Honokiol Mitigates Metabolic-Associated Fatty Liver Disease by Regulating Nrf2 and RIPK3 Signaling Pathways.

IF 1.4 4区医学 Q4 GASTROENTEROLOGY & HEPATOLOGY

Turkish Journal of Gastroenterology Pub Date : 2024-07-01 DOI:10.5152/tjg.2024.23470

Wen Cao, Zengdian Chen, Chenhui Lin, Xiaojin Lin, Yang Chen, Jingjuan Zhang

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引用次数: 0

Abstract

Background/aims: Metabolic-associated fatty liver disease (MAFLD) is a common cause of chronic liver disease worldwide. However, there is currently no recognized effective drugs for treating it.

Materials and methods: In this study, we investigated the efficacy of Honokiol (HNK) in vitro for mitigating MAFLD. Then, 0.4 mM palmitic acid (PA) and LO2 cells were used to establish the MAFLD model. The protective effect of HNK on MAFLD was confirmed by Oil Red O staining and cell counting kit (CCK-8) assay in LO2 cell line. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were carried out to analyze the regulatory role of HNK on Nrf2 and RIPK3 signaling pathways. The effect of HNK and its downstream signaling pathways on oxidative stress were verified by the detection of reactive oxygen species (ROS), malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD). The concentration of IL-1β, IL-6L, and TNF-α was assessed by enzyme-linked immunosorbent assay (ELISA).

Results: The middle concentration of HNK (50 μmol/L) was selected as the best option for inhibiting lipidosis and oxidative stress in MAFLD models. Honokiol mitigates MAFLD via activation of nuclear factor E2-related factor 2 (Nrf2) signaling pathways in vitro. Honokiol suppressed MAFLD via activating the Nrf2 signaling pathway to play an antioxidant and anti-inflammatory role. Also, HNK regulates Nrf2 and RIPK3 signaling pathways to mitigate MAFLD.

Conclusion: Our results showed that HNK may suppress the oxidative stress and inflammation in MAFLD via activation of Nrf2 signaling pathway.

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Honokiol通过调节Nrf2和RIPK3信号通路缓解代谢相关性脂肪肝疾病

背景/目的：代谢相关性脂肪肝（MAFLD）是全球慢性肝病的常见病因。然而，目前尚无公认有效的治疗药物：在本研究中，我们在体外研究了Honokiol（HNK）对减轻MAFLD的疗效。然后，用 0.4 mM 棕榈酸（PA）和 LO2 细胞建立 MAFLD 模型。油红 O 染色和细胞计数试剂盒（CCK-8）检测证实了 HNK 对 LO2 细胞株 MAFLD 的保护作用。实时定量聚合酶链反应（qRT-PCR）和Western印迹分析了HNK对Nrf2和RIPK3信号通路的调控作用。通过检测活性氧（ROS）、丙二醛（MDA）、过氧化氢酶（CAT）和超氧化物歧化酶（SOD），验证了HNK及其下游信号通路对氧化应激的影响。通过酶联免疫吸附试验（ELISA）评估了 IL-1β、IL-6L 和 TNF-α 的浓度：结果：HNK的中等浓度（50 μmol/L）被认为是抑制MAFLD模型脂质沉积和氧化应激的最佳选择。Honokiol通过激活体外核因子E2相关因子2（Nrf2）信号通路缓解MAFLD。Honokiol通过激活Nrf2信号通路发挥抗氧化和抗炎作用，从而抑制MAFLD。此外，HNK还能调节Nrf2和RIPK3信号通路，从而缓解MAFLD：我们的研究结果表明，HNK可通过激活Nrf2信号通路抑制MAFLD中的氧化应激和炎症反应。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Turkish Journal of Gastroenterology 医学-胃肠肝病学

CiteScore

1.90

自引率

0.00%

发文量

127

审稿时长

6 months

期刊介绍： The Turkish Journal of Gastroenterology (Turk J Gastroenterol) is the double-blind peer-reviewed, open access, international publication organ of the Turkish Society of Gastroenterology. The journal is a bimonthly publication, published on January, March, May, July, September, November and its publication language is English. The Turkish Journal of Gastroenterology aims to publish international at the highest clinical and scientific level on original issues of gastroenterology and hepatology. The journal publishes original papers, review articles, case reports and letters to the editor on clinical and experimental gastroenterology and hepatology.