深低温停循环大鼠海马组织中蛋白激酶CK2α表达情况及其在脑保护中的作用
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摘要
目的探讨深低温停循环大鼠海马组织中蛋白激酶CK2α表达情况及其在脑保护中的作用。方法 39只SD大鼠随机分为常温不停循环组、常温停循环组和深低温停循环组,常温不停循环组大鼠在37℃下体外循环20min;常温停循环组大鼠在37℃下体外循环10 min,停循环10 min;深低温停循环组大鼠在<20℃下体外循环10 min,停循环10min。动物模型建立后,取3组大鼠海马组织行组织病理学检查,采用免疫组织化学法和免疫荧光法检测海马组织蛋白激酶CK2α表达情况。结果 3组大鼠均建模成功;常温不停循环组和深低温停循环组大鼠神经细胞和椎体细胞形态和数量均正常,未见缺血性改变,常温停循环组大鼠少量神经元肿胀、变性,少量胶质细胞增生和少量炎性细胞浸润,呈轻度缺血性改变;常温不停循环组大鼠海马组织有极少量蛋白激酶CK2α表达,常温停循环组大鼠海马组织有大量蛋白激酶CK2α表达,深低温停循环组大鼠海马组织有少量蛋白激酶CK2α表达;常温停循环组大鼠海马组织蛋白激酶CK2α灰度值(99.54±3.28)低于常温不停循环组(189.43±8.86)和深低温停循环组(133.65±8.02)(P<0.05),深低温停循环组低于常温不停循环组(P<0.05)。结论停循环可引起海马组织中蛋白激酶CK2α含量升高,深低温能降低停循环状态下海马组织中蛋白激酶CK2α含量,发挥一定脑保护作用。
Objective To explore the expression of protein kinase CK2αin hippocampal tissue and its cerebral protective role in deep hypothermic circulatory arrest in rats. Methods Thirty-nine rats were randomly divided into roomtemperature cyclic group,room-temperature circulatory arrest group and deep hypothermic circulatory arrest group.The rats in room-temperature cyclic group received cardiopulmonary bypass(CPB)for 20 min at the temperature of 37 ℃without circulatory arrest.The rats in room-temperature circulatory arrest group received CPB for 10 min at the temperature of 37 ℃,followed by circulatory arrest for 10 min.The rats in deep hypothermic circulatory arrest group received CPB for 10 min followed by circulatory arrest for 10 min at the temperature below 20 ℃.The histopathological changes of hippocampal tissue were observed in 3groups after model establishment.The expression of hippocampal tissue protein kinase CK2αwas detected by immunohistochemistry and immunofluorescence staining in three groups.Results All models were successfully established in three groups.Hippocampal tissue staining showed normal morphology and quantity of nerve and vertebral cells with no ischemic changes in room-temperature cyclic group and deep hypothermic circulatory arrest group.Room-temperature circulatory arrest group had swelling and degeneration of a small amount of neurons,proliferation of a small amount of glial cells,and infiltration of a small amount inflammatory cells,showing mild ischemic changes.A very small amount of protein kinase CK2αwas expressed in hippocampal tissue in room-temperature cyclic group,a large amount of protein kinase CK2αwas expressed in room-temperature circulatory arrest group,and a small amount of protein kinase CK2αwas expressed in deep hypothermic circulatory arrest group.The average gray value of protein kinase CK2αin hippocampus tissue was significantly lower in room-temperature circulatory arrest group(99.54±3.28)than that in room-temperature cyclic group(189.43±8.86)and deep hypothermic circulatory arrest group(133.65±8.02)(P<0.05),and lower in deep hypothermic circulatory arrest group than that in room-temperature cyclic group(P<0.05).Conclusion Circulatory arrest can raise the levels of protein kinase CK2αin hippocampus tissue,deep hypothermia can reduce the protein kinase CK2αlevels in hippocampus tissue under circulatory arrest,which plays a cerebral protective role.
