This often leads to portal circulation-mediated translocation of gut-derived microbial products, such as lipopolysaccharide (LPS), to the liver, where these products engage Toll-like receptor 4 (TLR4) and initiate hepatic inflammation, which promotes alcoholic liver disease (ALD).
The present study demonstrated that the anti-inflammatory effect of cerebrolysin can decrease the TLR2 and TLR4 expressions through downregulating nuclear factor-κB pathway in the ALD disease.
Dietary inulin ameliorates ALD via suppressing LPS-TLR4-Mψ axis and modulating gut microbiota in mice, thus potentially provides theoretical foundation for inulin intervention in the prevention and treatment of ALD.
This study aimed to explore the influence of gut microbiota alterations induced by Linderae radix ethanol extract (LREE) on alcoholic liver disease (ALD) in rats and to study the anti-inflammatory effect of LREE on ALD through the lipopolysaccharide (LPS) toll-like receptor 4 (TLR4)-nuclear factor kappa B (NF-κB) pathway.
The results showed significant elevated levels of plasma LPS, hepatic TNF-α, IL-1β and IL-6 in ALD rats (P < 0.05), and heightened gene expressions of LBP, CD14, TLR4, NF-κB and TNF-α (P < 0.05); Taurine no matter administered preventively or curatively can reduce the levels of plasma LPS, hepatic TNF-α, IL-1β, IL-6, and down-regulate the gene expressions of LBP, CD14, TLR4, NF-κB and TNF-α.
Moreover, a comprehensive literature mining reveals that there are four signaling pathways with crosstalk (TLR4, NF- [Formula: see text]B, MAPK and Apoptosis) which play a major role in ALD.
Activation of innate immunity components such as Kupffer cells, LPS/TLR4, and complements in response to alcohol exposure plays a key role in the development and progression of alcoholic liver disease (ALD).