone group, corticotropin group and corticotropin group A total of four groups (n = 96) were divided into long and short-term treatment dose groups and four-week withdrawal group after drug administration, four-week long and short-term dose groups, Control group, a total of 12 observation group (n = 8). The level of NSE in serum, the expression of Bax and Bcl-2 in brain and nerve cells were detected. Results After administration of prednisone or corticotropin to short and long-term therapeutic doses, the level of serum neuron specific enolase (NSE) was significantly higher than that of the control group (50.6% -103.2) %, While those in long-term and low-dose groups increased by 38.3% -60.3% (P> 0.05). However, these NSE-elevated groups were associated with significantly increased Bax protein expression (P <0.01) and Bax / Bcl-2 ratio Increased (between 1.91 and 2.40 times) and TUNEL-positive cells increased. However, adult rats only showed significant abnormalities in serum NSE, immunohistochemistry and TUNEL after long-term administration of prednisone or corticotropin. Four weeks after drug withdrawal, there was no significant difference in each index of infant or adult mice compared with the control group. Conclusion Activation of excessive apoptosis and necrosis is an important mechanism of brain injury induced by hormones in infants and young children.