Objective To explore the expression of protein kinase CK2αin hippocampal tissue and its cerebral protective role in deep hypothermic circulatory arrest in rats. Methods Thirty-nine rats were randomly divided into roomtemperature cyclic group,room-temperature circulatory arrest group and deep hypothermic circulatory arrest group.The rats in room-temperature cyclic group received cardiopulmonary bypass(CPB)for 20 min at the temperature of 37 ℃without circulatory arrest.The rats in room-temperature circulatory arrest group received CPB for 10 min at the temperature of 37 ℃,followed by circulatory arrest for 10 min.The rats in deep hypothermic circulatory arrest group received CPB for 10 min followed by circulatory arrest for 10 min at the temperature below 20 ℃.The histopathological changes of hippocampal tissue were observed in 3groups after model establishment.The expression of hippocampal tissue protein kinase CK2αwas detected by immunohistochemistry and immunofluorescence staining in three groups.Results All models were successfully established in three groups.Hippocampal tissue staining showed normal morphology and quantity of nerve and vertebral cells with no ischemic changes in room-temperature cyclic group and deep hypothermic circulatory arrest group.Room-temperature circulatory arrest group had swelling and degeneration of a small amount of neurons,proliferation of a small amount of glial cells,and infiltration of a small amount inflammatory cells,showing mild ischemic changes.A very small amount of protein kinase CK2αwas expressed in hippocampal tissue in room-temperature cyclic group,a large amount of protein kinase CK2αwas expressed in room-temperature circulatory arrest group,and a small amount of protein kinase CK2αwas expressed in deep hypothermic circulatory arrest group.The average gray value of protein kinase CK2αin hippocampus tissue was significantly lower in room-temperature circulatory arrest group(99.54±3.28)than that in room-temperature cyclic group(189.43±8.86)and deep hypothermic circulatory arrest group(133.65±8.02)(P<0.05),and lower in deep hypothermic circulatory arrest group than that in room-temperature cyclic group(P<0.05).Conclusion Circulatory arrest can raise the levels of protein kinase CK2αin hippocampus tissue,deep hypothermia can reduce the protein kinase CK2αlevels in hippocampus tissue under circulatory arrest,which plays a cerebral protective role.
引文
[1]朱耀斌,李志强,范祥明,等.深低温停循环大鼠大脑缺氧诱导因子-1α和信号转导分子2表达情况[J].中华实用诊断与治疗杂志,2016,30(12):1162-1165.
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[9]Ye ZY,Li L,Li DP,et al.Casein kinase 2-mediated synaptic GluN2A up-regulation increases N-methyl-D-aspartate receptor activity and excitability of hypothalamic neurons in hypertension[J].J Biol Chem,2012,287(21):17438-17446.
[10]Elmistekawy EM,Rubens FD.Deep hypothermic circulatory arrest:alternative strategies for cerebral perfusion.A review article[J].Perfusion,2011,26Suppl 1:27-34.
[11]李斌,刘爱军,李晓锋,等.深低温停循环猪脑组织中小泛素样修饰蛋白表达实验研究[J].中华实用诊断与治疗杂志,2015,29(6):531-534.
[12]曹传辉,陈勃,梁基韵,等.蛋白激酶CK2α在食管癌中的表达及意义[J].广东医学,2013,34(11):1680-1683.
[13]Yang D,Wang T,Ni Y,et al.Apamin-sensitive K+current upregulation in volume-overload heart failure is associated with the decreased interaction of CK2with SK2[J].J Membr Biol,2015,248(6):1181-1189.
[14]Kim S,Jin B,Choi SH,et al.Casein kinaseⅡinhibitor enhances production of infectious genotype 1ahepatitis C virus(H77S)[J].PLoS One,2014,9(12):e113938.
[15]王建亭,龚树生.蛋白激酶CK2α对喉癌细胞凋亡和超微结构的影响[J].中华医学杂志,2010,90(40):2869-2872.
