Inhibition of Antimicrobial Peptide 17BIPHE2 on Lung Adenocarcinoma A549 Cells and Related Mechanism

Objective To investigate the inhibition of antimicrobial peptide 17BIPHE2 on lung adenocarcinoma A549 cells and the related mechanism.

Methods The viabilities of A549 cells treated with 17BIPHE2(0-40μmol/L) were measured by MTT method; flow cytometry and TUNEL were used to observe cell apoptosis; Real-time PCR and Western blot were used to measure the expression of Bax and Bcl-2. Transmission electron microscope was used to observe the ultrastructure change of A549 cells.

Results MTT results showed that 17BIPHE2 could inhibit the proliferation of A549 cells, and the IC₅₀ was 34.33μmol/L. The inhibitory rates at different concentrations (20, 25, 30, 35 and 40μmol/L) of 17BIPHE2 was (1.8±2.7)%, (6.1±2.1)%, (24.6±4.6)%, (55.2±1.1)% and (76.3±1.2)%, respectively. The apoptosis rates of A549 cells treated with 17BIPHE2 (25, 35μmol/L) for 24h were significantly higher than that of the control group(P < 0.05); the nucleus of A549 presented karyopyknosis, hyperchromatin mitochondrial crest fracture, endoplasmic reticulum swelling and other characteristics of apoptosis. Real-time PCR and Western blot results showed that 17BIPHE2 significantly upregulated Bax expression(P < 0.05) and downregulated Bcl-2 expression(P < 0.05) respectively, and the ratio of Bax/Bcl-2 was upregulated.

Conclusion Antimicrobial peptide 17BIPHE2 may induce the apoptosis and suppress the proliferation of A549 cells by upregulating Bax expression and downregulating Bcl-2 expression.