Study of mechanisms of hesperidin onanti-lung cancer effect based on microfluidic chip technology
10.3969/j.issn.1001-1978.2017.09.015
- VernacularTitle:基于微流控芯片技术橙皮苷抗肺肿瘤作用机制研究
- Author:
Jiaxin FAN
;
Shuai WANG
;
Xiansheng MENG
;
Yongrui BAO
;
Tianjiao LI
- Keywords:
hesperidin;
lung cancer cell A549;
microfluidic chip technology;
real-time PCR;
PI3K-Akt signal pathway;
Cyclin B1;
Bcl-2;
cell apoptosis
- From:
Chinese Pharmacological Bulletin
2017;33(9):1260-1265
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect of hesperidin on human lung cancer cell A549 and the possible mechanism.Methods The cell apoptosis and necrosis of A549 treated with hesperidin were measured by the Hoechst 33342/PI fluorescent dye based on microfluidic chip technology.Cell cycle and apoptosis rate were evaluated by flow cytometry(FCM).The expressions of the related genes were detected through the real-time fluorescent quantitative PCR technology(RT-PCR) including VEGF, PI3K and PTEN.The protein expressions of Bcl-2, Cyclin B1, PI3K, Akt and PTEN were detected by Western blot after hesperidin intervention.Results The proliferation of A549 cells was significantly inhibited by hesperidin in a dose-dependent manner.FCM results showed that hesperidin could not only influence the G0/G1 phase and S phase, but also promote the apoptosis of lung cancer cells.Meanwhile, the apoptosis and necrosis rate was increased from(6.7±0.6)% to(27.9±1.1)% compared with that of control group(P<0.05).From the level of molecular, the gene expressions of VEGF and PI3K were decreased, while the PTEN was increased after hesperidin stimulation.Western blot results showed that the expression of protein Bcl-2, Cyclin B1 and Akt were decreased, which all showed close relationship with cell apoptosis, cell cycle and PI3K-Akt signaling pathway.The expression of PI3K was increased, but the change of PTEN was not statistically significant compared with that of control group.Conclusion Hesperidin induces lung cancer cell apoptosis through PI3K-Akt signaling pathway, which blocks cancer cell division and destroys the balance of related protein expression.
