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目的:研究参附注射液对新生大鼠缺氧缺血性脑损伤(hypoxic-ischemic brain damage,HIBD)的干预作用。方法:建立新生大鼠HIBD模型,应用HE染色、Annexin V/PI染色法、免疫组化染色法观察正常对照组、假手术组、生理盐水组及参附干预组在缺氧缺血后2 h、12 h、24 h、3天、7天、14天的病理变化、神经细胞凋亡及Bax、Bcl-2蛋白表达。结果:①缺氧缺血后生理盐水组海马CA1区病理变化明显,参附干预组上述变化减轻。②正常对照组及假手术组海马CA1区Bcl-2表达较弱,手术后该区Bcl-2表达仍弱,Bax表达增强,出现凋亡细胞,以24 h最明显;参附干预组Bcl-2表达较生理盐水组增强,而Bax表达减弱(P<0.05),凋亡细胞减少。结论:HIBD后Bax蛋白表达增强,细胞凋亡增加。参附可上调Bcl-2表达,下调Bax表达,使凋亡细胞减少,这可能是参附注射液治疗新生儿缺氧缺血性脑损伤的机制之一。
Objective: To study the effect of Shenfu injection on hypoxic-ischemic brain damage (HIBD) in neonatal rats. METHODS: A neonatal rat HIBD model was established. HE staining, Annexin V/PI staining, and immunohistochemical staining were used to observe the normal control group, sham operation group, normal saline group, and Shenfu intervention group 2 h after hypoxia-ischemia. Pathological changes, neuronal apoptosis and Bax, Bcl-2 protein expression at 12 h, 24 h, 3 days, 7 days, and 14 days. RESULTS: 1 Pathological changes in hippocampal CA1 region of the normal saline group after hypoxia-ischemia were obvious, and the above changes in the Shenfu intervention group were alleviated. 2The expression of Bcl-2 in hippocampal CA1 region was weak in normal control group and sham operation group. The expression of Bcl-2 was still weak in the region after surgery, and the expression of Bax was increased. The apoptotic cells appeared, which was the most obvious at 24 h; The expression of 2 was stronger than that of normal saline group, while that of Bax was weakened (P<0.05). The number of apoptotic cells decreased. Conclusion: The expression of Bax protein is increased and the apoptosis is increased after HIBD. Shenfu can up-regulate Bcl-2 expression, down-regulate Bax expression, and reduce apoptotic cells, which may be one of the mechanisms of Shenfu injection in treating neonatal hypoxic-ischemic brain damage.