NDLI: Poloxamer-188 Can Attenuate Blood–Brain Barrier Damage to Exert Neuroprotective Effect in Mice Intracerebral Hemorrhage Model

Content Provider	Springer Nature Link
Author	Wang, Tao Chen, Xiping Wang, Zufeng Zhang, Mingyang Meng, Huanhuan Gao, Yuan Luo, Bin Tao, Luyang Chen, Yijiu
Copyright Year	2014
Abstract	Blood–brain barrier (BBB) disruption and brain edema formation play important roles in the secondary neuronal death and neurological dysfunction induced by intracerebral hemorrhage (ICH). Poloxamer 188 (P188), a multiblock copolymer surfactant, has been shown to be capable of sealing damaged cell membranes and decrease neuronal cell death. In this study, we explored whether P188 had a protective effect against ICH and its underlying mechanisms. Male ICR mice were subjected to infusion of type IV collagenase (to induce ICH) of saline (for shams) into the left striatum. The results showed that P188-12 mg post-treatment by tail intravenous injection significantly ameliorated the neurological symptoms and brain edema, attenuated BBB permeability, and decreased cell insults and injury volume at 24 and 72 h after ICH. Furthermore, P188 maintained the protein levels of tight junction (TJ) proteins including claudin-5, occludin, and zonula occludens-1, and reversed the increases of nuclear factor-kappaB (NF-κB), matrix metalloproteinase (MMP)-2, and MMP-9 protein expression at 72 h post ICH. Immunofluorescence showed P188 treatment rearranged the structure of TJ proteins in a continuous and linear pattern. Therefore, the present study concludes that P188 can protect against ICH, and the protective effect was associated with preventing BBB disruption through NF-κB-MMPs-mediated TJ proteins degradation.
Starting Page	240
Ending Page	250
Page Count	11
File Format	PDF
ISSN	08958696
Journal	Journal of Molecular Neuroscience
Volume Number	55
Issue Number	1
e-ISSN	15591166
Language	English
Publisher	Springer US
Publisher Date	2014-04-29
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Intracerebral hemorrhage Poloxamer 188 Blood–brain barrier Matrix metalloproteinases Tight junction Neurosciences Neurochemistry Cell Biology Proteomics Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Cellular and Molecular Neuroscience

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Anti-Necroptosis Chemical Necrostatin-1 Can Also Suppress Apoptotic and Autophagic Pathway to Exert Neuroprotective Effect in Mice Intracerebral Hemorrhage Model

Vascular disruption and blood–brain barrier dysfunction in intracerebral hemorrhage

Poloxamer-188 Attenuates TBI-Induced Blood–Brain Barrier Damage Leading to Decreased Brain Edema and Reduced Cellular Death

Deficiency of TREK-1 potassium channel exacerbates blood-brain barrier damage and neuroinflammation after intracerebral hemorrhage in mice

Mechanism of Low-Frequency Ultrasound in Opening Blood–Tumor Barrier by Tight Junction

Effects of Erythropoietin on Blood–Brain Barrier Tight Junctions in Ischemia–Reperfusion Rats

Specific Role of Tight Junction Proteins Claudin-5, Occludin, and ZO-1 of the Blood–Brain Barrier in a Focal Cerebral Ischemic Insult

Blood–brain barrier permeability change and regulation mechanism after subarachnoid hemorrhage

Profiling of Blood-Brain Barrier Disruption in Mouse Intracerebral Hemorrhage Models: Collagenase Injection vs. Autologous Arterial Whole Blood Infusion

Poloxamer-188 Can Attenuate Blood–Brain Barrier Damage to Exert Neuroprotective Effect in Mice Intracerebral Hemorrhage Model

Similar Documents

Anti-Necroptosis Chemical Necrostatin-1 Can Also Suppress Apoptotic and Autophagic Pathway to Exert Neuroprotective Effect in Mice Intracerebral Hemorrhage Model

Vascular disruption and blood–brain barrier dysfunction in intracerebral hemorrhage

Poloxamer-188 Attenuates TBI-Induced Blood–Brain Barrier Damage Leading to Decreased Brain Edema and Reduced Cellular Death

Deficiency of TREK-1 potassium channel exacerbates blood-brain barrier damage and neuroinflammation after intracerebral hemorrhage in mice

Mechanism of Low-Frequency Ultrasound in Opening Blood–Tumor Barrier by Tight Junction

Effects of Erythropoietin on Blood–Brain Barrier Tight Junctions in Ischemia–Reperfusion Rats

Specific Role of Tight Junction Proteins Claudin-5, Occludin, and ZO-1 of the Blood–Brain Barrier in a Focal Cerebral Ischemic Insult

Blood–brain barrier permeability change and regulation mechanism after subarachnoid hemorrhage

Profiling of Blood-Brain Barrier Disruption in Mouse Intracerebral Hemorrhage Models: Collagenase Injection vs. Autologous Arterial Whole Blood Infusion

Poloxamer-188 Can Attenuate Blood–Brain Barrier Damage to Exert Neuroprotective Effect in Mice Intracerebral Hemorrhage Model