[1]汪　雷　胡火军　马金阳　黄　松　董元训　王旭光　周有东.七叶皂苷钠对大鼠脑缺血再灌注损伤的保护作用[J].中国临床神经外科杂志,2021,26(08):616-621.[doi:10.13798/j.issn.1009-153X.2021.08.013]
　WANG Lei,HU Huo-jun,MA Jin-yang,et al.Protective effect of sodium aescinate on adult rats after cerebral ischemia-reperfusion injury[J].,2021,26(08):616-621.[doi:10.13798/j.issn.1009-153X.2021.08.013]
点击复制

七叶皂苷钠对大鼠脑缺血再灌注损伤的保护作用()
分享到：

《中国临床神经外科杂志》[ISSN:1009-153X/CN:42-1603/TN]

卷:
26
期数:
2021年08期
页码:
616-621
栏目:
实验研究
出版日期:
2021-08-25

文章信息/Info

Title:
Protective effect of sodium aescinate on adult rats after cerebral ischemia-reperfusion injury
文章编号:
1009-153X（2021）08-0616-06
作者:
汪　雷　胡火军　马金阳　黄　松　董元训　王旭光　周有东
Author(s):
WANG Lei;  HU Huo-jun;  MA Jin-yang;  HUANG Song;  DONG Yuan-xun;  WANG Xu-guang;  ZHOU You-dong.
Institute of Neurology, China Three Gorges University; Department of Neurosurgery, Yichang Central People’s Hospital, Yichang 441021, China
关键词:
脑缺血再灌注损伤; 七叶皂苷钠; 炎症反应; 氧化应激反应; 细胞凋亡
Keywords:
Cerebral ischemia-reperfusion injury;  Aescinate;  Adult rat;  Inflammation;  Oxidative stress;  Neuronal apoptosis
分类号:
R 743
DOI:
10.13798/j.issn.1009-153X.2021.08.013
文献标志码:
A
摘要:
目的 探讨七叶皂苷钠对大鼠脑缺血再灌注损伤的作用及机制。方法 60只成年SD大鼠随机分为假手术组、模型组和七叶皂苷钠组，各20只。采用线栓法建立大鼠局灶性大脑中动脉闭塞再灌注损伤模型，七叶皂苷钠组建模成功后1 h腹腔注射七叶皂苷钠（2.8 mg/kg），假手术组和模型组腹腔注射等量生理盐水。造模后24 h，使用Longa评分评估大鼠神经功能损伤程度，使用称重法检测大鼠脑水肿程度，使用ELISA法测定大鼠损伤脑组织超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、丙二醛（MDA）、肿瘤坏死因子（TNF-α）、白细胞介素6（IL-6）及白细胞介素1β（IL-1β）的含量，使用TUNEL法检测损伤脑组织神经元凋亡率，使用蛋白免疫印迹法检测损伤脑组织双特异性磷酸酶1（DUSP1）、核转录因子-κB（NF-κB）p65、Bcl-2及Bax蛋白的表达。结果 与假手术组比较，模型组大鼠Longa评分显著增加（P<0.01），脑含水量显著升高（P<0.01），损伤脑组织MDA、TNF-α、IL-1β和IL-6水平显著增高（P<0.001），损伤脑组织SOD和CAT水平显著降低（P<0.001），损伤脑组织神经元凋亡率显著升高（P<0.01），损伤脑组织DUSP1和Bcl-2蛋白表达水平显著降低（P<0.05），损伤脑组织NF-kB p65和Bax蛋白表达水平显著增高（P<0.05）。七叶皂苷钠显著逆转大鼠上述反应（P<0.05）。结论 七叶皂苷钠显著改善大鼠脑缺血再灌注损伤，机制可能与减轻炎症反应、氧化应激反应、神经元凋亡等有关。
Abstract:
Objective To explore the effect of sodium aescinate on the adult rats after cerebral ischemia-reperfusion injury (CIRI). Methods Sixty adult SD rats were randomly divided into sham operation group, model group and aescinate group, with 20 rats in each group. A rat model of focal middle cerebral artery occlusion and reperfusion injury was established by the modified Zea-Longa method. The aescinate group was intraperitoneally injected with sodium aescinate (2.8 mg/kg) 1 hour after the injury, and the sham operation and model groups were intraperitoneally injected with saline. Twenty-four hours after the injury, the Longa score was used to evaluate the neurological damage, the weighing method was used to detect the degree of brain edema, the ELISA method was used to detect the levels of superoxide dismutase (SOD) and catalase (CAT), malondialdehyde (MDA), tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β in the injured brain tissues, the TUNEL method was used to detect the neuronal apoptosis rate in the injured brain tissues, and the Western blotting was used to detect the expression levels of dual-specific phosphatase 1 (DUSP1), nuclear transcription factor-κB (NF-κB) p65, Bcl-2 and Bax in the damaged brain tissues. Results after CIRI, the Longa score was significantly increased (P<0.01), the brain water content, the neuronal apoptosis rate, the levels of MDA, TNF-α, IL-1β, IL-6 NF-kB p65 and Bax were significantly increased in the injured cerebral tissues (P<0.001), and the levels of SOD, CAT, DUSP1 and Bcl-2 were significantly reduced in the injured cerebral tissues (P<0.001). Sodium aescinate significantly reversed the above reactions in the CIRI rats (P<0.05). Conclusions Sodium aescinate significantly improves the CIRI in adult rats, and the mechanism may be related to reducing inflammation, oxidative stress, and neuronal apoptosis.

