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提取物对饮食诱导性脂肪变性模型的抗氧化和抗炎作用

Antioxidant and Anti-Inflammatory Effects of Extracts on a Model of Diet-Induced Steatosis.

作者信息

Besné-Eseverri Irene, Martín María Ángeles, Lobo Gloria, Cano M Pilar, Portillo María P, Trepiana Jenifer

机构信息

Nutrition and Obesity Group, Department of Nutrition and Food Sciences, Faculty of Pharmacy, University of the Basque Country (UPV/EHU) and Lucio Lascaray Research Centre, 01006 Vitoria-Gasteiz, Spain.

CIBER Physiopathology of Obesity and Nutrition (CIBERobn), Institute of Health Carlos III, 28029 Madrid, Spain.

出版信息

Antioxidants (Basel). 2024 Nov 19;13(11):1416. doi: 10.3390/antiox13111416.

Abstract

Oxidative stress and inflammation are widely recognised as factors that can initiate and facilitate the development of MAFLD. The aim of this study is to analyse the effect of low and high doses of var. peel extract (L-OD and H-OD, respectively) and var. pulp extract (L-OFI and H-OFI, respectively), which are rich in betalains and phenolic compounds, on oxidative stress, inflammation, DNA damage and apoptosis in rat livers with diet-induced steatosis. Steatotic diet led to increased final body and liver weight, serum transaminases, hepatic TG content, oxidative status and cell death. H-OFI treatment decreased serum AST levels, while L-OFI reduced hepatic TG accumulation. Oxidative stress was partially prevented with H-OD and H-OFI supplementation, and pro-inflammatory cytokines levels were especially improved with H-OFI treatment. Moreover, H-OFI appears to prevent DNA damage markers. Finally, H-OD and L-OFI supplementation down-regulated the apoptotic pathway. In conclusion, both H-OD and H-OFI supplementation were effective in regulating the progression to metabolic steatohepatitis, triggering different mechanisms of action.

摘要

氧化应激和炎症被广泛认为是可引发和促进MAFLD发展的因素。本研究的目的是分析富含甜菜碱和酚类化合物的低剂量和高剂量的[品种名]果皮提取物(分别为L-OD和H-OD)和[品种名]果肉提取物(分别为L-OFI和H-OFI)对饮食诱导的脂肪变性大鼠肝脏中的氧化应激、炎症、DNA损伤和细胞凋亡的影响。致脂肪变性饮食导致终末体重和肝脏重量增加、血清转氨酶升高、肝脏TG含量增加、氧化状态改变以及细胞死亡。H-OFI处理降低了血清AST水平,而L-OFI减少了肝脏TG积累。补充H-OD和H-OFI可部分预防氧化应激,并通过H-OFI处理特别改善了促炎细胞因子水平,此外,H-OFI似乎可预防DNA损伤标志物。最后,补充H-OD和L-OFI下调了凋亡途径。总之,补充H-OD和H-OFI均能有效调节向代谢性脂肪性肝炎的进展,触发不同的作用机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/11591152/4b569e214dd8/antioxidants-13-01416-g001.jpg

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