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通过抑制NLRP3炎性小体激活和氧化应激,探索花青素锦葵色素在博来霉素诱导的小鼠肺纤维化模型中的缓解潜力。

Exploring the mitigating potential of anthocyanin Malvidin in a mouse model of bleomycin-induced pulmonary fibrosis by inhibiting NLRP3 inflammasome activation and oxidative stress.

作者信息

Zhou Dingzi, Cai Lin, Xu Jie, Fu Daigang, Yan Ling, Xie Linshen

机构信息

West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, 610041, China.

出版信息

J Inflamm (Lond). 2025 Mar 31;22(1):14. doi: 10.1186/s12950-025-00441-1.

DOI:10.1186/s12950-025-00441-1
PMID:40165218
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11959746/
Abstract

BACKGROUND

Malvidin (MV), an essential anthocyanin, has antioxidant and anti-inflammatory effects that may help treat pulmonary fibrosis (PF), a progressive and occasionally fatal condition characterized by severe lung scarring, oxidative stress, and inflammation.

OBJECTIVE

This study aims to evaluate the therapeutic potential of MV in PF by assessing its effects on inflammation, oxidative stress, and fibrotic markers through in vitro and in vivo models.

METHODS AND MATERIALS

The compound was evaluated by molecular docking. BEAS-2B and RLE-6TN cells were treated with 200 µg/mL BLM to induce inflammation, followed by MV treatment. Cell viability, ROS levels, and wound healing were analyzed. In vivo, BLM-induced mice were evaluated to assess fibrotic and antioxidant biomarkers.

RESULTS

MV interacted with NLRP3 with a binding energy of -7 kcal/mol. MV increased cell viability in BLM-induced cells, reducing ROS and oxidative stress. Wound healing was enhanced in MV-treated groups. A decrease in HYP proteins confirms MV's antifibrotic effects. In the mice model, MV reduced TXNIP, MDA, and MPO while increasing CAT, GSH, and SOD, confirming its antioxidant capacity.

CONCLUSION

MV alleviated PF in the BLM-induced model via the NLRP3 inflammasome pathway, demonstrating its potential as an antifibrotic and antioxidant agent.

摘要

背景

锦葵色素(MV)是一种重要的花青素,具有抗氧化和抗炎作用,可能有助于治疗肺纤维化(PF),这是一种以严重肺瘢痕形成、氧化应激和炎症为特征的进行性且偶有致命的疾病。

目的

本研究旨在通过体外和体内模型评估MV对炎症、氧化应激和纤维化标志物的影响,以评价其在PF中的治疗潜力。

方法和材料

通过分子对接对该化合物进行评估。用200μg/mL博来霉素(BLM)处理BEAS-2B和RLE-6TN细胞以诱导炎症,随后进行MV处理。分析细胞活力、活性氧(ROS)水平和伤口愈合情况。在体内,对BLM诱导的小鼠进行评估以检测纤维化和抗氧化生物标志物。

结果

MV与NLRP3相互作用,结合能为-7 kcal/mol。MV增加了BLM诱导细胞的活力,降低了ROS和氧化应激。MV处理组的伤口愈合得到增强。HYP蛋白的减少证实了MV的抗纤维化作用。在小鼠模型中,MV降低了硫氧还蛋白互作蛋白(TXNIP)、丙二醛(MDA)和髓过氧化物酶(MPO),同时增加了过氧化氢酶(CAT)、谷胱甘肽(GSH)和超氧化物歧化酶(SOD),证实了其抗氧化能力。

结论

MV通过NLRP3炎性小体途径减轻了BLM诱导模型中的PF,证明了其作为抗纤维化和抗氧化剂的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/a97bfed48d56/12950_2025_441_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/813ec9c529fd/12950_2025_441_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/d87bdffc07e4/12950_2025_441_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/3a3b393cd653/12950_2025_441_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/cc6cda507d4e/12950_2025_441_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/175b80708994/12950_2025_441_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/4c235dbe4006/12950_2025_441_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/8f1d2ef7987d/12950_2025_441_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/a97bfed48d56/12950_2025_441_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/813ec9c529fd/12950_2025_441_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/d87bdffc07e4/12950_2025_441_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/3a3b393cd653/12950_2025_441_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/cc6cda507d4e/12950_2025_441_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/175b80708994/12950_2025_441_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/4c235dbe4006/12950_2025_441_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/8f1d2ef7987d/12950_2025_441_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11959746/a97bfed48d56/12950_2025_441_Fig8_HTML.jpg

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