丁基苯酞对大鼠弥漫性脑损伤后排斥性导向分子表达的影响

EFFECT OF BUTYLPHTHALIDE ON EXPRESSION OF RGMA IN DIFFUSION BRAIN INJURY

目的探讨丁基苯酞对弥漫性脑损伤(DBI)后大鼠海马排斥性导向分子(RGMa)表达的影响。方法160只成年雄性Sprague-Dawlley大鼠,随机分为正常对照组(n=40),模型组(n=40),低剂量丁基苯酞干预组(n=40,80mg/kg),高剂量丁基苯酞干预组(n=40,160mg/kg)。参照Marmarou's法建立脑损伤模型,选取伤后1、2、7、14d作为时间点,干预组均在致伤后采用腹腔注射丁基苯酞,1次/24h,连续注射14d。通过行为学评分量表测评神经功能;光镜观察神经细胞形态结构变化,免疫组织化学观察RGMa的表达情况。结果与对照组比较,模型组动物各时间点行为学评分降低(P<0.05);死亡神经元数量升高(P<0.05);各时间点RGMa阳性表达增加(P<0.05)。与模型组比较,高低剂量丁基苯酞干预组中1、2d时行为学评分差异无统计学意义(P>0.05),7d和14d行为学评分升高(P<0.05),但在7d和14d丁基苯酞高、低剂量组间差异无统计学意义(P>0.05)。与模型组比较,丁基苯酞高、低剂量组死亡神经元数量降低(P<0.05);丁基苯肽高、低剂量组之间差异无统计学意义(P>0.05)。与模型组比较,丁基苯酞高、低剂量组中RGMA阳性表达1d差异无统计学意义(P>0.05),2、7、14d时RGMa阳性表达明显减少(P<0.05)。但在2、7、14d丁基苯肽高、低剂量组间差异无统计学意义(P>0.05)。与对照组比较,模型组各时间点RGMamRNA表达水平增加。与模型组比较,丁基苯酞高、低剂量组中1d时差异无统计学意义(P>0.05),2、7、14d时减少(P<0.05)。丁基苯酞高、低剂量组间各时间点差异无统计学意义(P>0.05)。结论丁基苯酞可减少弥漫性脑损伤大鼠大脑海马区RGMa表达。

Objective To investigate the impact of hutylphthalide on RGMA expression in rats＂ hippocampus in diffusion brain injury（DBI）. Methods Animal mode was established by using Marmarou＇s method. SD rats were randomly divided into normal group, diffuse brain injury group, lowdose Butylphthalide treatment group （80mg/kg）, and high-dose Butylphthalide treatment group （160mg/kg）. Treatment groups were intraperitoneal injection of butylphthalide （low dose： 80mg/kg; high dose groups： 160mg/kg） after injury, once for 24h, continued to 14d, and ld, 2d, 7d, 14d were selected as a point in time after injury. Evaluated the neural function by behavior rating scale, observed the morphology and structure of nerve cells by optical microscopes, and observed the expression of RGMA by immunohistochemical and RT - PCR. Results Compared with the normal group, model group animals behaviors score were low at each time point （P〈0.05）; death of neurons increases （P〈0.05）, RGMA positive cells significantly increased at each time point （ P〈0.05 ）. Compared with model group, NBP low - dose and high- dose group animals behavioural scores at ld, 2d had no statistically significant differences （P〉0.05） , behavior score at 7d and 14d increased （P〈0.05）. But the two treatment groups had no statistically significant differences （P〉0. 05）. Compared with model group, The number of animals＂ dead neurons were died down in NBP low- dose and high - dose group （ P〈0. 05）, but at each time point of two groups animals＂ dead neurons had no statistically significant differences（P〉0. 05）. Compared with model group, the RGMA and RGMAmRNA positive cell in NBP low- dose and high- dose group at ld had no statistically significant differences {P〉0.05） ; at 2d , 7d and 14d were reduced （P〈0.05） ; at 2d , 7d and 14d point of two groups animals＂ expression of RGMA and RGMAmRNA had no statistically significant differences（P〉0.05）. Conclusion The NBP can reduce the expression of RGMA in hippocampus of rats with DBI.