TLR4型
炎症
氧化应激
肝损伤
脂多糖
生物
化学
药理学
免疫学
肿瘤坏死因子α
生物化学
作者
Sixuan Guo,Wanyan Li,Feiyue Chen,Shuzhan Yang,Yunmao Huang,Yunbo Tian,Nan Cao
标识
DOI:10.1016/j.intimp.2021.107692
摘要
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, IKBα and NFκB, increased cytokines IL-1β, IL-4, IL-6 and TNF-α 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-NFκB signalling pathway, reduce the levels of IL-1β, IL-6 and TNF-α, 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.
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