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提取物通过维持肠道微生态和脂质代谢的稳态改善果糖诱导的小鼠肝脏脂肪变性。

Extract Ameliorates Fructose-Induced Hepatic Steatosis in Mice by Sustaining the Homeostasis of Intestinal Microecology and Lipid Metabolism.

作者信息

Chen Liang, Song Yingying, Huang Yurou, Hu Junjie, Meng Yan, Yuan Ming, Zheng Guohua, Wang Xuanbin, Zhang Cong, Qiu Zhenpeng

机构信息

School of Pharmacy, Hubei University of Chinese Medicine Wuhan China.

Laboratory of Chinese Herbal Pharmacology, Department of Pharmacy Renmin Hospital, Biomedical Research Institute, Hubei Key Laboratory of Wudang Local Chinese Medicine Research, Hubei University of Medicine Shiyan China.

出版信息

Food Sci Nutr. 2025 Jun 11;13(6):e70425. doi: 10.1002/fsn3.70425. eCollection 2025 Jun.

DOI:10.1002/fsn3.70425
PMID:40501499
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12152365/
Abstract

Sieb. et Zucc. (), an edible natural plant fruit, has beneficial effects on a multitude of metabolic diseases, but the mechanism to improve hepatic steatosis remains elusive. In this study, the curative effect of extract (COE) is evaluated in a fructose-induced NAFLD mouse model using biochemical indicators monitoring, histological staining, 16S rRNA sequencing analysis, and fecal microbiota transplantation. Our results showed that COE attenuates hepatic steatosis in fructose-fed mice. Mechanistically, COE repairs intestinal barrier damage and gut flora dysbiosis to suppress proinflammatory microbe-derived metabolite transportation to the liver, thus inhibiting the hepatic inflammation and lipid metabolic dysfunction. Notably, transplantation of fecal microbiota isolated from the fructose-fed mice could reverse the beneficial effect of COE on attenuating NAFLD. Therefore, our study demonstrates that COE delays the progression of fructose-driven NAFLD by suppressing lipid metabolic dysfunction and gut microbiota-mediated liver inflammation, highlighting the potential of as a resource for the treatment of NAFLD drugs.

摘要

Sieb. et Zucc.(一种可食用的天然植物果实)对多种代谢性疾病具有有益作用,但改善肝脂肪变性的机制仍不清楚。在本研究中,使用生化指标监测、组织学染色、16S rRNA测序分析和粪便微生物群移植,在果糖诱导的非酒精性脂肪性肝病(NAFLD)小鼠模型中评估了提取物(COE)的治疗效果。我们的结果表明,COE减轻了果糖喂养小鼠的肝脂肪变性。从机制上讲,COE修复肠道屏障损伤和肠道菌群失调,以抑制促炎微生物衍生代谢产物向肝脏的转运,从而抑制肝脏炎症和脂质代谢功能障碍。值得注意的是,移植从果糖喂养小鼠分离的粪便微生物群可以逆转COE对减轻NAFLD的有益作用。因此,我们的研究表明,COE通过抑制脂质代谢功能障碍和肠道微生物群介导的肝脏炎症来延缓果糖驱动的NAFLD的进展,突出了作为NAFLD药物治疗资源的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/6395cb4ea7c6/FSN3-13-e70425-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/6f90765f51ba/FSN3-13-e70425-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/128bf143bfc2/FSN3-13-e70425-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/faf7bec16263/FSN3-13-e70425-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/2da8bc574b03/FSN3-13-e70425-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/1161555b48ef/FSN3-13-e70425-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/3266f9c9fcd9/FSN3-13-e70425-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/53f4fcb34dfe/FSN3-13-e70425-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/6395cb4ea7c6/FSN3-13-e70425-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/6f90765f51ba/FSN3-13-e70425-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/128bf143bfc2/FSN3-13-e70425-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/faf7bec16263/FSN3-13-e70425-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/2da8bc574b03/FSN3-13-e70425-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/1161555b48ef/FSN3-13-e70425-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/3266f9c9fcd9/FSN3-13-e70425-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/53f4fcb34dfe/FSN3-13-e70425-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f5/12152365/6395cb4ea7c6/FSN3-13-e70425-g001.jpg

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本文引用的文献

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Transitioning from NAFLD to MAFLD and MASLD: Consistent prevalence and risk factors in a Chinese cohort.从非酒精性脂肪性肝病向代谢相关脂肪性肝病及代谢相关脂肪性肝炎的转变:中国队列中的一致患病率及危险因素
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α-D-1,3-glucan from Radix Puerariae thomsonii improves NAFLD by regulating the intestinal flora and metabolites.粉葛中的α-D-1,3-葡聚糖通过调节肠道菌群和代谢产物改善非酒精性脂肪性肝病。
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An adipocentric perspective on the development and progression of non-alcoholic fatty liver disease.
从脂肪细胞角度探讨非酒精性脂肪性肝病的发生发展。
J Hepatol. 2023 May;78(5):1048-1062. doi: 10.1016/j.jhep.2023.01.024. Epub 2023 Feb 3.
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Anthocyanins from Murray Ameliorated High-Fructose Diet-Induced Neuroinflammation through the Promotion of the Integrity of the Intestinal Barrier and the Proliferation of .花色苷通过促进肠道屏障完整性和增殖来改善高果糖饮食诱导的神经炎症。
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Global incidence and prevalence of nonalcoholic fatty liver disease.全球非酒精性脂肪性肝病的发病率和患病率。
Clin Mol Hepatol. 2023 Feb;29(Suppl):S32-S42. doi: 10.3350/cmh.2022.0365. Epub 2022 Dec 14.
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Loganin Prevents Hepatic Steatosis by Blocking NLRP3 Inflammasome Activation.马钱子苷通过阻断NLRP3炎性小体激活预防肝脂肪变性。
Biomol Ther (Seoul). 2023 Jan 1;31(1):40-47. doi: 10.4062/biomolther.2022.077. Epub 2022 Sep 16.
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Cornus officinalis vinegar reduces body weight and attenuates hepatic steatosis in mouse model of nonalcoholic fatty liver disease.山茱萸醋可降低非酒精性脂肪肝模型小鼠的体重并减轻肝脂肪变性。
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Interleukin-17 Weakens the NAFLD/NASH Process by Facilitating Intestinal Barrier Restoration Depending on the Gut Microbiota.白细胞介素-17 通过促进肠道屏障的恢复来减弱 NAFLD/NASH 进程,这取决于肠道微生物群。
mBio. 2022 Apr 26;13(2):e0368821. doi: 10.1128/mbio.03688-21. Epub 2022 Mar 10.
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and -A Comparison of Antioxidant and Immunomodulatory Activities of Standardized Fruit Extracts in Human Neutrophils and Caco-2 Models.标准化水果提取物在人中性粒细胞和Caco-2模型中的抗氧化和免疫调节活性比较
Plants (Basel). 2021 Oct 30;10(11):2347. doi: 10.3390/plants10112347.