摘要
背景:脊髓缺血再灌注损伤的机制是多因素综合作用的结果,其尚无有效的治疗手段。目的:探讨脂氧素受体激动剂BML-111对大鼠脊髓缺血再灌注损伤时炎性因子和细胞凋亡的影响。方法:随机数字法将72只成年健康雄性SD大鼠随机等分为假手术组、缺血再灌注组和BML-111组。后2组大鼠通过夹闭腹主动脉的方法建立大鼠脊髓缺血再灌注损伤模型。缺血再灌注组和BML-111组大鼠分别于造模后30 min给予尾静脉注射0.1 m L生理盐水及1 mg/kg BML-111。结果与结论:与缺血再灌注组相比,BML-111组大鼠BBB评分显著提高,脊髓组织病理损伤明显减轻,脊髓组织中细胞凋亡数量、肿瘤坏死因子α、白细胞介素1β表达、髓过氧化物酶活性以及丙二醛浓度减少。提示脂氧素受体激动剂BML-111可通过抑制神经细胞凋亡及炎症反应,从而减轻脊髓损伤。
BACKGROUND： The mechanisms of spinal cord ischemia-reperfusion injury are the result of the combined effects of multiple factors, but there is no effective treatment. OBJECTIVE： To investigate the effect of lipoxin receptor agonist BML-111 on inflammatory factor and apoptosis in rats with spinal cord ischemia-reperfusion injury. METHODS： A total of 72 healthy adult male Sprague-Dawley rats were randomly divided into sham surgery group, ischemia-reperfusion group and BML-111 group. Rat models of spinal cord ischemia-reperfusion injury were established by clamping the abdominal aorta in the later two groups. Rats in the ischemia-reperfusion group and BML-111 group were injected with 0.1 mL of saline and 1 mg/kg BML-111 through caudal vein at 30 minutes after model establishment. RESULTS AND CONCLUSION： Compared with ischemia-reperfusion group, BBB scores were significantly improved, pathological injury of spinal cord tissue significantly reduced, the number of apoptotic cel s, tumor necrosis factor α and interleukin-1β expression, myeloperoxidase oxide activity and malondialdehyde content decreased in the BML-111 group. These findings indicate that lipoxin receptor agonist BML-111 can inhibit neuronal apoptosis and inflammation so as to reduce spinal cord injury.
出处
《中国组织工程研究》
CAS
北大核心
2016年第18期2642-2647,共6页
Chinese Journal of Tissue Engineering Research
基金
新乡医学院科研项目培育基金(2013ZD120)~~
