Abstract

Objective To observe the inhibitory effect of gambogic acid on the proliferation of liver cancer cells HepG2 and explore its mechanism. Methods The vitro cultured liver cancer cells HepG2 were divided into the control group, low dose gambogic acid group, medium dose gambogic acid group and high dose gambogic acid group according to random number table method, 5 multiple holes in each group. The control group was cultured in normal medium and 0.5% DMSO was added as the solvent control. The 0.1, 1 and 10 μmol/L of gambogic acid were added to low, medium and high dose group of gambogic acid for intervention. MTT method was used to detect the inhibition rate of cell proliferation, flow cytometry was used to detect the apoptosis rate, Hoechst nuclear staining was used to observe the nucleus apoptosis, and Western blot was used to detect the expression of Bcl-2 and Bax protein. Results Compared with the control group, the HepG2 cells proliferation rate (68.00% ± 3.55%, 51.93% ± 4.36%, 47.16% ± 4.73% vs. 99.87% ± 4.53%) in low, medium and high dose gambogic acid group significantly decreased (P<0.01); apoptosis rate (23.00% ± 1.22%, 40.09% ± 4.65%, 70.32% ± 4.99% vs. 4.33% ± 0.57%) significantly elevated (P<0.01); Bcl-2 experssion (0.73 ± 0.10, 0.25 ± 0.10, 0.19 ± 0.08 vs. 0.97 ± 0.11) significantly decreased (P<0.01); and Bax expression (0.39 ± 0.14, 0.88 ± 0.15, 0.85 ± 0.13 vs. 0.22 ± 0.08) significantly elevated (P<0.01); Bax/Bcl-2 (0.34 ± 0.10, 1.87 ± 0.29, 1.63 ± 0.23 vs. 0.13 ± 0.06) significantly increased (P<0.01). Hoechst staining showed that the apoptosis rate of HepG2 cells increased in a dose-dependent manner with the increasing concentration of gambogic acid. Conclusions Gambogic acid could inhhibit HepG2 cells proliferation by regulating the expression of Bax and Bcl-2. Key words: Gambogic acid; Hep G2 cells; Cell proliferation; Apoptosis

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