参考文献/References:

[1] Go AS, Mozaffarian D, Roger VL, et al. Heart disease and stroke statistics--2014 update: a report from the American Heart Association [J]. Circulation, 2014, 129(3): e28-e292.
[2] Nilupul Perera M, Ma HK, Arakawa S, et al. Inflammation following stroke [J]. J Clin Neurosci, 2006, 13(1): 1-8.
[3] Mizuma A, Yenari MA. Anti-inflammatory targets for the treatment of reperfusion injury in stroke [J]. Front Neurol, 2017, 8: 467.
[4] 贺斌峰，海　乐，魏征华，等. 七叶皂苷钠对模拟高原低氧大鼠脑损伤的干预作用及对水通道蛋白4表达的影响[J]. 中国急救医学，2012，32（1）：47-50.
[5] 刘士民. 大鼠局灶脑缺血/再灌注模型缺血神经元损伤和胶质细胞反应以及TGFβ表达的时空关系[D]. 中国协和医科大学，1997.
[6] Wang YK, Han J, Xiong WJ, et al. Evaluation of in vivoanti-oxidant and immunity enhancing activities of sodium aescinate injection liquid [J]. Molecules, 2012, 17(9):10267-10275.
[7] Longa EZ, Weinstein PR, Carlson S, et al. Reversible middlecerebral artery occlusion without craniectomy in rats [J]. Stroke, 1989, 20(1): 84-91.
[8] Khadir A, Tiss A, Abubaker J, et al. MAP kinase phospha-tase DUSP1 is overexpressed in obese humans and modula-ted by physical exercise [J]. Am J Physiol Endocrinol Metab, 2015, 308(1): E71-83.
[9] Kapoor D, Trikha D, Vijayvergiya R, et al. Conventional therapies fail to target inflammation and immune imbalance in subjects with stable coronary artery disease: a system-based approach [J]. Atherosclerosis, 2014, 237(2): 623-631.
[10] Wu R, Li X, Xu P, et al. TREM2 protects against cerebral ischemia/reperfusion injury [J]. Mol Brain, 2017, 10(1): 20.
[11] Fonarow GC, EE Smith, Saver JL, et al. Timeliness of tissue-type plasminogen activator therapy in acute ischemic stroke:patient characteristics, hospital factors, and outcomes asso-ciated with door-to-needle times within 60 minutes [J].Circulation, 2011, 123(7): 750-758.
[12] Wu H, Tang C, Tai LW, et al. Flurbiprofen axetil attenuates cerebral ischemia reperfusion injury by reducing inflam-mation in a rat model of transient global cerebral ischemia reperfusion [J]. Biosci Rep, 2018, 38(4): BSR20171562.
[13] Khandelwal P, Yavagal DR, Sacco RL. Acute ischemic stroke intervention [J]. J Am Coll Cardiol, 2016, 67(22):2631-2644.
[14] Zhu Y, Guan YM, Huang HL, et al. Human umbilical cord blood mesenchymal stem cell transplantation suppresses inflammatory responses and neuronal apoptosis during early stage of focal cerebral ischemia in rabbits [J]. Acta Pharmacol Sin, 2014, 35(5): 585-591.
[15] Letteria M, Domenico P, Mariagrazia R, et al. ROS-mediated NLRP3 inflammasome activation in brain, heart, kidney, and testis ischemia/reperfusion injury [J]. Oxid Med Cell Long, 2016, 2016: 2183026.
[16] Maslov LN, Naryzhnaia NV, Podoksenov IK, et al. Reactive oxygen species are triggers and mediators of an increase in cardiac tolerance to impact of ischemia-reperfusion [J]. Ross Fiziol Zh Im I M Sechenova, 2015, 101(1): 3-24.
[17] 王大贵，李　梅，李　竣，等. 七叶皂苷钠对小鼠变应性接触性皮炎作用研究[J]. 中国民族民间医药，2020，29（1）：8-12.
[18] 范永会，王星利，张永丽，等. 七叶皂苷钠通过上调SOCS-1表达抑制脑内出血诱发的炎症反应[J]. 实用药物与临床，2018，21（6）：632-636.
[19] Chuang HC, Tan TH. MAP4K family kinases and DUSP family phosphatases in T-cell signaling and systemic lupuserythematosus [J]. Cells, 2019, 8(11): 1433.
[20] Auger-Messier M, Accornero F, Goonasekera SA, et al.Unrestrained p38 MAPK activation in Dusp1/4 double-null mice induces cardiomyopathy [J]. Circ Res, 2013; 112(1):48-56.
[21] Li S, Hao G, Li J, et al. Comparative analysis of dual speci-ficity protein phosphatase genes 1, 2 and 5 in response to immune challenges in Japanese flounder Paralichthys olivaceus [J]. Fish Shellfish immunol, 2017, 68: 368-376.
[22] Jin Q, Li R, Hu N, et al. DUSP1 alleviates cardiac ischemia/reperfusion injury by suppressing the Mff-required mito-chondrial fission and Bnip3-related mitophagy via the JNK pathways [J]. Redox biology, 2018, 14: 576-587.
[23] Gil-Araujo B, Lobo MT, Gutiérrez-Salmerón M, et al. Dual specificity phosphatase 1 expression inversely correlates with NF-κB activity and expression in prostate cancer and promotes apoptosis through a p38 MAPK dependent mechanism [J]. Mol Oncol, 2014, 8(1): 27-38.
[24] Gaynor RB, Williams NS, Scoggin S, et al. Identification of NF-kappaB-regulated genes induced by TNFalpha utilizingexpression profiling and RNA interference [J]. Oncogene, 2004, 22(13): 2054-2064.

