Puerarin inhibits vascular smooth muscle cells proliferation induced by fine particulate matter via suppressing of the p38 MAPK signaling pathway.
Puerarin inhibits vascular smooth muscle cells proliferation induced by fine particulate matter via suppressing of the p38 MAPK signaling pathway.
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葛根素通过抑制 p38 MAPK 信号通路抑制细颗粒物诱导的血管平滑肌细胞增殖
DOI：
10.1186/s12906-018-2206-9
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发表时间：
2018-05-04
影响因子：
--
通讯作者：
Yang Y
中科院分区：
文献类型：
--
作者：
Wan Q;Liu Z;Yang Y
细颗粒物（PM2.5）是动脉粥样硬化发生和发展的主要危险因素。血管平滑肌细胞（VSMCs）从血管介质向内膜的增殖和浸润是动脉粥样硬化病理生理的关键步骤。葛根素是一种天然的葛根提取物，具有显著的抗动脉粥样硬化特性。然而，葛根素对PM2.5诱导的VSMCs增殖作用的潜在分子机制尚不清楚。本研究旨在探讨葛根素对pm2.5诱导的VSMCs增殖的影响，并探讨p38丝裂原活化蛋白激酶（p38 MAPK）的信号机制。方法采用CCK-8法检测svsmcs活力，BrdU免疫荧光法检测VSMCs增殖，比色法检测超氧化物歧化酶（SOD）和丙二醛（MDA）水平，硝酸还原酶法和放射免疫法检测一氧化氮（NO）和内皮素-1 （ET-1）水平，ELISA法检测血管细胞粘附分子-1 （VCAM-1）、白细胞介素-6 （IL-6）和肿瘤坏死因子-α (TNF-α)水平。Western blot检测VSMCs中磷酸化-p38 MAPK （p-p38 MAPK）蛋白和增殖细胞核抗原（PCNA）蛋白的表达。结果与pm2.5处理的细胞相比，葛根素除抑制pm2.5诱导的VSMCs增殖外，还下调p-p38 MAPK和PCNA蛋白表达，降低ET-1、VCAM-1、IL-6、TNF-α和MDA水平，升高NO和SOD水平。此外，与经葛根素处理的细胞相比，葛根素与p38 MAPK选择性抑制剂SB203580共孵生后，葛根素的抗增殖作用显著增强。结论葛根素可能通过抑制p38 MAPK信号通路抑制pm2.5诱导的VSMCs增殖。
BackgroundFine particulate matter (PM2.5) is a major risk factor for the development and progression of atherosclerosis. Proliferation and infiltration of vascular smooth muscle cells (VSMCs) from the blood vessel media into the intima is a crucial step in the pathophysiology of atherosclerosis. Puerarin, a natural extract fromRadix Puerariae, possesses significant anti-atherosclerosis properties. However, the underlying molecular mechanisms responsible for the effect of puerarin on the VSMCs proliferation induced by PM2.5 remain unclear. The present study was designed to examine the effect of puerarin on PM2.5-induced VSMCs proliferation, and to explore the p38 mitogen-activated protein kinase (p38 MAPK) signal mechanism involved.MethodsVSMCs viability was measured by CCK-8 assay, VSMCs proliferation was assessed by BrdU immunofluorescence, the levels of superoxide dismutase (SOD) and malonaldehyde (MDA) were assayed by colorimetric assay kits, the levels of nitric oxide (NO) and endothelin-1 (ET-1) were determined by nitrate reductase method and radioimmunoassay, the levels of vascular cell adhesion molecule-1 (VCAM-1), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were measured by ELISA. The protein expressions of phospho-p38 MAPK (p-p38 MAPK) and proliferating cell nuclear antigen (PCNA) in the VSMCs were subjected by Western blot.ResultsCompared to the PM2.5-treated cells, in addition to inhibiting the PM2.5-induced VSMCs proliferation, puerarin also down-regulated the protein expressions of p-p38 MAPK and PCNA, decreased the levels of ET-1, VCAM-1, IL-6, TNF-α and MDA, increased the levels of NO and SOD. Moreover, the anti-proliferative effects of puerarin were significantly enhanced by the co-incubation of puerarin with SB203580, a selective inhibitor of p38 MAPK, as compared to the puerarin-treated cells.ConclusionThese results suggest that puerarin might suppress the PM2.5-induced VSMCs proliferation via the inhibition of the p38 MAPK signaling pathway.
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影响因子：
24
作者：
Krishnan, Ranjini M.;Adar, Sara D.;Szpiro, Adam A.;Jorgensen, Neal W.;Van Hee, Victor C.;Barr, R. Graham;O'Neill, Marie S.;Herrington, David M.;Polak, Joseph F.;Kaufman, Joel D.
通讯作者：
Kaufman, Joel D.
影响因子：
10.4
作者：
Krall JR;Anderson GB;Dominici F;Bell ML;Peng RD
通讯作者：
Peng RD
DOI：
10.1152/ajpheart.00327.2006
发表时间：
2006-12-01
影响因子：
4.8
作者：
Hashim, Shehla;Li, Yuan;Anand-Srivastava, Madhu B.
通讯作者：
Anand-Srivastava, Madhu B.
影响因子：
0.9
作者：
Bao, Lidao;Zhang, Ying;Agula, B.
通讯作者：
Agula, B.
影响因子：
20.1
作者：
Gimbrone MA Jr;García-Cardeña G
通讯作者：
García-Cardeña G