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在雌性C57BL/6小鼠多发性硬化症动物模型中,MS14下调脊髓组织中脂质运载蛋白2的表达。

MS14 down-regulates lipocalin2 expression in spinal cord tissue in an animal model of multiple sclerosis in female C57BL/6.

作者信息

Ebrahimi-Kalan Abbas, Soleimani Rad Jafar, Kafami Laya, Mohammadnejad Daryoush, Habibi Roudkenar Mehryar, Khaki Amir Afshin, Aliyari Serej Zeynab, Mohammadi Roushandeh Amaneh

出版信息

Iran Biomed J. 2014;18(4):196-202. doi: 10.6091/ibj.1375.2014.

DOI:10.6091/ibj.1375.2014
PMID:25326017
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4225058/
Abstract

Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis, which is a demyelinating and an inflammatory disease of central nervous system. Recent studies have established that some molecules such as Lipocaline2 (LCN2), which expresses during inflammatory conditions, play an important role in EAE pathogenesis and might involve in its treatment process. Recently, it has been proved that MS14, an herbal-marine drug, has anti-inflammatory properties through reduction of TNF-α and IL-1β. Thus, the present study investigated the effects of MS14 on the course of EAE and its relation to LCN2 expression in both protein and gene levels. EAE was induced in female C57BL/6 mice using Hooke kits. Animals were scored for clinical signs of the disease according to a 10-point EAE scoring system. On 21 and 35 days after immunization, mice (n = 4/group) were deeply anesthetized, and the spinal cords were removed. Inflammatory cell infiltration and LCN2 expression in spinal cord were assessed by hematoxylin and eosin staining, immuno-histochemistry, and real-time PCR methods. MS14 significantly ameliorated EAE symptoms and decreased lymphocyte infiltration into the spinal cord (<0.05). Our data also revealed that LCN2 expression was significantly down-regulated in acute and chronic phases of EAE both at protein and gene levels after MS14 treatment (<0.05). The results demonstrated that MS14 regulatory effect on EAE is accompanied by LCN2 down-regulation after treatment with the herb; however, more studies are required for clarifying the other involved mechanisms.

摘要

实验性自身免疫性脑脊髓炎(EAE)是多发性硬化症的动物模型,多发性硬化症是一种中枢神经系统的脱髓鞘和炎症性疾病。最近的研究表明,一些分子,如在炎症条件下表达的脂质运载蛋白2(LCN2),在EAE发病机制中起重要作用,并且可能参与其治疗过程。最近,已证明一种草药-海洋药物MS14通过降低TNF-α和IL-1β具有抗炎特性。因此,本研究在蛋白质和基因水平上研究了MS14对EAE病程的影响及其与LCN2表达的关系。使用胡克试剂盒在雌性C57BL/6小鼠中诱导EAE。根据10分EAE评分系统对动物的疾病临床症状进行评分。在免疫后第21天和第35天,将小鼠(每组n = 4)深度麻醉,然后取出脊髓。通过苏木精和伊红染色、免疫组织化学和实时PCR方法评估脊髓中的炎性细胞浸润和LCN2表达。MS14显著改善了EAE症状,并减少了淋巴细胞向脊髓的浸润(<0.05)。我们的数据还显示,在MS14治疗后,EAE的急性和慢性期LCN2表达在蛋白质和基因水平上均显著下调(<0.05)。结果表明,MS14对EAE的调节作用伴随着该草药治疗后LCN2的下调;然而,需要更多的研究来阐明其他涉及的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ce7/4225058/7366c50e007c/ibj-18-196-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ce7/4225058/86327a11bea1/ibj-18-196-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ce7/4225058/d237bad2aa62/ibj-18-196-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ce7/4225058/76f851bfa64c/ibj-18-196-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ce7/4225058/7366c50e007c/ibj-18-196-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ce7/4225058/86327a11bea1/ibj-18-196-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ce7/4225058/d237bad2aa62/ibj-18-196-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ce7/4225058/76f851bfa64c/ibj-18-196-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ce7/4225058/7366c50e007c/ibj-18-196-g004.jpg

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