Abstract:
OBJECTIVE:The aim of this study was to explore whether Dl-3-n-butylphthalide (DBT) could protect blood-brain barrier (BBB) of mice with experimental cerebral infarction and the relevant mechanism. MATERIALS AND METHODS:Adult male CD-1 mice were selected as the study objects. The permanent middle cerebral artery occlusion (MCAO) model was prepared by Longa's modified suture-occluded method. The mice were randomly divided into 3 groups: the sham operation group (Sham group), the cerebral infarction model group (CI group) and the DBT (120 mg/kg) intervention group (DBT group). Neurologic function deficits were evaluated by Longa's modified scoring method after 24 h of permanent MCAO. The wet and dry weight method was used for measuring water content in brain tissues. 2% 2,3,5-triphenyltetrazolium chloride (TTC) staining method was applied to determine the volume of cerebral infarction. Changes in the protein and messenger ribonucleic acid (mRNA) expression levels of matrix metallopeptidase 9 (MMP-9), claudin-5, vascular endothelial growth factor (VEGF), glial fibrillary acidic protein (GFAP), NF-E2 related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1) in ischemic brain tissues were detected using immunohistochemistry, Western blotting and quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). Ultrastructure changes in BBBs were observed under an electron microscope. RESULTS:DBT improved the neurologic function deficits of mice and reduced the infarction volume of mice with cerebral infarction. DBT alleviated edema and decreased the permeability of BBBs of mice with cerebral infarction. DBT down-regulated the expression of MMP-9 and up-regulated the expression of claudin-5 in brain tissues of mice with cerebral infarction. DBT increased the expressions of VEGF and GFAP. DBT improved the ultrastructure in capillary endothelial cells of BBBs and increased the expressions of Nrf-2 and HO-1. CONCLUSIONS:DBT may protect BBB by activating the Nrf-2/HO-1 signaling pathway, thus achieving its protective effect on the brain.
journal_name
Eur Rev Med Pharmacol Scijournal_title
European review for medical and pharmacological sciencesauthors
Zhao YJ,Nai Y,Ma QS,Song DJ,Ma YB,Zhang LH,Mi LXdoi
10.26355/eurrev_201804_14744subject
Has Abstractpub_date
2018-04-01 00:00:00pages
2109-2118issue
7eissn
1128-3602issn
2284-0729journal_volume
22pub_type
杂志文章abstract:BACKGROUND:Breast cancer is categorized into two broad groups: estrogen receptor positive (ER+) and ER negative (ER-) groups. Previous study proposed that under trastuzumab-based neoadjuvant chemotherapy, tumor initiating cell (TIC) featured ER- tumors response better than ER+ tumors. Exploration of the molecular diffe...
journal_title:European review for medical and pharmacological sciences
pub_type: 杂志文章
doi:
更新日期:2014-01-01 00:00:00
abstract:OBJECTIVE:In this study, we investigated whether circulating microRNA-137 (miR-137) could be a potential biomarker for patients with glioblastoma (GBM). PATIENTS AND METHODS:Serum samples were collected from 64 GBM patients and 64 healthy controls. The expression level of circulating miR-137 was compared by quantitati...
journal_title:European review for medical and pharmacological sciences
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更新日期:2016-09-01 00:00:00
abstract:OBJECTIVE:Atherosclerosis is featured as artery wall thickness as a result of invasion and accumulation of white blood cells and proliferation of intimal smooth muscle cells. Endothelial dysfunction has been linked to a variety of vascular diseases, including atherosclerosis. MicroRNAs play essential roles during the a...
journal_title:European review for medical and pharmacological sciences
pub_type: 杂志文章
doi:
更新日期:2016-07-01 00:00:00
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journal_title:European review for medical and pharmacological sciences
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doi:10.26355/eurrev_202012_24204
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pub_type: 杂志文章,评审
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更新日期:2008-08-01 00:00:00
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journal_title:European review for medical and pharmacological sciences
pub_type: 杂志文章,收录出版
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