OBJECTIVE: To evaluate the proliferation inhibitory effect of Lappaconitine (LAP) on non-small cell lung cancer cell line A549 cells in vitro and its possible mechanism. METHODS: A549 cell was cultured with different concentrations of LAP. Cellular proliferation was determined with MTT. Cell cycle and apoptosis were detected with FCM technology. The Cyclin E1 gene expression was checked by Real-time Quantitative PCR method. RESULTS: LAP could inhibit the proliferation of A549 cells in vitro in a dose-dependent manner. LAP could induce apoptosis of A549 cell. Cell cycle was stopped at the G1 + G0 phase by LAP with FCM technology. With the increasement of LAP concentration, the ratio of G1 + G0 phase was increased and the ratio of S phase and G2 + M phase was decreased; The apoptotic rate was gradually increased, and the Cyclin E1 gene expression was down-regulated. CONCLUSION: LAP has the inhibitory effect on the growth of A549 cells, which is related to the cell cycle arrest in G0/G1 phase, apoptosis and down-regulation of Cyclin E1 gene expression.
OBJECTIVE: To evaluate the proliferation inhibitory effect of Lappaconitine (LAP) on non-small cell lung cancer cell line A549 cells in vitro and its possible mechanism. METHODS: A549 cell was cultured with different concentrations of LAP. Cellular proliferation was determined with MTT. Cell cycle and apoptosis were detected with FCM technology. The Cyclin E1 gene expression was checked by Real-time Quantitative PCR method. RESULTS:LAP could inhibit the proliferation of A549 cells in vitro in a dose-dependent manner. LAP could induce apoptosis of A549 cell. Cell cycle was stopped at the G1 + G0 phase by LAP with FCM technology. With the increasement of LAP concentration, the ratio of G1 + G0 phase was increased and the ratio of S phase and G2 + M phase was decreased; The apoptotic rate was gradually increased, and the Cyclin E1 gene expression was down-regulated. CONCLUSION:LAP has the inhibitory effect on the growth of A549 cells, which is related to the cell cycle arrest in G0/G1 phase, apoptosis and down-regulation of Cyclin E1 gene expression.