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已发表论文
京尼平苷通过 PPARγ 信号通路诱导 M2 极化稳定动脉粥样硬化斑块
Authors Jin Z, Chu Q, Du Z, Li J, Wu W , Zhou X, Zhao H
Received 23 October 2024
Accepted for publication 23 August 2025
Published 30 September 2025 Volume 2025:19 Pages 8805—8821
DOI https://doi.org/10.2147/DDDT.S499890
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Yan Zhu
Zheng Jin, Qingmin Chu, Zhiyi Du, Junlong Li, Wei Wu, Xiaoxiong Zhou, Huanyi Zhao
First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510000, People’s Republic of China
Correspondence: Xiaoxiong Zhou, First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510000, People’s Republic of China, Email zhouxiaoxiong0825@163.com Huanyi Zhao, First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510000, People’s Republic of China, Email zhao_banli@163.com
Objective: The instability of atherosclerotic (AS) plaque constitutes a critical trigger for acute intravascular thrombosis and cardiovascular disease. Prior studies have found that Geniposide (Gen) is capable of regulating macrophage polarization and stabilizing AS plaque. However, its potential mechanism is not clear. Given the role of peroxisome proliferator-activated receptor γ (PPARγ) in mediating macrophage polarization, this study aims to investigate the relationship between Gen, PPARγ and macrophage polarization.
Methods: In vitro, RAW264.7 was used to investigate the effects of Gen on polarization phenotype, anti-inflammatory activity, and its correlation with PPARγ. In vivo, ApoE−/− mice were fed with a high-fat diet to induce AS and were used to evaluate the pharmacological effects of Gen. Additionally, the relationship between Gen, PPARγ and M2 polarization in AS was verified.
Results: In vitro, Gen upregulated the expressions of M2 macrophage markers (CD163, IL-10, Arg-1). Moreover, Gen increased the expressions of PPARγ target genes (CD36, ABCG1) and activated PPARγ activity, which could be inhibited by PPARγ antagonist GW9662. In vivo, the intervention of Gen on AS model of ApoE−/− mice played a role in reducing the blood lipid, stabilizing AS plaques and down-regulating the level of inflammatory factors. Consistent with the results in vitro, Gen was able to regulate the expression of macrophage polarization and increase the expression of PPARγ, while GW9662 treatment inhibited the expression of M2 phenotypic markers.
Conclusion: Gen regulates macrophage polarization to M2 phenotype and plays a role in inhibiting inflammation and stabilizing plaque by mediating PPARγ activation, which suggests that Gen may be a promising agent for AS.
Keywords: atherosclerosis, geniposide, macrophage polarization, inflammation, PPARγ
First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510000, People’s Republic of China
Correspondence: Xiaoxiong Zhou, First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510000, People’s Republic of China, Email zhouxiaoxiong0825@163.com Huanyi Zhao, First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510000, People’s Republic of China, Email zhao_banli@163.com
Objective: The instability of atherosclerotic (AS) plaque constitutes a critical trigger for acute intravascular thrombosis and cardiovascular disease. Prior studies have found that Geniposide (Gen) is capable of regulating macrophage polarization and stabilizing AS plaque. However, its potential mechanism is not clear. Given the role of peroxisome proliferator-activated receptor γ (PPARγ) in mediating macrophage polarization, this study aims to investigate the relationship between Gen, PPARγ and macrophage polarization.
Methods: In vitro, RAW264.7 was used to investigate the effects of Gen on polarization phenotype, anti-inflammatory activity, and its correlation with PPARγ. In vivo, ApoE−/− mice were fed with a high-fat diet to induce AS and were used to evaluate the pharmacological effects of Gen. Additionally, the relationship between Gen, PPARγ and M2 polarization in AS was verified.
Results: In vitro, Gen upregulated the expressions of M2 macrophage markers (CD163, IL-10, Arg-1). Moreover, Gen increased the expressions of PPARγ target genes (CD36, ABCG1) and activated PPARγ activity, which could be inhibited by PPARγ antagonist GW9662. In vivo, the intervention of Gen on AS model of ApoE−/− mice played a role in reducing the blood lipid, stabilizing AS plaques and down-regulating the level of inflammatory factors. Consistent with the results in vitro, Gen was able to regulate the expression of macrophage polarization and increase the expression of PPARγ, while GW9662 treatment inhibited the expression of M2 phenotypic markers.
Conclusion: Gen regulates macrophage polarization to M2 phenotype and plays a role in inhibiting inflammation and stabilizing plaque by mediating PPARγ activation, which suggests that Gen may be a promising agent for AS.
Keywords: atherosclerosis, geniposide, macrophage polarization, inflammation, PPARγ