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朴尔提取物通过SIRT1/AMPK信号轴改善小鼠酒精性脂肪肝疾病。

Pursh extract ameliorates alcohol-related fatty liver disease in mice via the SIRT1/AMPK signaling axis.

作者信息

Zhuge Hui, Pan Yan, Lai Shanglei, Chang Kaixin, Ding Qinchao, Cao Wenjing, Song Qing, Li Songtao, Dou Xiaobing, Ding Bin

机构信息

College of Life Science, Zhejiang Chinese Medical University, Hangzhou, 310053, China.

Molecular Medicine Institute, Zhejiang Chinese Medical University, Hangzhou, 310053, China.

出版信息

Heliyon. 2024 May 16;10(11):e31195. doi: 10.1016/j.heliyon.2024.e31195. eCollection 2024 Jun 15.

DOI:10.1016/j.heliyon.2024.e31195
PMID:38832279
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11145240/
Abstract

Pursh (), a functional food, has been applied to protect the liver against alcohol-related fatty liver disease (ALD) for a long history in China. This study was designed to evaluate the ameliorative activity of the polyphenolic fraction in (PGF) depending on the relief of ALD. The ALD mouse model was established by exposing the mice to a Lieber-DeCarli alcohol liquid diet. We found that PGF administration significantly ameliorated alcohol-induced liver injury, steatosis, oxidative stress, and inflammation in mice. Furthermore, alcohol-increased levels of the critical hepatic lipid synthesis proteins sterol regulatory element binding transcription factor (SREBP-1) and diacylglycerol -acyltransferase 2 (DGAT2) were attenuated by PGF. Similarly, PGF inhibited the expression of the lipid transport protein very low-density lipoprotein receptor (VLDLR). Interestingly, PGF restored alcohol-inhibited expression of carnitine palmitoyltransferase 1 (CPT1) and peroxisome proliferator-activated receptor alpha (PPARα), essential fatty acid β-oxidation proteins. Mechanistic studies revealed that PGF protects against alcohol-induced hepatocyte injury and lipid deposition via the SIRT1/AMPK signaling pathway. In sum, this research clearly demonstrated the protective effects of PGF against ALD, which was mediated by activating SIRT1/AMPK pathways in hepatocytes. We provide a new theoretical basis for using as a functional food in ALD.

摘要

在中国，功能性食品朴树（音译）长期以来一直被用于保护肝脏免受酒精性脂肪肝病（ALD）的侵害。本研究旨在根据ALD的缓解情况评估朴树多酚组分（PGF）的改善活性。通过让小鼠食用Lieber-DeCarli酒精液体饮食建立ALD小鼠模型。我们发现，给予PGF可显著改善小鼠酒精诱导的肝损伤、脂肪变性、氧化应激和炎症。此外，PGF可减轻酒精导致的关键肝脏脂质合成蛋白固醇调节元件结合转录因子（SREBP-1）和二酰甘油酰基转移酶2（DGAT2）水平的升高。同样，PGF抑制脂质转运蛋白极低密度脂蛋白受体（VLDLR）的表达。有趣的是，PGF恢复了酒精抑制的肉碱棕榈酰转移酶1（CPT1）和过氧化物酶体增殖物激活受体α（PPARα）的表达，这两种蛋白是必需脂肪酸β氧化所必需的。机制研究表明，PGF通过SIRT1/AMPK信号通路保护肝细胞免受酒精诱导的损伤和脂质沉积。总之，本研究清楚地证明了PGF对ALD的保护作用，这是通过激活肝细胞中的SIRT1/AMPK通路介导的。我们为将朴树用作ALD功能性食品提供了新的理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290a/11145240/cde8c08b2bd4/gr7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290a/11145240/cde8c08b2bd4/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290a/11145240/57b68e51f3c7/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290a/11145240/046f0dea4a56/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290a/11145240/f86c4ada6324/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290a/11145240/e14326e23ecf/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290a/11145240/25085111ea8e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290a/11145240/2c5dd4f3c70e/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290a/11145240/e5880fbaab1f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290a/11145240/cde8c08b2bd4/gr7.jpg

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