摘要
目的探讨抗氧化剂丹参提取物764-3对高氧损伤后新生大鼠脑细胞凋亡和血管内皮生长因子(vascular endothelial growth factor,VEGF)表达的影响。方法采用Spraque-Dawley(SD)新生大鼠持续暴露于≥90%高氧14 d建立高氧脑损伤模型,分别用764-3进行预防和治疗干预后,采用HE染色对比脑细胞病理变化,SABC免疫组化法检测VEGF表达水平以及脱氧核糖核酸转移酶介导的细胞凋亡标记法(TUNEL)检测脑细胞凋亡情况。结果高氧对照组与空气对照组相比:可见神经元变性,VEGF表达下降,凋亡指数(apoptosis index,AI)增多。干预组14 d与高氧对照组14 d相比:764-3预防组VEGF表达高于高氧对照组,但差异无显著性(P>0.05),764-3治疗组VEGF表达显著高于高氧对照组(P<0.05),两干预组间差异无显著性(P>0.05)。两干预组凋亡指数均明显下降且差异显著(P<0.01),764-3治疗组显著低于预防组(P<0.01)。结论 764-3可通过上调脑组织中VEGF的表达来抑制脑细胞凋亡从而发挥保护作用。
Objective To investigate the effect of 764-3 on VEGF expression and apoptosis in the brain of neonatal rats after hyperoxia injury. Methods Hyperoxia brain injury model was established by exposing to ≥90% oxygen in the neonatal period of SD rats for 14 days. Interfered with 764-3,the neuronal degeneration was observed by HE staining;VEGF expression was measured by means of immunohistochemistry. Meanwhile,terminal deoxyribonucleotidyl biotin-dUTP nick end labeling （TUNEL） was utilized to detect the mumber of apoptosis of brain cells. Results Compared with the air control group,the AI of hyperoxia-exposed group increased and the expression of VEGF reduced. Interfered with 764-3,the VEGF expression in the brain increased,the protective effect of those two groups were sim- ilar（P〉0.05）. The AI in 764-3 groups were lower than those in hyperoxia-exposed group （P〈0.01）,the treatment group showed significantly difference comparing with the prevention group （P〈0.01）. Conclusion 764-3 could inhibit apoptosis by increasing the expression of VEGF, thus alleviate injury on hyperoxia injuried rats.
出处
《中国现代医生》
2013年第28期16-18,24,共4页
China Modern Doctor
关键词
细胞凋亡
VEGF
高氧症
脑损伤
丹参提取物
Apoptosis
VEGF
Hyperoxia
Brain injury
Radix salvia miltiorrhiza extract
