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土木香内酯可减轻非酒精性脂肪性肝病的高脂饮食诱导的炎症和氧化应激。

Alantolactone attenuates high-fat diet-induced inflammation and oxidative stress in non-alcoholic fatty liver disease.

机构信息

Joint Research Center on Medicine, the Affiliated Xiangshan Hospital of Wenzhou Medical University, Ningbo, 315700, Zhejiang, China.

Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China.

出版信息

Nutr Diabetes. 2024 Jun 10;14(1):41. doi: 10.1038/s41387-024-00300-7.

Abstract

BACKGROUND

Nonalcoholic fatty liver disease (NAFLD) is a chronic disease with an increasing incidence, which can further develop into liver fibrosis and hepatocellular carcinoma at the end stage. Alantolactone (Ala), a sesquiterpene lactone isolated from Asteraceae, has shown anti-inflammatory effects in different models. However, the therapeutic effect of Ala on NAFLD is not clear.

METHODS

C57BL/6 mice were fed a high-fat diet (HFD) to induce NAFLD. After 16 weeks, Ala was administered by gavage to observe its effect on NAFLD. RNA sequencing of liver tissues was performed to investigate the mechanism. In vitro, mouse cell line AML-12 was pretreated with Ala to resist palmitic acid (PA)-induced inflammation, oxidative stress and fibrosis.

RESULTS

Ala significantly inhibited inflammation, fibrosis and oxidative stress in HFD-induced mice, as well as PA-induced AML-12 cells. Mechanistic studies showed that the effect of Ala was related to the induction of Nrf2 and the inhibition of NF-κB. Taken together, these findings suggested that Ala exerted a liver protective effect on NAFLD by blocking inflammation and oxidative stress.

CONCLUSIONS

The study found that Ala exerted a liver protective effect on NAFLD by blocking inflammation and oxidative stress, suggesting that Ala is an effective therapy for NAFLD.

摘要

背景

非酒精性脂肪性肝病(NAFLD)是一种发病率不断增加的慢性疾病,其终末期可进一步发展为肝纤维化和肝细胞癌。从菊科植物中分离得到的艾兰素(Ala)是一种倍半萜内酯,在不同模型中表现出抗炎作用。然而,Ala 对 NAFLD 的治疗效果尚不清楚。

方法

用高脂肪饮食(HFD)喂养 C57BL/6 小鼠以诱导 NAFLD。16 周后,通过灌胃给予 Ala 观察其对 NAFLD 的作用。对肝组织进行 RNA 测序以研究其作用机制。体外,用 Ala 预处理小鼠细胞系 AML-12 以抵抗棕榈酸(PA)诱导的炎症、氧化应激和纤维化。

结果

Ala 显著抑制 HFD 诱导的小鼠的炎症、纤维化和氧化应激,以及 PA 诱导的 AML-12 细胞的炎症、纤维化和氧化应激。机制研究表明,Ala 的作用与 Nrf2 的诱导和 NF-κB 的抑制有关。综上所述,这些发现表明,Ala 通过阻断炎症和氧化应激对 NAFLD 发挥肝脏保护作用。

结论

本研究发现,Ala 通过阻断炎症和氧化应激对 NAFLD 发挥肝脏保护作用,表明 Ala 是治疗 NAFLD 的有效方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8876/11164993/2b1b99fb9c67/41387_2024_300_Fig1_HTML.jpg

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