摘要
目的观察不同剂量伊桐苷对大鼠弥散性脑损伤(DBI)的防治作用,并探讨其可能机制。方法 50只SD大鼠随机分为5组,A、B、C、D组均制备DBI模型,E组仅做头皮切口并暴露颅骨,不致脑损伤。A、B、C组另分别以40、80、160 g/kg伊桐苷灌胃,造模前7 d开始给药,造模后继续给药14 d,1次/d;D、E组给予等量生理盐水。采用感觉运动功能测试方法评价大鼠神经生理功能的缺陷程度,HE染色法观察大鼠脑组织病理形态学变化,化学比色法测定脑组织谷胱甘肽过氧化物酶(GSH-PX)活性及丙二醛(MDA)含量。结果与E组比较,D组神经功能评分降低,病理形态学变化明显,脑组织MDA含量升高、GSH-PX活性减弱(P均<0.01)。与D组比较,A、B、C组神经功能评分增加,病理形态学改变减轻,脑组织MDA含量降低、GSH-PX活性增强(P均<0.01)。结论伊桐苷能够改善弥漫性脑损伤大鼠的神经功能,减轻脑组织的病理损害,尤以160 g/kg剂量的伊桐苷效果最好;其机制可能与伊桐苷能够减少脑组织内过氧化物的生成并增强抗氧化酶的活性有关。
Objective To observe the preventive and therapeutic effect of different doses of Itoside on rats with diffuse brain injury （ DBI） and to investigate its mechanism. Methods SD rats were randomly divided into 5 groups： groups A, B, C, D and E. DBI models were prepared in the groups A, B, C and D. Rats in the group E only received scalp incision and skull was exposed. Rats in the groups A, B and C were given Itoside （40, 80 and 160 g/kg） by gavage, respectively, starting from 7 days before modeling, and continuing for 14 days after modeling, once a day. Groups D and E received e-qual volume of saline. We used the sensory and motor function test to evaluate the nerve function′s defect degree after DBI, and observed morphological changes of the cerebral cortex of rats by HE staining. We determined the content of glutathione peroxidase （ GSH-PX） and malondialdehyde （ MDA） through the chemical colorimetric method. Results Compared with group E, neurological score was decreased, pathological changes were significant, the content of MDA in brain tissues was increased, and the activity of GSH-PX was decreased in the group D （all P〈0. 01）. Compared with group D, neurological score was increased, pathological changes alleviated, the content of MDA in brain tissues was decreased, and the activity of GSH-PX was increased in the groups A, B and C （all P〈0. 01）. Conclusions Itoside can improve the neural function of rats with DBI and alleviate the pathological damage of brain tissue with the best effect of 160 g/kg Itoside. The mechanism may be related to that Itoside can reduce the formation of oxidation products in the brain tissues and enhance the activity of antioxidant enzymes.
出处
《山东医药》
CAS
北大核心
2016年第15期19-22,共4页
Shandong Medical Journal
基金
广西教育厅科研立项项目(10JKT-111)
桂林市科学研究与技术开发计划项目(11SKT-66)
