BDNF对缺糖缺氧小鼠mPFC脑区GFAP蛋白的影响
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摘要
目的探讨BDNF在缺糖缺氧复灌条件下对小鼠mPFC脑区胶质纤维酸性蛋白GFAP蛋白的影响。方法 2017年12月—2018年2月,徐州医科大学麻醉学重点实验室,将18只小鼠随机平均分为正常组(mPFC脑片低糖DMEM培养基培养)、缺糖缺氧复灌组(mPFC脑片EBSS培养基培养15 min后复灌1 h)、缺糖缺氧复灌给药组(mPFC脑片EBSS培养基中加入BDNF培养15 min后复灌1 h)。给与相应的处理后,对GFAP蛋白表达量进行测定。结果正常组GFAP蛋白的相对表达量为(1.066 33±0.356 753),缺糖缺氧复灌组GFAP蛋白的相对表达量为(2.317 57±0.578 685),缺糖缺氧复灌给药组GFAP蛋白的相对表达量为(1.377 63±0.061 996)。缺糖缺氧复灌组与正常组相比GFAP蛋白的相对表达量升高,差异有统计学意义(P<0.05),缺糖缺氧复灌给药组与缺糖缺氧复灌组相比GFAP的蛋白相对表达量降低,差异有统计学意义(P<0.05)。缺糖缺氧复灌给药组与正常组相比GFAP的蛋白相对表达量升高,差异无统计学意义(P>0.05)。结论 mPFC脑区中的胶质纤维酸性蛋白GFAP在缺糖缺氧条件下有明显升高,BDNF对星形胶质细胞起抑制作用。
Objective This paper tries to investigate the effect of BDNF on the expression of glial fibrillary acidic protein GFAP in the brain of mice mPFC under hypoxia and hypoxia-reperfusion conditions. Methods From December 2017 to February 2018, the Key Laboratory of Anesthesiology of Xuzhou Medical University, 18 mice were randomly divided into normal group(mPFC brain slice lowglucose DMEM medium culture), hypoxia and hypoxia re-irrigation group(mPFC). Brain slices were cultured in EBSS medium for 15 minutes and then refilled for 1 hour) and hypoxia-hypoxia-reperfusion group(mPFC brain slices were supplemented with BDNF for15 minutes after BDNF incubation for 1 hour). After corresponding treatment, the GFAP protein expression level was measured. Re-sults The relative expression level of GFAP protein in the normal group was(1.066 33±0.356 753). The relative expression level of GFAP protein in the hypoxia-hypoxia-reperfusion group was(2.317 57±0.578 685). The relative expression level of GFAP protein in the hypoxia-hypoxia-reperfusion group was(1.377 63±0.061 996). The relative expression of GFAP protein in the hypoxia and hypoxia-reperfusion group was significantly higher than that in the normal group(P<0.05). The hypoxia-ischemia-reperfusion group was compared with the hypoxia-hypoxia-reperfusion group. The relative protein expression of GFAP decreased, there was a statistical dif-ference(P<0.05). Compared with the normal group, the relative protein expression of GFAP increased in the hypoxia-ischemia-reperfusion group but there was no statistical difference(P>0.05). Conclusion The glial fibrillary acidic protein GFAP in mPFC brain regions was significantly increased under hypoxia and hypoxia conditions. BDNF inhibited astrocytes.
Objective This paper tries to investigate the effect of BDNF on the expression of glial fibrillary acidic protein GFAP in the brain of mice mPFC under hypoxia and hypoxia-reperfusion conditions. Methods From December 2017 to February 2018, the Key Laboratory of Anesthesiology of Xuzhou Medical University, 18 mice were randomly divided into normal group(mPFC brain slice lowglucose DMEM medium culture), hypoxia and hypoxia re-irrigation group(mPFC). Brain slices were cultured in EBSS medium for 15 minutes and then refilled for 1 hour) and hypoxia-hypoxia-reperfusion group(mPFC brain slices were supplemented with BDNF for15 minutes after BDNF incubation for 1 hour). After corresponding treatment, the GFAP protein expression level was measured. Re-sults The relative expression level of GFAP protein in the normal group was(1.066 33±0.356 753). The relative expression level of GFAP protein in the hypoxia-hypoxia-reperfusion group was(2.317 57±0.578 685). The relative expression level of GFAP protein in the hypoxia-hypoxia-reperfusion group was(1.377 63±0.061 996). The relative expression of GFAP protein in the hypoxia and hypoxia-reperfusion group was significantly higher than that in the normal group(P<0.05). The hypoxia-ischemia-reperfusion group was compared with the hypoxia-hypoxia-reperfusion group. The relative protein expression of GFAP decreased, there was a statistical dif-ference(P<0.05). Compared with the normal group, the relative protein expression of GFAP increased in the hypoxia-ischemia-reperfusion group but there was no statistical difference(P>0.05). Conclusion The glial fibrillary acidic protein GFAP in mPFC brain regions was significantly increased under hypoxia and hypoxia conditions. BDNF inhibited astrocytes.
引文
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[13]唐启盛,司银楚,裴清华,等.颐脑解郁方对脑卒中后抑郁状态模型大鼠脑内GFAP、BDNF、b FGF的影响[J].北京中医药大学学报,2005,28(4):32-35.
[14]张兵.(一)左旋千金藤啶碱抗抑郁的药理机制研究(二)新型离子通道的功能机制探究[D].上海:中国科学院大学(中国科学院上海药物研究所),2017.
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[3]刘志娟.脑源性神经营养因子在突触可塑性中的作用[J].国际神经病学神经外科学杂志,2015,42(2):185-188.
[4]Koyama Y,Tsujikawa K,Matsuda T,et al.Intracerebroventricular administration of an endothelin ETB receptor agonist increases expressions of GDNF and BDNF in rat brain[J].European Journal of Neuroscience,2015,18(4):887-894.
[5]Luo L,Liu X L,Li J,et al.Macranthol promotes hippocampal neuronal proliferation in mice via BDNF-Trk B-PI3K/Akt signaling pathway[J].European Journal of Pharmacology,2015(762):357-363.
[6]Sasi M,Vignoli B,Canossa M,et al.Neurobiology of local and intercellular BDNF signaling:[J].Pflügers Archiv-European Journal of Physiology,2017,469(5):1-18.
[7]吕秀芳,胡宝英,巩秀,等.内侧前额叶皮层神经元可塑性改变在吗啡奖赏记忆形成中的作用[J].中华行为医学与脑科学杂志,2014,23(12):1061-1064.
[8]杜成昊,万海同,周惠芬,等.谷红注射液对新生乳鼠海马神经元缺氧缺糖损伤的保护作用[J].中华中医药杂志,2017(1):289-293.
[9]董梅,程树彬,郭彦芳,等.器官型脑片培养OGD复氧复糖模型中丁苯酞对于bcl-2/bax、及bim蛋白的调节作用[J].中风与神经疾病,2017,34(1):16-20.
[10]李钊,程树彬,郭彦芳,等.器官型脑片糖氧剥夺模型的建立[J].脑与神经疾病杂志,2017,25(11):707-710.
[11]李青,何顺厚,周作华,等.氯胺酮、异丙酚对谷氨酸诱导大鼠海马星形胶质细胞损伤的影响[J].湖北医药学院学报,2007,26(3):137-140.
[12]Kang J W M,Keay K A,Mor D.Resolving the contributions of anaesthesia,surgery,and nerve injury on brain derived neurotrophic factor expression in the medial prefrontal cortex of male rats in the CCI model of neuropathic pain[J].Journal of Neuroscience Research,2017.
[13]唐启盛,司银楚,裴清华,等.颐脑解郁方对脑卒中后抑郁状态模型大鼠脑内GFAP、BDNF、b FGF的影响[J].北京中医药大学学报,2005,28(4):32-35.
[14]张兵.(一)左旋千金藤啶碱抗抑郁的药理机制研究(二)新型离子通道的功能机制探究[D].上海:中国科学院大学(中国科学院上海药物研究所),2017.