Blood-brain barrier breakdown by PAF and protection by XQ-1H due to antagonism of PAF effects

Deng, Yan; Fang, Weirong; Li, Yunman; Cen, Juan; Fang, Fang; Lv, Peng; Gong, Shubo; Mao, Lishun

doi:10.1016/j.ejphar.2009.06.017

Cited by 35 publications

(24 citation statements)

References 29 publications

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“…As an autacoid, extensive studies in the past have been focused on PAF's effects on neurological functions and inflammation. [55][56][57][58] A role of PAF in developing TBI-associated coagulopathy remains largely unknown, but should be expected because it is a potent platelet agonist. In addition, PAF also contributes to the hypoxiainduced breakdown of the blood brain barrier, 58 potentially resulting in the release of PAF and other brain-derived prothrombotic molecules to the systemic circulation.…”

Section: Zhang Et Almentioning

confidence: 98%

Traumatic Brain Injury-Associated Coagulopathy

Zhang

Jiang

Liu

et al. 2012

Journal of Neurotrauma

127

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Traumatic injury is a common cause of coagulopathy, primarily due to blood loss and hemodilution secondary to fluid resuscitation. Traumatic injury-associated coagulopathy often follows a course of transition from hyper- to hypocoagulable state exemplified in disseminated intravascular coagulation. The incidence of coagulopathy is significantly higher in patients with traumatic brain injury (TBI), especially those with penetrating trauma compared to injury to the trunk and limbs. This occurs despite the fact that patients with isolated TBI bleed less and receive restricted volume load of fluids. TBI-associated coagulopathy is extensively documented to associate with poor clinical outcomes, but its pathophysiology remains poorly understood. Studies in the past have shown that brain tissue is highly enriched in key procoagulant molecules. This review focuses on the biochemical and cellular characteristics of these molecules and pathways that could make brain uniquely procoagulant and prone to coagulopathy. Understanding this unique procoagulant environment will help to identify new therapeutic targets that could reverse a state of coagulopathy with minimal impacts on hemostasis, a critical requirement for neurosurgical treatments of TBI.

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Section: Zhang Et Almentioning

confidence: 98%

Traumatic Brain Injury-Associated Coagulopathy

Zhang

Jiang

Liu

et al. 2012

Journal of Neurotrauma

127

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“…Therefore, the inhibition of neuroinflammation likely represents a crucial therapy for the treatment of secondary brain injury [5,6]. As one of the str ngest inflammatory factors, PAF plays a key role in the modulation of neuroinflammation [7]. PAF is expressed in neurons as well as neuroglial cells, and previous studies report that PAF is increased after brain injury [8].…”

Section: Discussionmentioning

confidence: 99%

The Neuroinflammatory Response Induced by PAF Can Be Attenuated by BN52021 Administration

Han¹,

Hu²,

Su³

2011

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“…6 groups were set as follows: control (PBS), H/R (PBS), ozagrel (10 − 5 M) and N2 (3 × 10 − 5 M, 10 − 5 M, and 3 × 10 − 6 M). Oxygen-glucose deprivation (OGD) was used as an in vitro model for H/R damage (Deng et al, 2009). Briefly, N2, ozagrel or PBS-incubated RBMECs were exposed to 30 mM Na 2 S 2 O 4 in DMEM (low glucose) medium for 2 h (hypoxia) and then cultured in Na 2 S 2 O 4 -free DMEM-F12 medium for 2 h (reoxygenation).…”

Section: Drug Treatment and H/rmentioning

confidence: 99%