摘要
目的探讨正丁基苯酞(n-butylphthalide, NBP)对急性一氧化碳中毒(acute carbon monoxide poisoning,ACOP)大鼠脑损伤氧化应激的调节作用及机制。方法雄性SD大鼠36只,随机分为对照组、ACOP组和ACOP正丁基苯酞干预组(干预组)。染毒过程中观察各组大鼠的一般状态,检测ACOP组和干预组大鼠的血液碳氧血红蛋白浓度(COHb%);采用Morris水迷宫实验评估学习与记忆功能;检测海马和皮质丙二醛(malondialdehyde, MDA)、8-羟基脱氧鸟苷(8-hydroxydesoxyguanosine, 8-OHdG)和3-硝基酪氨酸(3-nitrotyrosine, 3-NT)水平;采用Western blotting法检测海马和皮质沉默信息调节因子3(sirtuin 3, SIRT3)蛋白表达水平。结果染毒过程中,ACOP组和干预组大鼠呈典型的ACOP表现,对照组大鼠无异常表现,ACOP组与干预组大鼠血液COHb%的差异无统计学意义。ACOP组与对照组或干预组大鼠相比,逃避潜伏期延长,第3象限游泳时间缩短。ACOP组与对照组或干预组大鼠相比,海马和皮质MDA和8-OHdG以及海马3-NT含量均升高,但各组大鼠皮质3-NT的差异无统计学意义。ACOP组与对照组或干预组大鼠相比,海马和皮质SIRT3蛋白表达水平下降。结论 NBP通过对脑组织SIRT3蛋白表达水平的调节抗氧化应激,降低脑组织MDA、8-OHdG和3-NT含量,从而发挥对ACOP大鼠脑损伤的神经保护作用。
Objective To explore the regulation and its mechanism of n-butylphthalide(NBP)on oxidative stress of brain tissue induced by acute carbon(ACOP)in rats.Methods Thirty-six male SD rats were divided into three groups:the air+vehicle group,the CO+vehicle group and the CO+NBP group according to the principle of random grouping.The manifestations of rats in each group were observed during the process of ACOP.The blood COHb%for the rats in CO+vehicle group and CO+NBP group were determined.Morris water maze experiment was used to evaluate the function of learning and memory for rats in each group.And the MDA,8-OHdG and 3-NT levels in the hippocampus and cortex for rats in each group were determined.Western blotting was used to determine the SIRT3 protein levels in the hippocampus and cortex for rats in each group.Results During the process of ACOP,typical manifestations of ACOP exhibited in CO+vehicle group and CO+NBP group,no abnormal manifestation exhibited in air+vehicle group.No significant difference was found in COHb%in the blood for CO+vehicle group and CO+NBP group.Longer escape latency and shorter time spent in quadrant 3 were found in CO+vehicle group than those in air+vehicle group or CO+NBP group.Higher MDA and 8-OHdG levels in the hippocampus and cortex and 3-NT level in the hippocampus were found in CO+vehicle group than those in air+vehicle group or CO+NBP group.However,there was no significant difference of 3-NT level in the cortex for rats in each group.Lower SIRT3 protein levels in the hippocampus and cortex were found in CO+vehicle group than those in air+vehicle group or CO+NBP group.Conclu?sions NBP could inhibit oxidative stress by regulating protein levels of SIRT3 and downregulate levels of MDA,8-OHdG,3-NT in the brain tissue,and then exert neuroprotective effect against ACOP induced brain injuries in rats.
作者
王鲲宇
唐圣桃
邱峰
王晴晴
任明
王文
戚晓昆
Wang Kunyu;Tang Shengtao;Qiu Feng;Wang Qingqing;Ren Ming;Wang Wen;Qi Xiaokun(Seven-year-program Clinical Medicine,Dalian Medical University,Dalian 116044,China)
出处
《北京医学》
CAS
2019年第5期389-392,共4页
Beijing Medical Journal
基金
北京医学奖励基金会(YXJL-2018-0296-0037)
