TLR4型
炎症
苍术
NF-κB
脂多糖
药理学
NFKB1型
传统医学
化学
医学
免疫学
生物化学
转录因子
中医药
病理
基因
替代医学
作者
Jian‐Fan Chen,Shuzhan Yang,Hai‐Bin Luo,Xinliang Fu,Wanyan Li,Bingxin Li,Fu Cheng,Feiyue Chen,Wanyan Li,Nan Cao
标识
DOI:10.1016/j.intimp.2024.113014
摘要
Non-alcoholic fatty liver disease (NAFLD) not only could cause abnormal lipid metabolism in the liver, but also could cause liver inflammation. Previous studies have shown that Polysaccharide of Atractylodes macrocephala Koidz (PAMK) could alleviate animal liver inflammatory damage and alleviate NAFLD in mice caused by high-fat diet(HFD), but regulation of liver inflammation caused by NAFLD has rarely been reported. In this study, an animal model of non-alcoholic fatty liver inflammation in the liver of mice was established to explore the protective effect of PAMK on the liver of mice. The results showed that PAMK could alleviate the abnormal increase of body weight and liver weight of mice caused by HFD, alleviate the abnormal liver structure of mice, reduce the level of oxidative stress and cytokine secretion in the liver of mice, and downregulate the mRNA expression of TLR4, MyD88, NF-κB and protein expression of P-IκB, P-NF-κB-P65, TLR4, MyD88, NF-κB in the liver. These results indicate that PAMK could alleviate hepatocyte fatty degeneration and damage, oxidative stress and inflammatory response of the liver caused by NAFLD in mice.
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