Polysaccharide of Atractylodes macrocephala Koidz regulates LPS-mediated mouse hepatitis through the TLR4-MyD88-NFκB signaling pathway

Feed corruption and poor breeding environment could cause widespread bacterial infection which could cause severe liver inflammation and lead to liver damage, even death. It has been proved that Polysaccharide of Atractylodes macrocephala Koidz (PAMK) could improve the immunity of animal, but the mechanism of its protective effect on hepatitis has been rarely reported. This study investigated the protective effect of PAMK on mouse liver through LPS-induced liver inflammatory. The results showed that LPS caused swelling of hepatocytes, disappearance of hepatic cord structure and infiltration of a large number of inflammatory cells, and LPS could up-regulated mRNA and protein expression levels of TLR4, MyD88, IKB alpha and NF kappa B, increased cytokines IL-1 beta, IL-4, IL-6 and TNF-alpha levels, enhance the levels of antioxidant enzymes CAT, GSH-PX, SOD, iNOs and MDA. PAMK pretreatment could relieved histopathological damage caused by LPS, and could activate the TLR4-MyD88-NF kappa B signalling pathway, reduce the levels of IL-1 beta, IL-6 and TNF-alpha, increase IL-4 levels, inhibit the levels of GSH-PX and MDA. These results indicate that PAMK could reduce inflammatory damage and oxidative stress in mice and play a protective role in the early stages of LPS invasion of the liver.

Automated summary

This study found that pretreatment with Polysaccharide of Atractylodes macrocephala Koidz (PAMK) could alleviate the histopathological damage caused by LPS-induced liver inflammation in mice. PAMK activated the TLR4-MyD88-NF-κB signaling pathway, reduced levels of IL-1β, IL-6, and TNF-α, increased IL-4 levels, and inhibited GSH-PX and MDA levels, indicating its potential protective role in reducing inflammatory damage and oxidative stress in the liver.