Allicin Improves Lung Injury Induced by Sepsis via Regulation of the Toll-Like Receptor 4 (TLR4)/Myeloid Differentiation Primary Response 88 (MYD88)/Nuclear Factor kappa B (NF-κB) Pathway.

PMID 30957795 ↗2019Reported benefit

Allicin Improves Lung Injury Induced by Sepsis via Regulation of the Toll-Like Receptor 4 (TLR4)/Myeloid Differentiation Primary Response 88 (MYD88)/Nuclear Factor kappa B (NF-κB) Pathway.

RatEndotoxin/LPSSprague-DawleyMalen = 54 rats randomised into 6 groups, n = 9 per group; n = 5 pe…Intraperitoneal injection25, 50 or 100 microgram/mL allicin at an injection volume o…Given at the same time as the LPS injection

Model: Sepsis-related acute lung injury induced by intraperitoneal injection of lipopolysaccharide (endotoxin, Escherichia coli) at 20 mg/kg

Allicin dose-dependently reduced histological lung injury score, apoptotic cell number, lung wet/dry ratio and bronchoalveolar lavage TNF-alpha, IL-6 and IL-1beta compared with LPS alone, and suppressed TLR4, MyD88, NF-kappaB, caspase-3 and caspase-9 protein expression.

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Allicin Improves Lung Injury Induced by Sepsis via Regulation of the Toll-Like Receptor 4 (TLR4)/Myeloid Differentiation Primary Response 88 (MYD88)/Nuclear Factor kappa B (NF-κB) Pathway.

Evidence by therapy association

Allicin Improves Lung Injury Induced by Sepsis via Regulation of the Toll-Like Receptor 4 (TLR4)/Myeloid Differentiation Primary Response 88 (MYD88)/Nuclear Factor kappa B (NF-κB) Pathway.