The Activation of PhosphatidylserineCD36TGF-β1 Pathway prior to Surgical Brain Injury Attenuates Neuroinflammation in Rats
Joint Authors
Zhang, John H.
Tang, Jiping
Tang, Hailiang
Lenahan, Cameron
Huang, Lei
Sherchan, Prativa
Boling, Warren
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-13, 13 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-08-12
Country of Publication
Egypt
No. of Pages
13
Main Subjects
Abstract EN
Neuroinflammation plays an important pathological role in experimental surgical brain injury (SBI).
Apoptotic associated with phosphatidylserine (PS) externalization promotes anti-inflammatory mediator TGF-β1 release.
In the present study, we investigated the anti-neuroinflammation effect of PS liposome or isoflurane pretreatment via PS/CD36/TGF-β1 signaling in a rat model of SBI.
A total of 120 male Sprague-Dawley rats (weighing 280-330 gms) were used.
SBI was induced by partial right frontal lobe corticotomy.
Intranasal PS liposome or isoflurane inhalation was administered prior to SBI induction.
CD36 small interfering RNA (siRNA) was administered intracerebroventricularly.
Recombinant Annexin V protein (rAnnexin V) was delivered intranasally.
Post-SBI assessments included neurological tests, brain water content, Western blot, and immunohistochemistry.
Endogenous CD36 protein levels but not TGF-β1 was significantly increased within peri-resection brain tissues over 72 h after SBI.
SBI rats were associated with increased brain water content surrounding corticotomy and neurological deficits.
PS liposome pretreatment significantly reduced brain water content and improved some neurological deficits at 24 hours and 72 hours after SBI.
PS liposome increased CD36 and TGF-β1 protein levels, but decreased IL-1β and TNFα protein levels in peri-resection brain tissues at 24 hours after SBI.
CD36 siRNA or rAnnexin V partially countered the protective effect of PS liposome.
Isoflurane pretreatment produced similar antineuroinflammation and neurological benefits in SBI rats partially by upregulating CD36/Lyn/TGF-β1 signaling.
Collectively, our findings suggest that the activation of PS/CD36/TGF-β1 pathway by PS liposome or isoflurane prior to SBI could attenuate neuroinflammation and improve neurological outcomes in rats.
PS liposome or isoflurane pretreatment may serve as an effective preventive strategy to minimize the brain injury caused by neurosurgical procedures in patients.
American Psychological Association (APA)
Huang, Lei& Tang, Hailiang& Sherchan, Prativa& Lenahan, Cameron& Boling, Warren& Tang, Jiping…[et al.]. 2020. The Activation of PhosphatidylserineCD36TGF-β1 Pathway prior to Surgical Brain Injury Attenuates Neuroinflammation in Rats. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-13.
https://search.emarefa.net/detail/BIM-1204651
Modern Language Association (MLA)
Huang, Lei…[et al.]. The Activation of PhosphatidylserineCD36TGF-β1 Pathway prior to Surgical Brain Injury Attenuates Neuroinflammation in Rats. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-13.
https://search.emarefa.net/detail/BIM-1204651
American Medical Association (AMA)
Huang, Lei& Tang, Hailiang& Sherchan, Prativa& Lenahan, Cameron& Boling, Warren& Tang, Jiping…[et al.]. The Activation of PhosphatidylserineCD36TGF-β1 Pathway prior to Surgical Brain Injury Attenuates Neuroinflammation in Rats. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-13.
https://search.emarefa.net/detail/BIM-1204651
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1204651