Zhang Ming-Yan, Fan Shu-Juan, Li Li-Ping, Wu Bian-Ying, Wang Yu
Hebei University Health Science Center, Baoding 071002, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2011 May;27(2):196-200.
To observe the protective effect of Breviscapine injection on the hypoxic ischemic brain damage of neonatal rats, and the expression of Bcl-2 and Bax.
In this experiment 7-day-old newborn rat with hypoxic-ischemic brain damage model was used and divided into four groups: sham group, model group, control with sterile water for injection group and Breviscapine injection group. Breviscapine injection group was divided into large, medium, and small doses. Used thionin staining and immunohistochemical staining to assay the neuronal density, histological grade, and the expresssion of Bcl-2 and Bax protein in the CA1 hippocampus of each group , the number of positive cells and the integral optical density (IOD) of the immunostaining on Bcl-2, Bax protein expression in the CA1 hippocampus.
Sham group, there was no significant neuronal damage and no obvious positive cells of Bcl-2 and Bax in the CA1 hippocampus. In model group and control with sterile water for injection group, the level of Bcl-2, Bax expression peaked at 3 d after hypoxic-ischemic brain damage (HIBD) (P < 0.05 vs other groups), the value of neuronal density (ND) was decreased, and histological grade (HG) was increased compared with that in the sham group (P < 0.05). Breviscapine injection group, compared with control with sterile water for injection group, the expression of Bcl-2 protein was further increased, IOD value increased, while the expression of Bax protein was decreased, IOD value decreased, the value of ND increased, and HG decreased.
Breviscapin injection maybe reduce the delayed neuronal death, and reduce the apoptosis of neuron after severe brain injury through improving the expression of Bcl-2 protein and inhibiting expression of Bax. The study would provide a fine theoretical foundation for clinical therapy of neonatal HIBD.
观察灯盏花素注射液对新生大鼠缺氧缺血性脑损伤的保护作用及Bcl-2和Bax的表达。
本实验采用7日龄新生大鼠缺氧缺血性脑损伤模型，分为假手术组、模型组、注射用水对照组和灯盏花素注射液组。灯盏花素注射液组再分为大、中、小剂量组。采用硫堇染色和免疫组织化学染色检测各组海马CA1区神经元密度、组织学分级以及Bcl-2和Bax蛋白的表达，免疫染色的阳性细胞数及Bcl-2、Bax蛋白在海马CA1区表达的积分光密度（IOD）。
假手术组海马CA1区无明显神经元损伤，Bcl-2和Bax无明显阳性细胞。模型组和注射用水对照组，缺氧缺血性脑损伤（HIBD）后3 d时Bcl-2、Bax表达水平达峰值（与其他组比较，P<0.05），神经元密度（ND）值降低，组织学分级（HG）升高，与假手术组比较差异有统计学意义（P<0.05）。灯盏花素注射液组与注射用水对照组比较，Bcl-2蛋白表达进一步增加，IOD值升高，而Bax蛋白表达降低，IOD值降低，ND值升高，HG降低。
灯盏花素注射液可能通过提高Bcl-2蛋白表达、抑制Bax表达减轻严重脑损伤后迟发性神经元死亡，减少神经元凋亡。本研究为新生儿HIBD的临床治疗提供良好的理论基础。
