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血必净在心肺复苏大鼠脑损伤中的神经保护作用
Neuroprotective effect of Xuebijing following the brain injury in the rat after cardiopulmonary resuscitation
目的 探讨中成药血必净对心肺复苏模型大鼠脑损伤的神经保护作用及相关机制。 方法 采用Utstein模式建立心肺复苏大鼠模型，45只SD大鼠随机分成假手术组、血必净组和生理盐水组。血必净组和生理盐水组在建立心肺复苏大鼠模型后分别给予腹腔注射血必净和生理盐水。10d后采集鼠脑连冷冻切片后利用3D-Doctor三维重建血必净组和生理盐水组大鼠脑损伤区域并测算脑损伤面积与体积；TUNEL法检测各组大鼠脑损伤区域神经细胞凋亡情况。 结果 成功建立心肺复苏大鼠模型，模型制作成功率50%；三维重建生理盐水组和血必净组大鼠鼠脑，经3D-Doctor4.0测算，血必净组鼠脑皮质损伤面积和梗死灶体积均低于生理盐水组.P<0.05；心肺复苏模型大鼠脑损伤区周围皮质出现凋亡细胞；给予血必净治疗后，与生理盐水组比较，血必净可以下调损伤区周围皮质神经细胞的凋亡指数（AI)。 结论 大鼠心肺复苏脑损伤后，给予血必净治疗后能减少大鼠脑内皮质损伤区面积和梗死灶体积, 抑制损伤区周围皮质神经细胞的凋亡，具有神经保护作用。
Objective To explore the effect of Chinese medicine Xuebijing against post cardiopulmonary-resuscitatied brain injury in rats and the related mechanisms involved.
Methods The rat model of cardiopulmonary-resuscitatied brain injury was established according to the model of Utstein. The rats were randomly divided into 3 groups: Sham group, Xuebijing group and physiological saline group. After the rat model of cardiopulmonary-resuscitatied brain injury had been established in Xuebijing group and physiological saline group, Xuebijing or physiological saline were injected into cardiopulmonary resuscitation model rats by intraperitoneal injection respectively. At 10 days after establishment rat model of cardiopulmonary resuscitatied brain injury, the continuous rat brain frozen sections were acquired to reconstruct theion rat brain by 3D-Doctor, and the volumes of the damaged region in the rat brain were calculated by 3D-Doctor. Frozen sections of brain damaged tissues were subjected to detect apoptotic cells by using the terminal deoxynucleotide transferase dUTP nick end labeling(TUNEL) assay. Results The rat model of cardiopulmonary-resuscitatied brain injury was established successfully,with 50% of thewhich success ratepercentage was 50%. Rat brains in physiological saline group and Xuebijing group were reconstructed successfully by 3D-Doctor, which showed the volume of infarction in Xuebijin group reduced significantly compared with that of the physiological saline group. TUNEL assay showed that apoptotic reaction occurred in the cortex around the injury site. After treatment with Xuebijing, the apoptosis index (AI) was significantly decreased compared with that of physiological saline group. Conclusion For cardiopulmonary resuscitatied brain damage in rats, intraperitoneal injection of Xuebijing can reduce the rat brain cortex injured area and infarct size. Xuebijing can also inhibit neural cells apoptosis around damaged cortex, which has the neuroprotective effect on brain injury in the rat after cardiopulmonary resuscitation.
心肺复苏脑损伤 / 血必净 / 神经保护 / 三维重建 / 大鼠
Cardiopulmonary-resuscitatied brain injury / Xuebijing / Neuroprotection / 3D reconstruction / Rat
［1］Nadkarni VM, Larkin GL, Peberdy MA,et al. First documented rhythm and clinical outcome from inhospital cardiac arrest among children and adults ［J］. JAMA, 2006, 295(1): 50-57.
［2］Laver S, Farrow C, Turner D, et al. Mode of death after admission to an intensive care unit following cardiac arrest ［J］.Intensive Care Med, 2012, 30(2): 2126-2128.
