Hu Wen-Jun, Zhang Zhen, Dai Min
College of Pharmacy, Anhui University of Chinese Medicine, Key Laboratory of Xin'an Medicine, Ministry of Education, Hefei 230038, China.
Zhongguo Zhong Yao Za Zhi. 2016 Jun;41(12):2298-2302. doi: 10.4268/cjcmm20161221.
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.
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。