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刺槐素腹腔注射对局灶性脑缺血小鼠脑再灌注损伤的预防作用及其机制 被引量:3

Preventive effect of intraperitoneal injection of acacetin on reperfusion injury in mice with focal cerebral ischemia
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摘要 目的观察刺槐素对局灶性脑缺血小鼠脑再灌注损伤的预防作用,并探讨其可能机制。方法 36只清洁级雄性C57BL/6J小鼠随机分为刺槐素组、模型组、对照组各12只,刺槐素组、模型组小鼠均制备局灶性脑缺血模型,刺槐素组于再灌注时腹腔注射刺槐素,模型组同时点给予等量0. 9%生理盐水;对照组小鼠仅分离颈内动脉,但不闭塞大脑中动脉,同时点给予等量刺槐素。制模24 h后,对各组小鼠进行神经功能评分,并测算小鼠脑梗死体积,计数小鼠海马区、皮层区离子钙接头蛋白1(Iba-1)阳性细胞数。结果刺槐素组、模型组、对照组小鼠神经功能评分分别为(1. 67±0. 52)、(2. 83±0. 41)、0分,刺槐素组与模型组比较,P <0. 05。刺槐素组、模型组、对照组小鼠梗死体积分别为(22. 15±3. 85)、(70. 48±12. 57)、0 mm^3,刺槐素组与模型组比较,P <0. 05。刺槐素组、模型组、对照组海马区Iba-1阳性细胞数分别为(8. 480±1. 633)、(12. 370±2. 150)、(3. 670±0. 790)个/HP,皮层区Iba-1阳性细胞数分别为(8. 330±0. 983)、(13. 130±1. 860)、(4. 470±0. 370)个/HP,刺槐素组、对照组分别与模型组比较,P均<0. 05。结论刺槐素对局灶性脑缺血小鼠脑再灌注损伤有预防作用,机制可能与抑制小胶质细胞的增殖及激活有关。 Objective To observe the preventive effect of acacetin on reperfusion injury in mice with focal cerebral ischemia and to explore its possible mechanism.Methods Thirty-six clean-grade male C57BL/6J mice were randomly divided into the acacetin group,model group,and control group,with 12 mice in each.The rats in the acacetin group and the model group were prepared for focal cerebral ischemia.The rats in the acacetin group were injected intraperitoneally with acacetin during reperfusion,and the rats in the model group were given 0.9%saline.In the control group,only the internal carotid artery was isolated,but the middle cerebral artery was not occluded,and the same amount of acacetin was administered at the same time.After 24 h of modeling,the neurological function scores were recorded in each group,and the infarct volume of the mice was measured.The number of Iba-1 positive cells in the hippocampus and cortex of mice was counted.Results The neurological function scores of the mice in the acacetin group,the model group,and the control group were 1.67±0.52,2.83±0.41,and 0,respectively;significant difference was found between the model group and acacetin group(P<0.05).The infarct volume of mice in the acacetin group,the model group,and the control group were(22.15±3.85),(70.48±12.57),and 0 mm 3,respectively.Compared with the model group,the infarct volume of the acacetin group significantly decreased(P<0.05).The number of Iba-1 positive cells in the hippocampus of the acacetin group,the model group,and the control group was(8.480±1.633),(12.370±2.150),(3.670±0.790)/HP,respectively;the number of Iba-1 positive cells in the cortical area was(8.330±0.983),(13.130±1.860),and(4.470±0.370)/HP,respectively;significant difference was found between the acacetin group and model group,and between the control group and model group(both P<0.05).Conclusion The acacetin has a preventive effect on reperfusion injury in mice with focal cerebral ischemia by inhibiting the proliferation and activation of microglia.
作者 马志 补娟 朱沂 MA Zhi;BU Juan;ZHU Yi(Xinjiang Clinical College of Anhui Medical University,Urumqi 830000,China)
出处 《山东医药》 CAS 2018年第39期39-42,共4页 Shandong Medical Journal
基金 新疆维吾尔自治区自然科学基金(2016D01C120)
关键词 缺血再灌注损伤 刺槐素 神经功能评分 脑梗死体积 小胶质细胞 离子钙接头蛋白1 ischemia-reperfusion injury acacetin neurological function scores infarct volume microglia Iba-1
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  • 1Lee SJ, Lee S. Toll-like receptors and inflammation in the CNS. Curr Drug Targets Inamm Allergy, 2002, 1:181-191.
  • 2Zwagerman N, Plumlee C, Guthikonda M, et al. Toll-like receptor- 4 and cytokine caseade in stroke after exercise. Neurol Res, 2010, 32: 123-126.
  • 3Walter S, Letiernbre M, Lin Y, et al. Role of the toll-like receptor 4 in neuroinflamrnation in Alzheimer's disease. Cell Physiol Biochem, 2007, 20: 947-956.
  • 4AravaUi RN, Peterson PK, Lokensgard JR. ToU-like receptors in defense and damage of the central nervotts system. J Neuroimmune Phamacol, 2007, 2: 297-312.
  • 5李鑫,毕桂南.核因子-κB在脑缺血预处理中的作用.国际脑虹管病杂志,2010,18:865-871.
  • 6Ridder DA, Schwaninger M. NF-κB sigmling in cerebral ischemia. Neuroscience, 2009, 158: 995-1006.
  • 7Longa EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral artery occlusion without craniectomy in rats. Stroke, 1989, 20: 84- 91.
  • 8Gao Y, Fang X, Tong Y, et al. TLR4-mediated MyD88-depcndent signaling pathway is activated by cerebral ischemia-reperfusion in cortex in mice. Biomed Phannacother, 2009, 63: 442-450.
  • 9Fan H, Li L, Zhang X, et al. Oxymatrine downregnlates TLR4, TLR2, MyD88, and NF-KB and protects rat brains against focal ischemia. Mediators Inflamm, 2009, 2009: 704706.
  • 10Akira S, Takeda K. Toll-like receptor sigaalling, Nat Rev Immunol, 2004, 4:499-511.

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