Alkaline processing of cantharidin can significanty improve the antitumor activity of cantharidin.
10.12122/j.issn.1673-4254.2020.09.17
- Author:
Xian LI
1
;
Shanshan LI
1
;
Jinlong PANG
1
;
Fuhao HUANG
1
;
Bin GUO
1
;
Hao LIU
1
Author Information
1. School of Pharmacy, Bengbu Medical College, Bengbu 2330302, China.
- Publication Type:Journal Article
- Keywords:
alkaline processed cantharis;
apoptosis;
inflammatory factors;
invasion;
migration
- From:
Journal of Southern Medical University
2020;40(9):1332-1339
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To assess the changes in the effects of cantharides after alkaline processing on proliferation, migration, invasion, and apoptosis of human lung cancer A549 cells.
METHODS:Human non-small cell lung cancer A549 cells were treated with cantharis extract (CTE) from raw cantharides and alkali processed cantharis extract (ACE). The proliferation of the cells was detected with CCK-8 assay, and the cell migration and invasion were assessed using wound healing assay and Transwell assay, respectively. The expressions of MMP1 and MMP2 in the cells were detected using Western blotting, the contents of IFN-γ, IL-1β and TNF-α were measured with ELISA, and cell apoptosis was analyzed with annexinV/PI fluorescent staining.
RESULTS:Both CTE and ACE significantly reduced the viability and inhibited the migration of A549 cells, and high-dose ACE produced a significantly stronger inhibitory effect on cell migration than high- dose CTE ( < 0.01). ACE showed more potent inhibitory effect than CTE on the invasion of A549 cells ( < 0.01). Both CTE and ACE inhibited the expressions of MMP1 and MMP2 and up-regulated the level of IFN-γ without significantly affecting the levels of IL-1β and TNF-α. Annexin V/PI staining showed that both CTE and ACE caused apoptosis of A549 cells, but ACE had a stronger proapoptotic effect.
CONCLUSIONS:Processing with sodium hydroxide can significantly improve the antitumor activity of cantharides, which inhibits the proliferation, migration and invasion of A549 cells possibly by down-regulating the expressions of MMP1 and MMP2, promoting apoptosis and increasing the level of IFN-γ.
