Anti-Atherosclerotic Effect of Afrocyclamin A against Vascular Smooth Muscle Cells Is Mediated via p38 MAPK Signaling Pathway.
Anti-Atherosclerotic Effect of Afrocyclamin A against Vascular Smooth Muscle Cells Is Mediated via p38 MAPK Signaling Pathway.
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非洲cy菌A对血管平滑肌细胞的抗动脉粥样硬化作用是通过p38 MAPK信号通路介导的。
DOI：
10.22074/cellj.2021.7148
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发表时间：
2021-07
期刊：
影响因子：
2
通讯作者：
Dou N
中科院分区：
文献类型：
--
作者：
Gu Y;Xiao ZH;Wu J;Guo M;Lv P;Dou N
研究表明，细颗粒物（PM2.5）有助于动脉粥样硬化的扩张和发展。血管平滑肌细胞（VSMC）从血管中膜向内膜的浸润和增殖，是动脉粥样硬化病理生理学的重要一步。 Afrocyclamin A 是一种齐墩果烷型三萜皂苷，从伞形花中分离出来，是常用的中草药。在这项研究中，我们检查了 Afrocyclamin A 对 PM2.5 诱导的 VSMC 增殖的影响，并仔细研究了可能的作用机制。 在实验研究中，计数Kit-8（CCK-8）测定法用于估计VSMCs的活力。 BrdU 免疫荧光用于评估 VSMC 增殖。抗氧化参数的水平，例如丙二醛（MDA）、超氧化物歧化酶（SOD）和谷胱甘肽（GSH）；估计了促炎细胞因子，例如白细胞介素-1β (IL-1β)、IL-6、肿瘤坏死因子-α (TNF-α)、一氧化氮 (NO)、内皮素-1 (ET-1) 和血管细胞粘附分子-1 (VCAM-1)。评估增殖细胞核抗原（PCNA）和磷酸-p38 MAPK（p-p38 MAPK）的表达。 与PM2.5处理的细胞相比，除了减少PM2.5诱导的VSMC增殖外，Afrocyclamin A还降低PCNA和p-p38 MAPK的表达，下调TNF-α、IL-1β、IL-6、VCAM-1、MDA和ET-1的水平，上调SOD、GSH和NO水平。此外，与 Afrocyclamin A 处理的细胞相比，Afrocyclamin A 与 SB203580（p38 MAPK 抑制剂）共孵育后，Afrocyclamin A 的抗增殖作用显着增强。 根据结果，我们可以得出结论，Afrocyclamin A 可能通过减少 p38 MAPK 信号通路来减少 PM2.5 诱导的 VSMC 增殖。
Research suggests that fine particulate matter (PM2.5) contributes to the expansion and development of atherosclerosis. Infiltration and proliferation of vascular smooth muscle cells (VSMCs) from the blood vessel media into the intima, is an important step in the atherosclerosis pathophysiology. Afrocyclamin A, is an oleanane-type triterpene saponin, isolated from Androsace umbellate, which is commonly used in Chinese herbal medicine. In the study, we examined the effect of Afrocyclamin A on PM2.5-induced VSMCs proliferation and scrutinized possible mechanisms of action. In the experimental study, counting Kit-8 (CCK-8) assay was used for estimation of VSMCs viability. BrdU immunofluorescence was used for estimation of VSMCs proliferation. The levels of antioxidant parameters such as malonaldehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH); proinflammatory cytokines such as interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), nitric oxide (NO), endothelin-1 (ET-1), and vascular cell adhesion molecule-1 (VCAM-1), were estimated. The expression of proliferating cell nuclear antigen (PCNA) and phospho-p38 MAPK (p-p38 MAPK) was assessed. Compared to PM2.5-treated cells, in addition to reducing PM2.5-induced VSMCs proliferation, Afrocyclamin A reduced the expression of PCNA and p-p38 MAPK, down-regulated the level of TNF-α, IL-1β, IL-6, VCAM-1, MDA and ET-1, and up-regulated SOD, GSH and NO level. Furthermore, the anti-proliferative effect of Afrocyclamin A was considerably increased following co-incubation of Afrocyclamin A with SB203580 (p38 MAPK inhibitor) in comparison with Afrocyclamin A-treated cells. Based on the results, we can conclude that Afrocyclamin A might reduce PM2.5-induced VSMCs proliferation via reduction of p38 MAPK signaling pathway.
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