College of Animal Science and Technology, Zhongkai University of Agriculture and Engineering, Guangzhou, Guangdong 510225, China.
Technology Center, Guangzhou Customs, Guangzhou, Guangdong 510623, China.
Int Immunopharmacol. 2024 Nov 15;141:113014. doi: 10.1016/j.intimp.2024.113014. Epub 2024 Aug 26.
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.
非酒精性脂肪性肝病(NAFLD)不仅可引起肝脏脂质代谢异常,还可引起肝脏炎症。既往研究表明,白术多糖(PAMK)可减轻动物肝炎症损伤,缓解高脂饮食(HFD)诱导的小鼠 NAFLD,但关于 PAMK 对 NAFLD 引起的肝脏炎症的调控鲜有报道。本研究通过建立小鼠非酒精性脂肪性肝炎症动物模型,探究 PAMK 对小鼠肝脏的保护作用。结果表明,PAMK 可减轻 HFD 引起的小鼠体重和肝脏重量的异常增加,改善小鼠肝脏结构异常,降低小鼠肝脏氧化应激和细胞因子分泌水平,下调 TLR4、MyD88、NF-κB 的 mRNA 表达及 P-IκB、P-NF-κB-P65、TLR4、MyD88、NF-κB 蛋白表达。这些结果表明,PAMK 可减轻 NAFLD 引起的小鼠肝细胞脂肪变性及损伤、氧化应激和肝脏炎症反应。