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目的观察地塞米松(DXM)对缺氧缺血新生大鼠脑组织兴奋性氨基酸(EAA)和C-fos蛋白表达的影响,探讨其在缺氧缺血性脑损伤(HIBD)中的应用价值。方法建立HIBD动物模型,应用高效毛细管电泳和免疫组化方法,分别检测假手术组、HIBD组、小剂量DXM干预组(0．5 mg/kg)及大剂量DXM干预组(10mg/kg)的脑组织EAA含量及C-fos蛋白表达水平。结果 HIBD组的EAA含量及C-fos蛋白表达均较假手术组明显升高(P<0．01);小剂量DXM组的EAA含量及C-fos蛋白表达较 HIBD组无明显变化(P>0．05);大剂量DXM组EAA含量较HIBD组明显减少(P<0．01),较小剂量 DXM组减少(P<0．05);大剂量DXM组C-fos蛋白表达较HIBD组及小剂量DXM组均明显降低(P< 0．01)。结论缺氧缺血促进脑组织EAA的释放,诱导C-fos蛋白表达;大剂量DXM干预可能通过抑制EAA释放,降低C-fos蛋白表达而对缺氧缺血脑损伤起保护作用。
Objective To investigate the effects of dexamethasone (DXM) on the expression of excitatory amino acids (EAA) and C-fos protein in neonatal rats with hypoxic-ischemic brain damage (HIBD), and to explore their potential value in hypoxic-ischemic brain damage . Methods HIBD animal models were established. HCC group, HIBD group, low dose DXM intervention group (0.5 mg / kg) and high dose DXM intervention group (10 mg / kg) were detected by high performance capillary electrophoresis and immunohistochemistry Brain EAA content and C-fos protein expression levels. Results The EAA content and the expression of C-fos protein in HIBD group were significantly higher than those in sham operation group (P <0.01). EAA content and C-fos protein expression in low dose DXM group were not significantly different from those in HIBD group (P> 0.05). Compared with HIBD group, EAA content in high dose DXM group decreased significantly (P <0.01) and decreased in low dose DXM group (P <0.05). Compared with HIBD group, the expression of C-fos protein in high dose DXM group And low-dose DXM group were significantly lower (P <0.01). Conclusions Hypoxia-ischemia can promote the release of EAA and induce the expression of C-fos protein in hippocampus. High-dose DXM may protect the hypoxic-ischemic brain injury by inhibiting the release of EAA and decreasing the expression of C-fos protein.