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参红通络胶囊通过激活 PPAR-/LXR-/ABCA1 通路减轻巨噬细胞炎症和脂质堆积。

Shen-Hong-Tong-Luo Formula Attenuates Macrophage Inflammation and Lipid Accumulation through the Activation of the PPAR-/LXR-/ABCA1 Pathway.

机构信息

Research Center of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, Jilin, China.

Jilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, Jilin, China.

出版信息

Oxid Med Cell Longev. 2020 Oct 1;2020:3426925. doi: 10.1155/2020/3426925. eCollection 2020.

DOI:10.1155/2020/3426925
PMID:33082908
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7556105/
Abstract

Atherosclerosis (AS) is the killer of human health and longevity, which is majorly caused by oxidized lipoproteins that attack macrophages in the endarterium. The Shen-Hong-Tong-Luo (SHTL) formula has shown great clinical efficacy and vascular protective effect for over 30 years in China, to attenuate AS progression. However, its pharmacological mechanism needs more investigation. In this study, we first investigated the chemical composition of SHTL by fingerprint analysis using high-performance liquid chromatography. In primary mouse peritoneal macrophages induced by lipopolysaccharide (LPS), we found that SHTL pretreatment suppressed reactive oxygen species accumulation and reversed the increases of the inflammatory factors, TNF- and IL-6. Moreover, lipid accumulation induced by oxidized low-density lipoprotein (Ox-LDL) in macrophages was inhibited by SHTL. Additionally, network pharmacology was used to predict the potential targets of SHTL as the PPAR-/LXR-/ABCA1 signaling pathway, which was validated in macrophages and ApoE mice by histopathological staining, qPCR, and Western blot analysis. Importantly, the protective effect of SHTL in the LPS- and Ox-LDL-induced macrophages against inflammation and lipid accumulation was attenuated by GW9662, a PPAR- antagonist, which confirmed the prediction results of network pharmacology. In summary, these results indicated that SHTL pretreatment reduced inflammation and lipid accumulation of macrophages by activating the PPAR-/LXR-/ABCA1 pathway, which may provide a new insight into the mechanism of SHTL in the suppression of AS progression.

摘要

动脉粥样硬化（AS）是人类健康和长寿的杀手，主要是由攻击内皮下巨噬细胞的氧化脂蛋白引起的。参红通脉方在中国已有 30 多年的临床疗效和血管保护作用，可减轻 AS 的进展。然而，其药理机制需要进一步研究。在这项研究中，我们首先通过使用高效液相色谱的指纹分析方法研究了 SHTL 的化学成分。在由脂多糖（LPS）诱导的原代小鼠腹腔巨噬细胞中，我们发现 SHTL 预处理抑制活性氧的积累，并逆转了促炎因子 TNF-α和 IL-6 的增加。此外，SHTL 抑制了氧化低密度脂蛋白（Ox-LDL）诱导的巨噬细胞中的脂质积累。此外，还使用网络药理学预测 SHTL 的潜在靶点作为 PPAR-/LXR-/ABCA1 信号通路，并用组织病理学染色、qPCR 和 Western blot 分析在巨噬细胞和 ApoE 小鼠中进行验证。重要的是，PPAR-拮抗剂 GW9662 减弱了 SHTL 在 LPS 和 Ox-LDL 诱导的巨噬细胞中对炎症和脂质积累的保护作用，这证实了网络药理学的预测结果。总之，这些结果表明，SHTL 预处理通过激活 PPAR-/LXR-/ABCA1 通路减少巨噬细胞的炎症和脂质积累，这可能为 SHTL 抑制 AS 进展的机制提供新的见解。

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