切换至 "中华医学电子期刊资源库"
高级检索
中华神经创伤外科电子杂志

中华神经创伤外科电子杂志 ›› 2018, Vol. 04 ›› Issue (02) : 98 -102. doi: 10.3877/cma.j.issn.2095-9141.2018.02.008

所属专题： 文献；

基础研究

Mcc950对小鼠脑创伤后神经元树突棘的保护作用
吴毅1, 刘镛2, 陈旭1, 刘成辉1,†()   
  1. 1. 528000　佛山市南海区人民医院神经外科
    2. 524400　湛江，广东医科大学药学院
  • 收稿日期:2018-03-06 出版日期:2018-04-15
  • 通信作者: 刘成辉

Protective function of Mcc950 on dendritic spine in mice after traumatic brain injury

Yi Wu1, Yong Liu2, Xu Chen1, Chenghui Liu1,†()   

  1. 1. Department of Neurosurgery, Nanhai Area People’s Hospital, Foshan 528000, China
    2. College of Pharmacy, Guangdong Medical University, Zhanjiang 524400, China
  • Received:2018-03-06 Published:2018-04-15
  • Corresponding author: Chenghui Liu
  • About author:
    Corresponding author: Liu Chenghui, Email:
全文 ( ) 下载PDF ( ) 导出引用
引用本文：

吴毅, 刘镛, 陈旭, 刘成辉. Mcc950对小鼠脑创伤后神经元树突棘的保护作用[J]. 中华神经创伤外科电子杂志, 2018, 04(02): 98-102.

Yi Wu, Yong Liu, Xu Chen, Chenghui Liu. Protective function of Mcc950 on dendritic spine in mice after traumatic brain injury[J]. Chinese Journal of Neurotraumatic Surgery(Electronic Edition), 2018, 04(02): 98-102.

目的

研究Nod样受体蛋白3（NLRP3）抑制剂Mcc950对小鼠脑创伤后神经元树突棘的保护作用。

方法

选取60只C56BL/6J成年小鼠通过液压打击的方法建立小鼠多次脑创伤模型，然后将小鼠随机分为对照组、生理盐水组、Mcc950组各20只进行创伤后的处理，8个月时取小鼠脑组织进行高尔基染色计数神经元树突棘计数比较，以分析Mcc950对神经元树突棘的保护效应，并取脑皮层蛋白进行蛋白印记实验分析树突棘调节蛋白差异。

结果

30 μm长树突上树突棘的数量：Mcc950组（32.080±1.831）明显高于对照组（20.820±2.252）和生理盐水组（19.380±1.623），差异具有统计学意义（Mcc950组vs对照组：t=3.921，P=0.001；Mcc950组vs生理盐水组：t=5.187，P<0.001；对照组vs生理盐水组：t=0.527，P=0.603）。Mcc950组在PSD95、Profilin1以及GTPase HRAS的表达量均明显高于对照组和生理盐水组，差异具有统计学意义（Mcc950组比较于对照组和生理盐水组表达倍数分别是：PSD95：4.64，4.34；Profilin1：4.43，4.47；GTPase HRAS：2.97，3.03。PSD95：对照组vs Mcc950组：t=8.880，P=0.012，生理盐水组vs Mcc950组：t=7.248，P=0.002；Profilin1：对照组vs Mcc950组：t=6.654，P=0.022，生理盐水组vs Mcc950组：t=5.340，P=0.033；GTPase HRAS：对照组vs Mcc950组：t=5.092，P=0.036，生理盐水组vs Mcc950组：t=4.469，P=0.047）。

结论

Mcc950作为NLRP3的抑制剂，对脑创伤后神经元树突棘数量的稳定具有保护效应。

关键词: Mcc950, 炎性小体, Nod样受体蛋白3, 树突棘
Objective

To explore the function of Nod-like receptor protein 3 (NLRP3) inhibitor Mcc950 on the dendritic spine.

Methods

Establishing traumatic brain injury mouse model via pressure hitting in 60 C56BL/6J adult mice, then average the mice into three different groups based on manage process after brain injury: group control, group with normal saline, group Mcc950. After 8 months, detect the dendritic spine by Golgi-Cox staining and detect the dendritic spine regulatory protein by Western Blot.

Results

The number of 30 μm dendritic spine in group Mcc950 (32.08±1.831) is higher than group control (20.82±2.252) and group normal (19.38±1.623) saline significantly (group control vs group Mcc950: t=3.921, P=0.0007; group normal saline vs group Mcc950: t=5.187, P<0.0001). The expression level of dendritic regulatory protein PSD95, Profilin1 and GTPase HRAS are higher in group Mcc950 than group control and group normal saline, the difference is significantly (The times of expression level group Mcc950 compare to group control and group normal saline of these protein are: PSD95: 4.64, 4.34; Profilin1: 4.43, 4.47; GTPase HRAS: 2.97, 3.03. PSD95: group control vs group Mcc950: t=8.880, P=0.012, group normal saline vs group Mcc950: t=7.248, P=0.002; Profilin1: group control vs group Mcc950: t=6.654, P=0.022; group normal saline vs group Mcc950: t=5.340, P=0.033; GTPase HRAS: group control vs group Mcc950: t=5.092, P=0.036, group normal saline vs group Mcc950: t=4.469, P=0.047).

Conclusion

Mcc950, a NLRP3 inhibitor, plays a protective role in dendritic spine number after traumatic brain injury in mice.