［3］Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology,pathophysiology,treatment, and prognostication. A consensus statement from the international liaison committee on resuscitation ［J］. Circulation,2008, 118(23): 2452-2483.
［4］Basu S, Liu X, Nozari A, et al. Evidence for time-dependent maximum increase of free radical damage and eicosanoid formation in the brain as related to duration of cardiac arrest and cardiac-pulmonary resuscitation［J］. Free Radical Res,2003, 37(11):251-256.
［5］Liu XL, Wiklund L, Nozari A, et al. Differences in cerebral reperfusion and oxidative injury after cardiac arrest ［J］. Acta Anaesthesiol Scand, 2003, 47(8): 958-967.
［6］Wang WT,Xu ZhJ,Li LN, et al. The intervention of ligustrazine on nitric oxide and endothelin of experimental myocardial ischemia reperfusion injury［J］. Chinese Journal of Pathophysiology,2011, 17(3):230-233. (in Chinese)
王万铁, 徐正祄, 林丽娜, 等. 川芎嗪对实验性心肌缺血再灌注损伤中一氧化氮和内皮素的干预 ［J］. 中国病理生理杂志, 2011,17(3): 230-233.
［7］Xu ZhJ,Wang WT,Li D,et al.The protective effect of ligustrazine on lipid peroxidation with the ischemia-reperfusion injury of rat liver［J］. Chinese Journal of Applied Physiology, 2012,18(2):173-177. (in Chinese)
徐正祄, 王万铁, 李东, 等. 川芎嗪对肝缺血/再灌注损伤脂质过氧化的影响 ［J］. 中国应用生理杂志,2012,18(2): 173-177.
［8］Dris AH, Beeker LB, Omato JP, et al. Utsetin-style guidelines of uniform reporting of laboratory CPR research［J］. Circulation,1996, 94(3): 2324-2336.
［9］Housseini AM, Bozlar U, Schmitt TM, et al. Comparison of three-dimensional rotational angiography and digital subtraction angiography for the evaluation of the liver transplants［J］. Clin Imaging, 2009, 33(2):102-109.
［10］Weninger WJ, Meng S, Streicher J, et al. A new episcopic method for rapid 3-D reconstruction: applications in anatomy and embryology ［J］. Anat Embryol (Berl)，1998, 197(5):341-348.
［11］Casselman J, Mermuys K, Delanote J, et al. MRI of crainal nerves-more than meets the eye: technical considerations and advanced anatomy ［J］. Neuroimaging Clin N Am, 2008, 18(2):197-231.
［12］Sun X, Cheng G, Hao M, et al. CXCL12/CXCR4/CXCR7 chemokine axis and cancer progression［J］. Cancer Metastasis Rev, 2010, 29(4): 709-722.
［13］Imitola J, Raddassi K, Park KI, et al. Directed migration of neural stem cells to sites of CNS injury by the stromal cell-derived factor 1alpha/CXC chemokine receptor 4 pathway ［J］. Proc Nati Acad Sci USA, 2004, 101(52): 18117-18122.
［14］Tapias V, Escames G, López LC, et al. Melatonin and its brain metabolite N(1)-acetyl-5-methoxykynuramine prevent mitochondrial nitric oxide synthase induction in parkinsonian mice ［ J］. J Neurosci Res, 2009, 87(2):3002-3010.
［15］Richardson RM, Sun D, Bullock MR. Neurogenesis after traumatic brain injury ［J］. Neurosurg Clin N Am, 2007, 18(1): 169-181.
［16］Wang X, Figueroa BE, Stavrovskaya IG, et al. Methazolamide and melatonin inhibit mitochondrial cytochrome C release and are neuroprotective in experimental models of ischemic injury ［J］. Stroke, 2009, 40(5): 1877-1885.
［17］Clark RS, Kochanek PM, Watkins SC, et al. Caspase-3 mediated neuronal death after traumatic brain injury in rats ［J］. J Neurochem, 2000, 74(2): 740-753.
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