摘要
目的:探讨牛磺酸对过氧化氢(H2O2)引起的神经元损伤的保护作用。方法:采用不同浓度的H2O2处理神经元,制备体外氧化应激模型,造模前24 h分别给予5、15、25 mmol/L牛磺酸预处理。采用特异性荧光探针DCFH-DA检测神经元活性氧自由基水平,检测乳酸脱氢酶(LDH)释放率反映神经元损伤程度,用免疫印迹法检测脑源性营养因子(brain-derived neurotrophic factor,BDNF)及突触相关蛋白的表达水平。结果:与Control组比较,不同浓度的H2O2(25、50、100μmol/L)均能使LDH向胞外释放增多(P<0.05),15、25 mmol/L的牛磺酸均能减少H2O2引起的LDH的释放(P<0.05)。100μmol/L H2O2使神经元胞内活性氧水平升高,仅25 mmol/L的牛磺酸能抑制H2O2诱导的胞内活性氧的增多(P<0.05)。100μmol/L H2O2处理神经元导致BDNF、突触相关蛋白Synapsin和Spinophilin表达水平下降,给予25 mmol/L的牛磺酸能部分逆转H2O2诱导的蛋白水平的下降(P<0.05)。结论:牛磺酸能够减轻H2O2引起的神经元损伤,具有较好的神经保护作用。
Objective:To explore the protective effect of taurine on injured neurons induced by hydrogen peroxide(H2O2).Methods:Neurons were treated with different doses of H2O2.Oxidative stress model was prepared in vitro.Taurine was applied at5,15 or 25 mmol / L 24 h prior to H2O2treatment.Specific fluorescent probe DCFH-DA was performed to analyze reactive oxygen species level of neurons.Lactic dehydrogenase(LDH) release assay was performed to detect the injury degree of neurons.Brainderived neurotrophic factor(BDNF) and synaptic-related protein levels were evaluated by Western blotting.Results:Compared with the control group,different doses of H2O2(5,50 and 100 μmol / L) increased LDH release to the extracellular medium(P〈0.05),while 15 and 25 mmol / L taurine decreased the release(P〈0.05).One hundred μmol / L H2O2led to an increase of reactive oxygen species level and decreased BDNF,synapsin and spinophilin protein expressions(P〈0.05).After treatment with 25 mmol / L taurine,the above indicators were attenuated(P〈0.05).Conclusion:Taurine can alleviate H2O2induced neuron damages and show neuroprotective effect against oxidative stress.
出处
《南京医科大学学报(自然科学版)》
CAS
CSCD
北大核心
2014年第8期1072-1076,共5页
Journal of Nanjing Medical University(Natural Sciences)