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作 者:刘颖 游平飞 程凤 王泽薇 戴晶 曹滨验 金红旭 LIU Ying;YOU Ping-fei;CHENG Feng;WANG Ze-wei;DAI Jing;CAO Bin-jian;JIN Hong-xu(Department of Emergency Medicine,General Hospital of Northern Theater Command,Shenyang 110016,China)
机构地区:[1]北部战区总医院急诊医学科,辽宁沈阳110016
出 处:《创伤与急危重病医学》2024年第5期263-266,共4页Trauma and Critical Care Medicine
摘 要:目的探讨人参皂苷Rg1对小鼠低温致远期认知功能损伤的作用及机制。方法将24只雄性健康成年C57BL/6小鼠分为对照组(n=8)、低温组(n=8)和人参皂苷Rg1组(n=8)。对照组小鼠不作处理;低温组小鼠在对照组小鼠的基础上,每天于4℃环境下饲养,每天3h,持续4周;人参皂苷Rg1组小鼠在低温组的基础上,每天腹腔注射30mg/kg人参皂苷Rg1,持续4周。通过水迷宫评价小鼠记忆能力,检测三组小鼠通神经元核抗原(NeuN)、微管相关蛋白2(MAP-2)、脑组织神经生长因子(NGF)、脑源性神经营养因子(BDNF)水平;酪氨酸激酶受体A(TrkA)和酪氨酸激酶受体B(TrkB)蛋白表达;丙二醛(MAD)和环氧化酶-2(COX2)表达水平。结果人参皂苷Rg1组小鼠不同训练时间逃避潜伏期缩短于低温组,穿越平台次数多于低温组,目标象限时间长于低温组,NeuN和MAP-2蛋白水平高于低温组,脑组织NGF和BDNF水平高于低温组,脑组织TrkA和TrkB蛋白水平高于低温组,脑组织MDA、COX2水平表达低于低温组,差异有统计学意义(P<0.05)。结论人参皂苷Rg1组能够改善小鼠低温致远期认知功能损伤,其机制与调节神经营养因子、TrkA和TrkB蛋白,降低氧化应激有关。Objective To explore the effects and mechanisms of ginsenoside Rg1 on long-term cognitive impairment caused by hypothermia in mice.Methods A total of 24 male healthy adult C57BL/6 mice were divided into the control group(n=8),the low-temperature group(n=8)and the ginsenoside Rg1 group(n=8).The mice in the low-temperature group were kept at 4℃for 3 h per day for 4 weeks,and the mice in the ginsenoside Rg1 group were intraperitoneally injected with 30 mg/kg of ginsenoside Rg1 per day.The memory capacity of rats was evaluated by the water maze,and the levels of mouse neuronal nuclei(NeuN),microtubule associated protein-2(MAP-2),brain nerve growth factor(NGF),brain-derived neurotrophic factors(BDNF),tyrosine kinase receptor A(TrkA)and tyrosine kinase receptor B(TrkB)protein expression,and malondialdehyde(MAD)and cyclooxygenase-2(COX2)were measured.Results The latency period of mice in the ginsenoside Rg1 group was shorter than that of low-temperature group,the number of crossing platforms was more than that of low-temperature group,the target quadrant time was longer than that of low-temperature group.The expression levels of NeuN and MAP-2 proteins were higher than that of low-temperature group,the expression levels of NGF and BDNF in brain tissues were higher than that of low-temperature group,the levels of TrkA and TrkB proteins in brain tissues were higher than that of low-temperature group,and the levels of MDA and COX2 in brain tissues were lower than that of low-temperature group,the differences were statistically significant(P<0.05).Conclusion Ginsenoside Rg1 can improve long-term cognitive function impairment caused by low temperature in mice,and its mechanism is related to the regulation of neurotrophic factors and TrkA/TrkB receptors,as well as the reduction of oxidative stress.
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