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.
- Author:
Wen-Jun HU
1
;
Zhen ZHANG
1
;
Min DAI
1
Author Information
- Publication Type:Journal Article
- Keywords: NF-kappa B signaling pathway; PI3K/AKT signaling pathway; co-culture; endothelial cells; paeonol; smooth muscle cells
- From: China Journal of Chinese Materia Medica 2016;41(12):2298-2302
- CountryChina
- Language:Chinese
- 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.
