Effects of cell proliferation and apoptosis of L-carnitine combined with epirubicin on different human lung adenocarcinoma cells / 国际生物医学工程杂志

ABSTRACT

Objective To investigate the effect of L-carnitine (LCNT) combined with epirubicin (EPI) on cell proliferation and apoptosis of two lung adenocarcinoma cell lines (GLC-82 and A549). Methods GLC-82 and A549 cells were divided into control group, EPI group, LCNT group and EPI+LCNT group, respectively. The cell proliferation rate was examined by MTT assay 24 h after the treatment, and the cell cycle and cell early apoptosis were analyzed by flow cytometry. The expression of P53 and Bcl-2 proteins were detected by Western Blot. Results Compared with the control group, the proliferation rate of GLC-82 and A549 cells was 37.56％(P<0.01) and 6.32％(P>0.05) after 24 hours of 20.00μg/ml LCNT treatment indicating LCNT could promote the proliferation of GLC-82 cells. Compared with the EPI group, EPI+LCNT had smaller inhibitory effect on the proliferation of GLC-82 cells, and the inhibition rate of the EPI+LCNT group was 12.14％lower than that of EPI group (P<0.05). Compared with the EPI group, EPI+LCNT could significantly increase the G0/G1 phase ratio of GLC-82 cells (50.42％±1.21％vs. 25.94％± 0.66％, P<0.01) and A549 cells (54.92％±1.71％vs. 38.63％±0.69％, P<0.01), decrease the S phase ratio of GLC-82 cells (34.21％±0.96％vs. 59.68％±1.25％, P<0.05), and prevent the early apoptosis of GLC-82 cells without affecting apoptosis of A549 cells. Moreover, in the EPI+LCNT group, the expression of P53 protein in GLC-82 and A549 cells was down-regulated (P<0.05), and the expression of Bcl-2 protein in GLC-82 cells was up-regulated (P<0.01) and no significant change in A549 cells (P>0.05). Conclusions Comparing with the EPI, the combination of LCNT and EPI has less proliferation inhibition and apoptosis induction on GLC-82 cells, and without significant effect on A549 cells. LCNT can promote the proliferation of GLC-82 cells and block the cell cycle at G0/G1 phase. This mechanism may be related to down-regulation of P53 protein and up-regulation of Bcl-2 protein expression.