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PRECLINICAL PUBLICATION · 2018

Inhibition of 2-AG hydrolysis differentially regulates blood brain barrier permeability after injury.

Mouse / Endotoxin/LPS

Evidence by therapy association

Study details and outcomes are extracted in the context of a specific intervention. Separate associations are retained rather than silently merged.

PMID 29759062 ↗2018Reported benefit

Inhibition of 2-AG hydrolysis differentially regulates blood brain barrier permeability after injury.

MouseEndotoxin/LPSCD1 (lipopolysaccharide model and pharmacokinetics); C57BL/6 (photothrombosis model)Male (CD1 lipopolysaccharide model)Subcutaneous10 mg/kg in 5:5:90 dimethyl sulfoxide:Cremophor:salineLipopolysaccharide model: 30-45 min after each lipopolysaccharide dose. Ischaem…

Model: Two models. Systemic inflammation with Salmonella enterica typhimurium lipopolysaccharide 3 mg/kg intraperitoneally at 0, 6 and 24 h; and focal photothrombotic cortical ischaemia by retro-orbital rose bengal (30 uL of 15 mg/mL) with 10 min green laser illumination over somatosensory cortex

CPD-4645 raised brain 2-arachidonoylglycerol, lowered arachidonic acid, IL-1beta and IL-6, reversed 74% of lipopolysaccharide-induced vascular gene induction and reduced barrier leakage in both models; CB1 and CB2 blockade partially reversed only the ischaemic protection.

Extraction: extract · Supplied extraction confidence: 0.82. Machine-extracted fields require source verification.