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叶酸通过降低同型半胱氨酸和抑制HepG2细胞中的NF-κB途径来改善棕榈酸酯诱导的炎症。

Folic acid ameliorates palmitate-induced inflammation through decreasing homocysteine and inhibiting NF-κB pathway in HepG2 cells.

作者信息

Bagherieh Molood, Kheirollahi Asma, Zamani-Garmsiri Fahimeh, Emamgholipour Solaleh, Meshkani Reza

机构信息

Department of Clinical Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Department of Comparative Biosciences, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran.

出版信息

Arch Physiol Biochem. 2023 Dec;129(4):893-900. doi: 10.1080/13813455.2021.1878539. Epub 2021 Feb 17.

Abstract

OBJECTIVE

Prevention of inflammation is one of the possible remedy procedure for steatohepatitis during NAFLD. In this study, we researched the folic acid (FA) potency to attenuate the inflammation of palmitate-treated HepG2 cells and the related signalling pathways.

METHODS

The molecular mechanisms related to FA anti-inflammatory effect in palmitate and Hcy-treated HepG2 cell line were assessed.

RESULTS

The results indicated that while palmitate enhances the expression and secretion of TNF-α, IL-6, and IL-1β, and also intracellular ROS level, FA at concentrations of 25, 50, and 75 g/mL significantly reversed these effects in HepG2 cells. In addition, FA could ameliorate inflammation and decrease ROS production induced by Hcy. Furthermore, FA pre-treatment suppress palmitate -induced (NF-κB) p65 level in palmitate or Hcy stimulated cells.

CONCLUSIONS

Overall, these results suggest that FA reduces inflammation in HepG2 cells through decreasing ROS and Hcy concentration level resulting in inhibiting the NF-κB pathway.

摘要

目的

预防炎症是治疗非酒精性脂肪性肝病(NAFLD)期间脂肪性肝炎的一种可能的补救措施。在本研究中,我们研究了叶酸(FA)减轻棕榈酸酯处理的HepG2细胞炎症及相关信号通路的能力。

方法

评估了FA在棕榈酸酯和同型半胱氨酸(Hcy)处理的HepG2细胞系中抗炎作用的分子机制。

结果

结果表明,棕榈酸酯可增强肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-1β(IL-1β)的表达与分泌,还可提高细胞内活性氧(ROS)水平,而浓度为25、50和75μg/mL的FA可显著逆转HepG2细胞中的这些作用。此外,FA可改善炎症并减少Hcy诱导的ROS产生。此外,FA预处理可抑制棕榈酸酯或Hcy刺激的细胞中棕榈酸酯诱导的核因子-κB(NF-κB)p65水平。

结论

总体而言,这些结果表明,FA通过降低ROS和Hcy浓度水平,从而抑制NF-κB途径,减轻HepG2细胞中的炎症。

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