摘要
目的观察右美托咪定对缺血缺氧性脑损伤(HIBD)新生大鼠皮层和海马组织中损伤因子肿瘤坏死因子(TNF-α)、白细胞介素-1β(IL-1β)及抗损伤因子神经生长因子(NGF)、脑源性神经营养因子(BDNF)表达的影响,初步探讨右美托咪定的神经保护机制。方法将45只7日龄SD大鼠,随机分为3组:假手术组,缺血缺氧组和右美托咪定组。缺血缺氧组和右美托咪定组新生大鼠建立HIBD动物模型,假手术组仅分离左侧颈总动脉,不结扎也不做缺氧处理。右美托咪定组于建立模型后立即按100μg/kg腹腔注射右美托咪定,假手术组和缺血缺氧组注射等量生理盐水。24 h后全部处死,采用ELISA法检测脑组织中TNF-α、IL-1β、NGF、BDNF水平。结果缺血缺氧组新生大鼠皮层和海马组织中TNF-α、IL-1β、NGF、BDNF水平高于假手术组;右美托咪定组的TNF-α、IL-1β水平低于缺血缺氧组,而NGF、BDN水平则高于缺血缺氧组,差异均具有统计学意义(P<0.05或P<0.01)。结论右美托咪定可保护新生大鼠缺血缺氧后引起的皮层和海马损伤,其作用机制可能与抑制损伤因子TNF-α、IL-1β表达和促进抗损伤因子NGF、BDNF表达相关。
Objective To study the effect of dexmedetomidine on the expression of the damage factors of tumor necrosis factor α（ TNF-α）,interleukin-1β（ IL-1β） and the anti-damage factors of nerve growth factor（ NGF）,brain derived neurotrophic factor（ BDNF）,and to discuss the protective molecular mechanisms of dexmedetomidine on neonatal rats with hypoxic-ischemic brain damage（ HIBD）. Methods A total of 45 7-day-old neonatal rats were randomly divided into 3 groups： shamoperated group,hypoxic-ischemic group and dexmedetomidine group. Rats in hypoxic-ischemic group and dexmedetomidine group were subjected to establish HIBD models,while rats in sham-operated group were separated the left common carotid artery,but the exposed carotid artery was not ligated and they didn＇t deal with hypoxic. Dexmedetomidine was immediately injected intraperitoneally into the rats at 100 μg / kg in dexmedetomidine group after hypoxic treatment,and equal saline solution was injected into the hypoxic-ischemic group and sham-operated group. All the rats were killed 24 h after operation,and the levels of TNF-α,IL-1β,NGF,BDNF were measured by enzyme linked immunosorbent assay（ ELISA）. Results The levels of TNF-α,IL-1β,NGF,BDNF in hypoxic-ischemic group were higher than those in sham-operated group. The levels of TNF-α,IL-1β in dexmedetomidine group were significantly lower than those in hypoxic-ischemic group,while the levelsof NGF,BDNF in dexmedetomidine group were significantly higher than those in hypoxic-ischem icgroup,the differences were statistical significance（ P 0. 0 5 or P 0. 0 1）. Conclusion Dexmedetomidine could protect the cortex and hippocampus damage in neonatal rats with hypoxic-ischemic brain damage,and the potent mechanisms were related to down-regulate the expression of damage factors TNF-α,IL-1β and up-regulate the expression of anti damage factors NGF,BDNF.
出处
《实用临床医药杂志》
CAS
2016年第1期13-15,共3页
Journal of Clinical Medicine in Practice
基金
中国高校医学期刊临床专项资金(11523788)