Key words: Mcc950, Inflammasome, Nod-like receptor protein 3, Dendritic spine
图1 3组的8月龄小鼠大脑皮层神经元树突棘分析
图2 Mcc950对树突棘调节蛋白的影响
[1]
Ismael S,Nasoohi S,Ishrat T. MCC950, the selective NLRP3 inflammasome inhibitor protects mice against traumatic brain injury[J]. J Neurotrauma, 2018, Epub ahead of print.
[2]
van der Heijden T,Kritikou E,Venema W, et al. NLRP3 inflammasome inhibition by Mcc950 reduces atherosclerotic lesion development in apolipoprotein E-deficient mice-brief report[J]. Arterioscler Thromb Vasc Biol, 2017, 37(8): 1457-1461.
[3]
van Hout GP,Bosch L,Ellenbroek GH, et al. The selective NLRP3-inflammasome inhibitor MCC950 reduces infarct size and preserves cardiac function in a pig model of myocardial infarction[J]. Eur Heart J, 2017, 38(11): 828-836.
[4]
Chin LH,Hsu YJ,Hsu SC, et al. The regulation of NLRP3 inflammasome expression during the development of cardiac contractile dysfunction in chronic kidney disease[J]. Oncotarget, 2017, 8(69): 113303-113317.
[5]
Wan Z,Wen W,Ren K, et al. Involvement of NLRP3 inflammasome in the impacts of sodium and potassium on insulin resistance in normotensive Asians[J]. Br J Nutr, 2018, 119(2): 228-237.
[6]
Torres MD,Garcia O,Tang C, et al. Dendritic spine pathology and thrombospondin-1 deficits in Down syndrome[J]. Free Radic Biol Med, 2018, 114: 10-14.
[7]
Padamsey Z,McGuinness L,Emptage NJ. Inhibition of lysosomal Ca(2+) signalling disrupts dendritic spine structure and impairs wound healing in neurons[J]. Commun Integr Biol, 2017, 10(5-6): e1344802.
[8]
郭国庆,查彩慧.树突棘AMPA受体转运的细胞骨架机制[J].暨南大学学报(自然科学与医学版), 2017, 38(1): 13-19.
[9]
Rosoklija GB,Petrushevski VM,Stankov A, et al. Reliable and durable Golgi staining of brain tissue from human autopsies and experimental animals[J]. J Neurosci Methods, 2014, 230: 20-29.
[10]
马丽娜,王蓉.大脑发育调节脑蛋白对神经元树突棘及突触可塑性的影响[J].中华老年心脑血管病杂志, 2013, 15(10): 1109-1111.
[11]
Alkam D,Feldman EZ,Singh A, et al. Profilin1 biology and its mutation, actin(g) in disease[J]. Cell Mol Life Sci, 2017, 74(6): 967-981.
[12]
Merchant B,Edelstein-Keshet L,Feng JJ. A Rho-GTPase based model explains spontaneous collective migration of neural crest cell clusters[J]. Dev Biol, 2018, Epub ahead of print.
[13]
Groswasser Z,Peled I. Survival and mortality following TBI[J]. Brain Inj, 2018, 32(2): 149-157.
[14]
梁芯,唐静,张杨,等.抑郁症CUS模型大鼠海马CA1区及CA3区内树突棘数目减少[J].中国组织化学与细胞化学杂志, 2016, 25(1): 59-66.
[1] 郑娟红, 陈怡. 重症溃疡性结肠炎患者血清NOD样受体蛋白3、半胱氨酸天冬氨酸特异性蛋白酶1和核因子κB mRNA表达水平及临床意义[J]. 中华危重症医学杂志(电子版), 2019, 12(01): 31-36.
[2] 孙超, 黄华星, 邓献. 核苷酸结合寡聚化结构域样受体蛋白3炎性小体、炎性因子、半胱氨酸天冬氨酸蛋白酶-1与烧伤合并吸入性损伤预后的相关性分析[J]. 中华损伤与修复杂志(电子版), 2020, 15(06): 428-433.
[3] 季媛, 魏巴金. NLRP3炎性小体在器官移植不良反应发病机制中的研究进展[J]. 中华移植杂志(电子版), 2023, 17(05): 308-312.
[4] 雷莲莲, 李力, 毕婧. 胃饥饿素对小鼠急性肺损伤的保护作用及其机制研究[J]. 中华细胞与干细胞杂志(电子版), 2021, 11(02): 83-89.
[5] 姬丽娅, 姬昂, 狄政莉, 熊婧, 刘志勤, 薛秀云, 费晓炜, 豆雅楠, 王利. 叶酸通过NLRP3/ASC/Caspase-1信号通路对HT22细胞拟帕金森损伤作用的研究[J]. 中华神经创伤外科电子杂志, 2022, 08(04): 196-203.
[6] 姜硕, 王梦楠, 赵慧颖, 郭晓夏, 王慧霞, 安友仲. cGAS/STING通过NLRP3炎性小体调控人肺微血管内皮细胞炎症的作用机制[J]. 中华重症医学电子杂志, 2021, 07(03): 233-240.
[7] 武文君, 沙莎, 田聪, 朱建. 急性心肌梗死老年患者NLRP3基因多态性与炎症指标的关联性[J]. 中华临床医师杂志(电子版), 2022, 16(03): 241-245.
阅读次数
全文


摘要

版权所有 中华医学会 中华医学电子音像出版社有限责任公司  京ICP备14006079号-1  网络出版服务许可证：(署)网出证(京)字第075号