Baicalin Attenuates Subarachnoid Hemorrhagic Brain Injury by Modulating Blood-Brain Barrier Disruption, Inflammation, and Oxidative Damage in Mice

Autor: Xian-Qing Shi, Yong-Jian Fu, Song-Song Zhang, Hao Ding, Jin Chen
Rok vydání: 2017
Předmět:
Male
0301 basic medicine
Aging
Nitric Oxide Synthase Type II
Brain Edema
Pharmacology
Occludin
Biochemistry
chemistry.chemical_compound
0302 clinical medicine
Barrier function
lcsh:Cytology
General Medicine
Microglial cell activation
Blood-Brain Barrier
Anesthesia
NADPH Oxidase 2
Cytokines
Inflammation Mediators
medicine.symptom
Neuroglia
Research Article
Subarachnoid hemorrhage
Article Subject
Perforation (oil well)
Inflammation
Models
Biological
Permeability
Proinflammatory cytokine
03 medical and health sciences
medicine
Animals
RNA
Messenger
lcsh:QH573-671
Flavonoids
Tight Junction Proteins
business.industry
Cell Biology
Subarachnoid Hemorrhage
medicine.disease
Mice
Inbred C57BL
Oxidative Stress
030104 developmental biology
Gene Expression Regulation
chemistry
Brain Injuries
Proteolysis
business
Baicalin
030217 neurology & neurosurgery
Zdroj: Oxidative Medicine and Cellular Longevity
Oxidative Medicine and Cellular Longevity, Vol 2017 (2017)
ISSN: 1942-0994
1942-0900
DOI: 10.1155/2017/1401790
Popis: In subarachnoid hemorrhagic brain injury, the early crucial events are edema formation due to inflammatory responses and blood-brain barrier disruption. Baicalin, a flavone glycoside, has antineuroinflammatory and antioxidant properties. We examined the effect of baicalin in subarachnoid hemorrhagic brain injury. Subarachnoid hemorrhage was induced through filament perforation and either baicalin or vehicle was administered 30 min prior to surgery. Brain tissues were collected 24 hours after surgery after evaluation of neurological scores. Brain tissues were processed for water content, real-time PCR, and immunoblot analyses. Baicalin improved neurological score and brain water content. Decreased levels of tight junction proteins (occludin, claudin-5, ZO-1, and collagen IV) required for blood-brain barrier function were restored to normal level by baicalin. Real-time PCR data demonstrated that baicalin attenuated increased proinflammatory cytokine (IL-1β, IL-6, and CXCL-3) production in subarachnoid hemorrhage mice. In addition to that, baicalin attenuated microglial cell secretion of IL-1βand IL-6 induced by lipopolysaccharide (100 ng/ml) dose dependently. Finally, baicalin attenuated induction of NOS-2 and NOX-2 in SAH mice at the mRNA and protein level. Thus, we demonstrated that baicalin inhibited microglial cell activation and reduced inflammation, oxidative damage, and brain edema.
Databáze: OpenAIRE
Externí odkaz: