4.6 Article

Membrane-Free Stem Cell Extract Enhances Blood-Brain Barrier Integrity by Suppressing NF-κB-Mediated Activation of NLRP3 Inflammasome in Mice with Ischemic Stroke

期刊

LIFE-BASEL
卷 12, 期 4, 页码 -

出版社

MDPI
DOI: 10.3390/life12040503

关键词

membrane-free stem cell extract; ischemic stroke; blood-brain barrier; brain edema; matrix metalloproteinase; Toll-like receptor 4; NF-kappa B

资金

  1. National Research Foundation of Korea (MSIT) [NRF-2017M3A9E9032772, 2018R1A6A3A01011531]
  2. Ministry of Health and Welfare of Korea [HI17C2397]
  3. National Research Foundation of Korea [2017M3A9E9032772, 2018R1A6A3A01011531] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

Membrane-free stem cell extract (MFSCE) from human adipose tissues has positive effects on blood-brain barrier dysfunction and brain damage. Pretreatment with MFSCE can reduce infarct volume and edema, improve neurological and motor functions, and suppress inflammatory responses.
Membrane-free stem cell extract (MFSCE) of human adipose tissues possesses various biological activities. However, the effects of MFSCE on blood-brain barrier dysfunction and brain damage are unknown. In this study, we determined the role of MFSCE in an ischemic stroke mouse model. Mice were treated with MFSCE once daily for 4 days and 1 h before ischemic damage. Experimental ischemia was induced by photothrombosis. Pretreatment with MFSCE reduced infarct volume and edema and improved neurological, as well as motor functions. Evans blue leakage and water content in the brain tissue were reduced by MFSCE pretreatment relative to those in the vehicle group. MFSCE increased the expression of the tight junction proteins zonula occludens 1 and claudin-5, as well as vascular endothelial-cadherin, but decreased that of matrix metalloproteinase 9. Notably, MFSCE treatment decreased cell death and the level of NOD-like receptor protein 3 inflammasome, consistent with the downregulated expression of the pro-inflammatory cytokines interleukin (IL)-1 beta and IL-18 in the ischemic brain. These effects might have occurred via the suppression of the expression of Toll-like receptor 4 and activation of nuclear factor-kappa B. The results highlighted the potential of MFSCE treatment as a novel and preventive strategy for patients at a high risk of ischemic stroke.

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