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樟芝多糖通过 ROS/TLR4/NF-κB 信号通路改善肝损伤中的炎症反应。

Antrodia camphorata polysaccharide improves inflammatory response in liver injury via the ROS/TLR4/NF-κB signal.

机构信息

Department of Pharmacy, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.

Department of Digestive, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.

出版信息

J Cell Mol Med. 2022 May;26(9):2706-2716. doi: 10.1111/jcmm.17283. Epub 2022 Mar 29.

DOI:10.1111/jcmm.17283
PMID:35352469
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9077287/
Abstract

Antrodia Camphorata Polysaccharide (ACP) refers to a kind of polysaccharide extracted from the natural porous fungus Antrodia camphorata. This study investigated the mechanism of action of ACP in protecting the liver. The results showed that ACP suppressed the LPS-induced KC cell activation, reduced the expression of inflammatory factors, increased the SOD level and suppressed ROS expression. In addition, N-acetylcysteine (NAC) was adopted for pre-treatment to suppress ROS. The results indicated that NAC synergistically exerted its effect with ACP, suggesting that ACP played its role through suppressing ROS. Further detection revealed that ACP activated the Nrf2 signal. It was discovered in the mouse model that, ACP effectively improved liver injury in mice, decreased ALT and AST levels, and suppressed the expression of inflammatory factors. This study suggests that ACP can exert its effect against oxidative stress via the Nrf2-ARE signalling, which further improves the production of ROS and the activation of TLR4-NF-κB signalling, and protects the liver against liver injury.

摘要

樟芝多糖(ACP)是从天然多孔真菌樟芝中提取的一种多糖。本研究探讨了 ACP 保护肝脏的作用机制。结果表明,ACP 抑制 LPS 诱导的 KC 细胞活化,降低炎症因子的表达,增加 SOD 水平并抑制 ROS 表达。此外,采用 N-乙酰半胱氨酸(NAC)进行预处理以抑制 ROS。结果表明,NAC 与 ACP 协同发挥作用,提示 ACP 通过抑制 ROS 发挥作用。进一步的检测表明,ACP 激活了 Nrf2 信号。在小鼠模型中发现,ACP 能有效改善小鼠的肝损伤,降低 ALT 和 AST 水平,并抑制炎症因子的表达。本研究表明,ACP 可以通过 Nrf2-ARE 信号通路发挥抗氧化应激作用,进一步提高 ROS 的产生和 TLR4-NF-κB 信号通路的激活,从而保护肝脏免受肝损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/e9ef9a9f1932/JCMM-26-2706-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/6c8d6591aab4/JCMM-26-2706-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/3ce83ce4605a/JCMM-26-2706-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/83b941de54c2/JCMM-26-2706-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/2b29bfb6ed16/JCMM-26-2706-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/f3e36dfc39ff/JCMM-26-2706-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/475220295c96/JCMM-26-2706-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/e9ef9a9f1932/JCMM-26-2706-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/6c8d6591aab4/JCMM-26-2706-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/3ce83ce4605a/JCMM-26-2706-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/83b941de54c2/JCMM-26-2706-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/2b29bfb6ed16/JCMM-26-2706-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/f3e36dfc39ff/JCMM-26-2706-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/475220295c96/JCMM-26-2706-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49c1/9077287/e9ef9a9f1932/JCMM-26-2706-g006.jpg

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