相似文献/References:

[1]黄　坦　黄书岚　陈谦学.NaHS抑制Nox4 和 p22p hox的表达保护小鼠脑缺血再灌注损伤[J].中国临床神经外科杂志,2016,(09):545.[doi:10.13798/j.issn.1009-153X.2016.09.011]
　HUANG Tan,HUANG Shu-lan,CHEN Qian-xue..NaHS induces neuroprotection against cerebral ischemia reperfusion injury by inhibiting Nox4 and p22phox expressions in cerebral tissues in mice[J].,2016,(08):545.[doi:10.13798/j.issn.1009-153X.2016.09.011]
[2]任大斌　郑　平　冯九庚　段　剑　邹树峰　洪　涛　赵　麟　陈　伟.抑制ERK1/2对大鼠脑缺血再灌注损伤的保护作用[J].中国临床神经外科杂志,2019,(05):295.[doi:10.13798/j.issn.1009-153X.2019.05.012]
　REN Da-bin,ZHENG Ping,FENG Jiu-geng,et al.Protective effetc of inhbition of ERK1/2 on rats after cerebral ischemia-repufusion injury[J].,2019,(08):295.[doi:10.13798/j.issn.1009-153X.2019.05.012]
[3]曹瑜,邢丹.阿托伐他汀对大鼠脑缺血再灌注损伤后神经细胞焦亡的影响[J].中国临床神经外科杂志,2024,29(02):92.[doi:10.13798/j.issn.1009-153X.2024.02.007]
　CAO Yu,XING Dan.Effect of atorvastatin on neuronal pyroptosis in rats after cerebral ischemia-reperfusion injury[J].,2024,29(08):92.[doi:10.13798/j.issn.1009-153X.2024.02.007]

备注/Memo

备注/Memo:
作者单位：441021 湖北宜昌，三峡大学神经病学研究所/宜昌市中心人民医院神经外科（汪　雷、胡火军、马金阳、黄　松、董元训、王旭光、周有东）
通讯作者：马金阳，E-mail：514632999@qq.com
更新日期/Last Update: 1900-01-01