[16]Chen SR,Zhou HY,Byun HS,et al.Casein kinaseⅡregulates N-methyl-D-aspartate receptor activity in spinal cords and pain hypersensitivity induced by nerve injury[J].J Pharmacol Exp Ther,2014,350(2):301-312.
[17]Sanz-Clemente A,Gray JA,Ogilvie KA,et al.Activated CaMKⅡcouples GluN2B and casein kinase 2 to control synaptic NMDA receptors[J].Cell Rep,2013,3(3):607-614.
[2]李斌,朱耀斌,刘爱军,等.大鼠深低温停循环模型的建立[J].中华实用诊断与治疗杂志,2015,29(7):634-636.
[3]孔繁熙,张晶,朱耀斌,等.海马线粒体通透性转换孔在深低温停循环大鼠模型中的开闭情况研究[J].中华实用诊断与治疗杂志,2016,30(12):1166-1169.
[4]Gutsche JT,Ghadimi K,Patel PA,et al.New frontiers in aortic therapy:focus on deep hypothermic circulatory arrest[J].J Cardiothorac Vasc Anesth,2014,28(4):1159-1163.
[5]Reed H,Berg KB,Janelle GM.Aortic surgery and deephypothermic circulatory arrest:anesthetic update[J].Semin Cardiothorac Vasc Anesth,2014,18(2):137-145.
[6]朱耀斌,李志强,范祥明,等.乳猪深低温停循环不同流量选择性脑灌注微透析实验研究[J].中华实用诊断与治疗杂志,2014,28(3):220-223.
[7]Mandal T,Bhowmik A,Chatterjee A,et al.Reduced phosphorylation of Stat3at Ser-727mediated by casein kinase 2-protein phosphatase 2A enhances Stat3 Tyr-705 induced tumorigenic potential of glioma cells[J].Cell Signal,2014,26(8):1725-1734.
[8]阮杰,王菲菲,刘新光,等.蛋白激酶CK2βSiRNA对肺腺癌细胞A549增殖的抑制作用[J].中国肿瘤临床,2009,36(12):701-706.
[9]Ye ZY,Li L,Li DP,et al.Casein kinase 2-mediated synaptic GluN2A up-regulation increases N-methyl-D-aspartate receptor activity and excitability of hypothalamic neurons in hypertension[J].J Biol Chem,2012,287(21):17438-17446.
[10]Elmistekawy EM,Rubens FD.Deep hypothermic circulatory arrest:alternative strategies for cerebral perfusion.A review article[J].Perfusion,2011,26Suppl 1:27-34.
[11]李斌,刘爱军,李晓锋,等.深低温停循环猪脑组织中小泛素样修饰蛋白表达实验研究[J].中华实用诊断与治疗杂志,2015,29(6):531-534.
[12]曹传辉,陈勃,梁基韵,等.蛋白激酶CK2α在食管癌中的表达及意义[J].广东医学,2013,34(11):1680-1683.
[13]Yang D,Wang T,Ni Y,et al.Apamin-sensitive K+current upregulation in volume-overload heart failure is associated with the decreased interaction of CK2with SK2[J].J Membr Biol,2015,248(6):1181-1189.
[14]Kim S,Jin B,Choi SH,et al.Casein kinaseⅡinhibitor enhances production of infectious genotype 1ahepatitis C virus(H77S)[J].PLoS One,2014,9(12):e113938.
[15]王建亭,龚树生.蛋白激酶CK2α对喉癌细胞凋亡和超微结构的影响[J].中华医学杂志,2010,90(40):2869-2872.
[16]Chen SR,Zhou HY,Byun HS,et al.Casein kinaseⅡregulates N-methyl-D-aspartate receptor activity in spinal cords and pain hypersensitivity induced by nerve injury[J].J Pharmacol Exp Ther,2014,350(2):301-312.
[17]Sanz-Clemente A,Gray JA,Ogilvie KA,et al.Activated CaMKⅡcouples GluN2B and casein kinase 2 to control synaptic NMDA receptors[J].Cell Rep,2013,3(3):607-614.
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