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丹皮酚通过抑制PI3K/AKT-NF-κB信号通路影响脂多糖诱导并与平滑肌细胞共培养的大鼠血管内皮细胞的增殖活性

[Paeonol affects proliferation activity of rat vasular endothelial cells induced by lipopolysaccharide and co-cultured with smooth muscle cells via inhibiting pathway of PI3K/AKT-NF-κB signaling].

作者信息

Hu Wen-Jun, Zhang Zhen, Dai Min

机构信息

College of Pharmacy, Anhui University of Chinese Medicine, Key Laboratory of Xin'an Medicine, Ministry of Education, Hefei 230038, China.

出版信息

Zhongguo Zhong Yao Za Zhi. 2016 Jun;41(12):2298-2302. doi: 10.4268/cjcmm20161221.

Abstract

This paper was aimed to observe the anti-atheroslerosis effect of paeonol (Pae) on the activation of PI3K/AKT-NF-κB and the proliferation activity of rat vasular endothelial cells induced by lipopolysaccharide (LPS) and co-cultured with smooth muscle cells. Primary rat vascular endothelial cells (VECs) and rat vascular smooth cells (VSMCs) were cultured by predigesting and adhering tissue blocks. The VEC-VSMC co-culture model was established by Transwell chamber. LPS (100 μg•L ⁻¹, 7 h) was used to induce VEC injury. MTT assay were used to determine the VEC proliferation activity. Western blot was used to detect PI3K/AKT and NF-κB's signaling pathways related protein expressions. The concentration of LPS-induced VECs injury was 100 μg•L ⁻¹, and the time was 7 h. After the intervention on the above cell model for 24 h, paeonol (15, 30, 60 μmol•L ⁻¹) could effectively inhibit LPS-induced VECs injury, block PI3K/AKT-NF-κB signal transduction pathway thereby significantly affecting the proliferation of LPS-induced VECs co-cultured with SMCs. The anti-atherosclerosis mechanism of paeonol may be related to the reducing the inhibitory effect of the signaling pathway associated proteins of VEC PI3K/AKT and NF-κB, thereby increasing the VEC livability under co-culture.

摘要

本文旨在观察丹皮酚(Pae)对脂多糖(LPS)诱导的大鼠血管内皮细胞活化PI3K/AKT-NF-κB及增殖活性的影响,并与平滑肌细胞共培养。采用组织块消化贴壁法培养原代大鼠血管内皮细胞(VECs)和大鼠血管平滑肌细胞(VSMCs)。通过Transwell小室建立VEC-VSMC共培养模型。用LPS(100μg•L⁻¹,7h)诱导VEC损伤。采用MTT法检测VEC增殖活性。用Western blot检测PI3K/AKT和NF-κB信号通路相关蛋白表达。LPS诱导VEC损伤的浓度为100μg•L⁻¹,时间为7h。对上述细胞模型干预24h后,丹皮酚(15、30、60μmol•L⁻¹)可有效抑制LPS诱导的VEC损伤,阻断PI3K/AKT-NF-κB信号转导通路,从而显著影响与SMC共培养的LPS诱导的VEC增殖。丹皮酚的抗动脉粥样硬化机制可能与降低VEC的PI3K/AKT和NF-κB信号通路相关蛋白的抑制作用有关,从而提高共培养条件下VEC的存活率。

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