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

BACKGROUND: The aim of this study was to assess the effects and mechanisms of allicin in a sepsis-induced lung injury in vivo study. MATERIAL/METHODS: The rats (n=54) were divided into 6 groups: Normal, DMSO, LPS, LPS+LD, LPS+MD, and LPS+HD groups. After being treated by different methods, we collected the lung tissues of different groups and evaluated the pathology by HE staining and positive apoptosis cells by TUNEL. We assessed the W/D ratio, inflammatory cytokines (TNF-α, IL-6 and IL-1β), and relative protein expressions (TLR4, MyD88, NF-κB, caspase-3, and caspase-9) by IHC assay. RESULTS: Compared with LPS group, the lung injury and positive cell number of allicin treated groups were significantly improved with dose-dependent (P<0.05, respectively) and the W/D ratio and TNF-α, IL-6 and IL-1β concentration were significantly down-regulation compared with those of LPS group with dose-dependent (P<0.05, respectively). By IHC, the TLR4, MyD88, NF-κB, caspase-3 and caspase-9 protein activities of allicin treated groups were significantly suppressed compared with those of LPS group (P<0.05, respectively) in lung tissues. CONCLUSIONS: This in vivo study shows that allicin improved sepsis-induced lung injury by regulation of TLR4/MyD88/NF-κB.