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梓醇通过调节雌激素受体α抑制巨噬细胞极化并预防绝经后动脉粥样硬化。

Catalpol Inhibits Macrophage Polarization and Prevents Postmenopausal Atherosclerosis Through Regulating Estrogen Receptor Alpha.

作者信息

Chen Qi, Qi Xu, Zhang Weiwei, Zhang Yuhan, Bi Yunhui, Meng Qinghai, Bian Huimin, Li Yu

机构信息

School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, China.

School of Medicine and Life Sciences, Nanjing University of Chinese Medicine, Nanjing, China.

出版信息

Front Pharmacol. 2021 Apr 30;12:655081. doi: 10.3389/fphar.2021.655081. eCollection 2021.

DOI:10.3389/fphar.2021.655081
PMID:33995075
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8120111/
Abstract

Lacking estrogen increases the risk of atherosclerosis (AS) in postmenopausal women. Inflammation plays a vital role in the pathological process of AS, and macrophages are closely related to inflammation. Catalpol is an iridoid glucoside extracted from the fresh roots of the traditional Chinese herb . In this study, we aimed to evaluate the effects of catalpol on macrophage polarization and postmenopausal AS. In addition, we investigated whether the mechanism of catalpol was dependent on regulating the expression of estrogen receptors (ERs). , lipopolysaccharides (LPS) and interferon-γ (IFN-γ) were applied to induce M1 macrophage polarization. , the ApoE mice were fed with a high-fat diet to induce AS, and ovariectomy was operated to mimic the estrogen cessation. We demonstrated catalpol inhibited M1 macrophage polarization induced by LPS and INF-γ, and eliminated lipid accumulation in postmenopausal AS mice. Catalpol not only suppressed the inflammatory response but also reduced the level of oxidative stress. Then, ERs (ERα and ERβ) inhibitors and ERα siRNA were also applied in confirming that the protective effect of catalpol was mediated by ERα, rather than ERβ. In conclusion, catalpol significantly inhibited macrophage polarization and prevented postmenopausal AS by increasing ERα expression.

摘要

雌激素缺乏会增加绝经后女性患动脉粥样硬化（AS）的风险。炎症在AS的病理过程中起着至关重要的作用，而巨噬细胞与炎症密切相关。梓醇是从传统中药新鲜根中提取的一种环烯醚萜苷。在本研究中，我们旨在评估梓醇对巨噬细胞极化和绝经后AS的影响。此外，我们还研究了梓醇的作用机制是否依赖于调节雌激素受体（ERs）的表达。采用脂多糖（LPS）和干扰素-γ（IFN-γ）诱导M1巨噬细胞极化。对载脂蛋白E（ApoE）小鼠喂食高脂饮食以诱导AS，并进行卵巢切除术以模拟雌激素缺乏。我们证明梓醇抑制了LPS和INF-γ诱导的M1巨噬细胞极化，并消除了绝经后AS小鼠的脂质积累。梓醇不仅抑制了炎症反应，还降低了氧化应激水平。然后，应用ERs（ERα和ERβ）抑制剂和ERα小干扰RNA（siRNA）证实梓醇的保护作用是由ERα介导的，而不是ERβ。总之，梓醇通过增加ERα表达显著抑制巨噬细胞极化并预防绝经后AS。

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