脂多糖刺激脂肪间充质干细胞对高脂饮食大鼠非酒精性脂肪肝治疗的影响

IF 0.2 4区 心理学 Q4 PSYCHIATRY
Contemporary Psychoanalysis Pub Date : 2023-06-24 eCollection Date: 2023-01-01 DOI:10.5812/ijpr-134807
Reza Afarin, Fereshteh Aslani, Shahla Asadizade, Bahar Jaberian Asl, Mehrnoosh Mohammadi Gahrooie, Elham Shakerian, Akram Ahangarpour
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引用次数: 0

摘要

背景:非酒精性脂肪肝(NAFLD)和非酒精性脂肪性肝炎(NASH非酒精性脂肪肝(NAFLD)和非酒精性脂肪性肝炎(NASH)是两种常见的肝病,目前缺乏有效的治疗方案:本研究旨在探讨脂多糖(LPS)刺激脂肪源性干细胞(ADSCs)对动物模型非酒精性脂肪肝治疗的影响:雄性Wistar大鼠以高脂肪饮食(HFD)诱导非酒精性脂肪肝7周。然后将大鼠分为3组:间充质干细胞(MSC)组、间充质干细胞+LPS组和非诺贝特(FENO)组。测量肝脏和体重,评估脂肪酸生物合成、β-氧化和炎症反应相关基因的表达:结果:与其他组相比,脂多糖刺激的 ADSCs 在调节肝脏和体重增加以及降低肝脏甘油三酯(TG)水平方面更有效。用LPS刺激的ADSCs治疗能有效纠正肝酶,包括丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST),以及血脂因子,包括低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)值,其效果优于FENO和间充质干细胞治疗。ADSCs + LPS 处理能显著降低转化生长因子β(TGF-β)和与炎症反应相关的基因。此外,经 ADSCs + LPS 处理的大鼠体内活性氧(ROS)水平也明显降低:结论:脂多糖刺激的 ADSCs 有可能通过减少高脂血症大鼠的炎症基因和 ROS 水平来缓解非酒精性脂肪肝,其效果优于单独使用 ADSCs 和 FENO 组。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The Effect of Lipopolysaccharide-Stimulated Adipose-Derived Mesenchymal Stem Cells on NAFLD Treatment in High-Fat Diet-Fed Rats.

The Effect of Lipopolysaccharide-Stimulated Adipose-Derived Mesenchymal Stem Cells on NAFLD Treatment in High-Fat Diet-Fed Rats.

The Effect of Lipopolysaccharide-Stimulated Adipose-Derived Mesenchymal Stem Cells on NAFLD Treatment in High-Fat Diet-Fed Rats.

The Effect of Lipopolysaccharide-Stimulated Adipose-Derived Mesenchymal Stem Cells on NAFLD Treatment in High-Fat Diet-Fed Rats.

Background: Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) are 2 common liver diseases that currently lack effective treatment options.

Objectives: This study aimed to investigate the effect of lipopolysaccharide (LPS)-stimulated adipose-derived stem cells (ADSCs) on NAFLD treatment in an animal model.

Methods: Male Wistar rats were fed a high-fat diet (HFD) to induce NAFLD for 7 weeks. The rats were then categorized into 3 groups: Mesenchymal stem cell (MSC), MSC + LPS, and fenofibrate (FENO) groups. Liver and body weight were measured, and the expression of genes involved in fatty acid biosynthesis, β-oxidation, and inflammatory responses was assessed.

Results: Lipopolysaccharide-stimulated ADSCs were more effective in regulating liver and body weight gain and reducing liver triglyceride (TG) levels compared to the other groups. Treatment with LPS-stimulated ADSCs effectively corrected liver enzymes, including alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and lipid factors, including low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) values, better than treatment with both FENO and MSCs. ADSCs + LPS treatment significantly decreased transforming growth factor β (TGF-β) and genes associated with inflammatory responses. Additionally, there was a significant reduction in reactive oxygen species (ROS) levels in the rats treated with ADSCs + LPS.

Conclusions: Lipopolysaccharide-stimulated ADSCs showed potential in alleviating NAFLD by reducing inflammatory genes and ROS levels in HFD rats, demonstrating better results than treatment with ADSCs and FENO groups alone.

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