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菝葜多酚通过NF-κB信号通路抑制LPS诱导的巨噬细胞M1极化,从而在体内外减轻炎症。

Smilaxchina L. polyphenols inhibit LPS-induced macrophage M1 polarization to alleviate inflammation through NF-κB signaling pathway in vitro and in vivo.

作者信息

Yu Longhui, Liu Shanshan, Liu Jiluan, Li Jingen, Zhang Wenkai, Lin Lezhen, Yang Licong, Zheng Guodong

机构信息

Jiangxi Key Laboratory of Natural Product and Functional Food, College of Food Science and Engineering, Jiangxi Agricultural University, Nanchang, 330045, China.

College of Biological Science and Engineering, Fuzhou University, Fuzhou, 350108, China.

出版信息

J Ethnopharmacol. 2025 Feb 27;342:119355. doi: 10.1016/j.jep.2025.119355. Epub 2025 Jan 10.

DOI:10.1016/j.jep.2025.119355
PMID:39800244
Abstract

ETHNOPHARMACOLOGICAL RELEVANCE

As an important component of the cell wall of Gram-negative bacteria, lipopolysaccharide (LPS) is an important inducer of inflammation in humans. Smilax china L. is known for its diverse bioactive functions, particularly its anti-inflammatory effects.

AIM OF THE STUDY

This study aimed to investigate the bioactive function of Smilax china L. polyphenols (SCLP) on LPS-induced inflammation.

MATERIALS AND METHODS

Inflammation in RAW264.7 macrophages and mice were induced using LPS. The cytotoxicity of SCLP was investigated by MTT assay. Inflammatory factors were detected by ELISA and RT-PCR. The expression of NF-κB pathway-related proteins was analyzed by Western Blotting.

RESULTS

The results demonstrated that SCLP significantly reduced the levels of pro-inflammatory factors (TNF-α, IL-1β, and IL-6) and inhibited M1 polarization of macrophages in both RAW264.7 macrophages and mice (p < 0.05). Western Blotting analysis revealed that the levels of NF-κB signaling pathway-associated proteins (p-p65, p-IKB, p-IKK) were significantly reduced (p < 0.05). Notably, SCLP significantly downregulated the expression of pro-apoptotic proteins, while upregulating the expression of anti-apoptotic proteins in RAW264.7 macrophages (p < 0.05). Additionally, the levels of antioxidant enzymes were enhanced in mice, suggesting a potential reduction in the inflammatory response.

CONCLUSIONS

These findings indicated that SCLP might inhibit LPS-induced M1 polarization through the NF-κB signaling pathway, thereby reducing inflammation. Consequently, SCLP might serve as a promising bioactive substance for preventing inflammation-related injury.

摘要

民族药理学相关性

脂多糖(LPS)作为革兰氏阴性菌细胞壁的重要组成部分,是人体内炎症的重要诱导剂。菝葜以其多样的生物活性功能而闻名,尤其是其抗炎作用。

研究目的

本研究旨在探讨菝葜多酚(SCLP)对LPS诱导的炎症的生物活性作用。

材料与方法

用LPS诱导RAW264.7巨噬细胞和小鼠发生炎症。通过MTT法研究SCLP的细胞毒性。通过ELISA和RT-PCR检测炎症因子。通过蛋白质免疫印迹法分析NF-κB信号通路相关蛋白的表达。

结果

结果表明,SCLP显著降低了促炎因子(TNF-α、IL-1β和IL-6)的水平,并抑制了RAW264.7巨噬细胞和小鼠中巨噬细胞的M1极化(p<0.05)。蛋白质免疫印迹分析显示,NF-κB信号通路相关蛋白(p-p65、p-IκB、p-IKK)的水平显著降低(p<0.05)。值得注意的是,SCLP显著下调了RAW264.7巨噬细胞中促凋亡蛋白的表达,同时上调了抗凋亡蛋白的表达(p<0.05)。此外,小鼠体内抗氧化酶的水平升高,表明炎症反应可能有所减轻。

结论

这些发现表明,SCLP可能通过NF-κB信号通路抑制LPS诱导的M1极化,从而减轻炎症。因此,SCLP可能是一种有前途的预防炎症相关损伤的生物活性物质。

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