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日本厚朴通过调控铁死亡和颈动脉结扎小鼠模型中的血管平滑肌细胞表型转换来抑制内膜增生。

Magnolia kobus DC. suppresses neointimal hyperplasia by regulating ferroptosis and VSMC phenotypic switching in a carotid artery ligation mouse model.

作者信息

Kim Jong Min, Kim Yiseul, Na Hyun-Jin, Hur Haeng Jeon, Lee Sang Hee, Sung Mi Jeong

机构信息

Aging and Metabolism Research Group, Korea Food Research Institute, Wanju‑gun, 55365, Republic of Korea.

出版信息

Chin Med. 2025 Jan 3;20(1):3. doi: 10.1186/s13020-024-01051-4.

DOI:10.1186/s13020-024-01051-4
PMID:39754271
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11699803/
Abstract

BACKGROUND

Magnolia kobus DC (MO), as a plant medicine, has been reported to have various physiological activities, including neuroprotective, anti-inflammatory, and anti-diabetic effects. However, vascular protective effects of MO remain incompletely understood. In this study, we evaluated the vascular protective effect of MO against ferroptosis in a carotid artery ligation (CAL)-induced neointimal hyperplasia mouse model and in aortic thoracic smooth muscle A7r5 cells.

METHODS

This study was conducted to estimate the vascular protective effects of MO by systematically measuring histopathological analysis and western blot analysis in CAL animal model. In vitro protective effects of MO were evaluated by estimating cell viability, reactive oxygen species (ROS) content, glutathione (GSH) levels, lipid peroxidation, mitochondrial morphological change, cell proliferation, migration, western blot analysis, and qRT-PCR against erastin (Era)-induced A7r5 cells.

RESULTS

MO intake significantly improved neointimal formation, inhibited ferroptosis and vascular smooth muscle cell (VSMC) phenotypes, and ameliorated the antioxidant system of carotid artery tissues. In addition, MO treatment effectively ameliorated Era-induced ferroptotic cytotoxicity, including cellular death, ROS production, and cell migration status. MO treatment also suppressed proliferation and migration in Era-induced A7r5 cells. MO considerably regulated Era-induced abnormal mechanisms related to ferroptotic changes, VSMC phenotype switching, and the ROS scavenging system in A7r5 cells.

CONCLUSION

MO has the potential for use as a functional food supplement, nutraceutical, or medicinal food, with protective effects on vascular health by regulating ferroptosis and VSMC phenotypic switching.

摘要

背景

辛夷作为一种植物药,已被报道具有多种生理活性,包括神经保护、抗炎和抗糖尿病作用。然而,辛夷的血管保护作用仍不完全清楚。在本研究中,我们在颈动脉结扎(CAL)诱导的内膜增生小鼠模型和胸主动脉平滑肌A7r5细胞中评估了辛夷对铁死亡的血管保护作用。

方法

本研究通过在CAL动物模型中系统地测量组织病理学分析和蛋白质印迹分析来评估辛夷的血管保护作用。通过评估细胞活力、活性氧(ROS)含量、谷胱甘肽(GSH)水平、脂质过氧化、线粒体形态变化、细胞增殖、迁移、蛋白质印迹分析和针对埃拉斯汀(Era)诱导的A7r5细胞的qRT-PCR来评估辛夷的体外保护作用。

结果

摄入辛夷可显著改善内膜形成,抑制铁死亡和血管平滑肌细胞(VSMC)表型,并改善颈动脉组织的抗氧化系统。此外,辛夷治疗有效改善了Era诱导的铁死亡细胞毒性,包括细胞死亡、ROS产生和细胞迁移状态。辛夷治疗还抑制了Era诱导的A7r5细胞的增殖和迁移。辛夷显著调节了Era诱导的与A7r5细胞中铁死亡变化、VSMC表型转换和ROS清除系统相关的异常机制。

结论

辛夷有潜力用作功能性食品补充剂、营养保健品或药用食品,通过调节铁死亡和VSMC表型转换对血管健康具有保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/3fcdefdb42b9/13020_2024_1051_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/0a349af6689f/13020_2024_1051_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/9d047be131d3/13020_2024_1051_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/47023ca562e4/13020_2024_1051_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/b47b3b1af94f/13020_2024_1051_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/42d52a7cdf65/13020_2024_1051_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/5dbb1235d87b/13020_2024_1051_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/e5e09d4a09ca/13020_2024_1051_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/ca7297dee7f8/13020_2024_1051_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/3fcdefdb42b9/13020_2024_1051_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/0a349af6689f/13020_2024_1051_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/9d047be131d3/13020_2024_1051_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/47023ca562e4/13020_2024_1051_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/b47b3b1af94f/13020_2024_1051_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/42d52a7cdf65/13020_2024_1051_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/5dbb1235d87b/13020_2024_1051_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/e5e09d4a09ca/13020_2024_1051_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/ca7297dee7f8/13020_2024_1051_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2672/11699803/3fcdefdb42b9/13020_2024_1051_Fig9_HTML.jpg

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