[1]李婧静),吴世政),薛孟周),等.经典瞬时受体电位通道3与缺氧预处理大鼠脑梗死的关系[J].郑州大学学报(医学版),2020,(06):806-810.[doi:10.13705/j.issn.1671-6825.2019.08.106]
 LI Jingjing),WU Shizheng),XUE Mengzhou),et al.Relationship of TRPC3 with cerebral infarction after hypoxia preconditioning in rats[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2020,(06):806-810.[doi:10.13705/j.issn.1671-6825.2019.08.106]
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经典瞬时受体电位通道3与缺氧预处理大鼠脑梗死的关系()
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《郑州大学学报(医学版)》[ISSN:1671-6825/CN:41-1340/R]

卷:
期数:
2020年06期
页码:
806-810
栏目:
论著
出版日期:
2020-11-20

文章信息/Info

Title:
Relationship of TRPC3 with cerebral infarction after hypoxia preconditioning in rats
作者:
李婧静1)吴世政2)薛孟周1)李飞翔1)闻 君1)崔 健1)刘伟利1)吴 睿1)
1)郑州大学第二附属医院神经康复科 郑州 450014 2)青海省人民医院神经内科 西宁 810016
Author(s):
LI Jingjing1)WU Shizheng2)XUE Mengzhou1)LI Feixiang1)WEN Jun1)CUI Jian1)LIU Weili1)WU Rui1)
1)Department of Neurological Rehabilitation,the Second Affiliated Hospital,Zhengzhou University,Zhengzhou 450014 2)Department of Neurology,Qinghai People's Hospital,Xining 810016
关键词:
缺氧预处理 脑梗死 TRPC3 大鼠
Keywords:
hypoxia preconditioning cerebral infarction TRPC3 rat
分类号:
R743.32
DOI:
10.13705/j.issn.1671-6825.2019.08.106
摘要:
目的:分析经典瞬时受体电位通道3(TRPC3)在缺氧预处理中的神经保护作用及可能的机制。方法:将雄性SD大鼠56只随机分成4组,每组14只。正常对照组常规饲养。梗死组不进行缺氧预处理,采用改良Longa法制备左侧大脑中动脉栓塞(MCAO)模型。缺氧预处理组进行缺氧预处理,但不制备MCAO模型。缺氧预处理加梗死组先进行缺氧预处理,然后制备MCAO模型。缺氧预处理方法为连续3 d,每天上午8:00将大鼠置于低压氧舱(模拟5 000 m海拔,压强0.53×105 Pa,氧分压为42 mmHg,1 mmHg=0.133 kPa)中2 h。预处理结束2 h后进行MCAO制作。MCAO后24 h进行神经功能评分(n=14),然后断头取脑,TTC染色法测定脑梗死面积百分比(n=4),实时荧光定量PCR法测定脑组织中TRPC3 mRNA的表达(n=6),免疫组化法检测TRPC3蛋白的表达(n=4)。结果:正常对照组和缺氧预处理组大鼠无神经功能缺损表现(评分为0),TTC染色结果显示未发生脑梗死。与梗死组比较,缺氧预处理加梗死组脑梗死面积百分比降低(P<0.05)。缺氧预处理增加大鼠脑组织中TRPC3 mRNA和蛋白的表达水平(P<0.05),MCAO则降低大鼠脑组织中TRPC3 mRNA和蛋白的表达水平(P<0.05),缺氧预处理可以拮抗MCAO对大鼠脑组织中TRPC3 表达的影响(P<0.05)。结论:缺氧预处理可以改善大鼠脑梗死损伤程度,其神经元保护作用可能与调控TRPC3的表达有关。
Abstract:
Aim:To investigate the neuroprotection effects of TRPC3 on hypoxia preconditioning and its possible mechanism.Methods: A total of 56 male SD rats were randomly allocated into 4 groups,14 rats in each group.The normal control group was fed with normal diet without hypoxia preconditioning or cerebral infarction.The infarction group was underwent the left middle cerebral artery occlusion(MCAO)by modified Longa method and without hypoxia preconditioning.The pretreatment group was treated with hypoxia preconditioning,but without MCAO.The hypoxia+infarction group was underwent MCAO after hypoxia preconditioning.Hypoxia preconditioning: rats were placed in a hypobaric oxygen chamber(simulated 5 000 m altitude,0.53×105 Pa,oxygen partial pressure 42 mmHg,1 mmHg=0.133 kPa)for 2 hours at 8:00 every day for 3 days,and MCAO was prepared 2 hours after hypoxia preconditioning.24 hours after MCAO,neurological function was evaluated(n=14),then the rat was decapitated and the percentage of cerebral infarction area(n=4)was determined by TTC staining,the expression of TRPC3 mRNA(n=6)in brain tissue was determined by real-time quantitative PCR,the expression of TRPC3 protein(n=4)was detected by immunohistochemistry.Results: The normal control group and hypoxia preconditioning group showed no neurologic deficit(score was 0),and TTC staining showed no cerebral infarction.Compared with those of the infarction group,the percentage of infarction area in the hypoxia+infarction group was lower(P<0.05).Hypoxia preconditioning increased the expressions of TRPC3 mRNA and protein(P<0.05),while MCAO decreased the expressions of TRPC3 mRNA and protein(P<0.05),hypoxia preconditioning antagonized the effects of MCAO on TRPC3 expression in rat brain(P<0.05).Conclusion: Hypoxia preconditioning can improve the degree of cerebral infarction injury in rats,and its neuroprotection effects may be related to regulating the expression of TRPC3 in the brain tissue.

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备注/Memo

备注/Memo:
【基金项目】国家自然科学基金面上项目(81870942)
【作者简介】吴睿,通信作者,男,1967年6月生,博士,主任医师,研究方向:脑血管病,E-mail:lvchenwutong@163.com
更新日期/Last Update: 2020-11-20