EFFECTS OF GANODERMA LUCIDUM TRITERPENOIDS ON MITOCHONDRIAL APOPTOSIS FACTORS IN MICE WITH PROSTATIC HYPERPLASIA INDUCED BY TESTOSTERONE PROPIONATE

HioHeng Cheng*

Cheng Hio Heng Clinic , Macau, Macao 99076, China

Objective: To investigate the effect of Ganoderma lucidum triterpenoids on mitochondrial apoptosis factors in mice with benign prostatic hyperplasia (BPH) induced by testosterone propionate.

Methods: Of the 80 mice collected, 16 were randomly selected as the blank control group, which had no intervention. The remaining 64 ICR mice were subcutaneously injected with 0.5mg/d testosterone propionate to establish a BPH model. After successful modelling, they were randomly divided into a negative control group, a low-concentration group, a medium-concentration group and a high-concentration group, with 16 mice in each group The mice in the negative control group were treated with an equal volume of normal saline. The histopathological changes of BPH were observed and analysed. The apoptosis rate of mitochondria, the release of reactive oxygen species (ROS), cell cycle and the expression of Caspase-3, Bad, Bax and Bcl-2 were compared.

Results: no obvious pathological changes were found in the blank control group. Papillary hyperplasia was found in the negative control group, inflammatory cell infiltration and cell arrangement were irregular, and the size was different. The situation of the Ganoderma acid D-concentration group was significantly improved compared with the negative control group, and the concentration dependence of the Ganoderma acid D groups was observed. The apoptosis rate of the negative control group was significantly lower than that of the blank control group. The apoptosis rate of the Ganoderma acid D group was significantly higher than that of the negative control group (P<0.05). The ROS content of BPH mice in the negative control group was significantly lower than that in the blank control group. The ROS content of BPH mice in the Ganoderma D concentration group was significantly higher than that in the negative control group in a concentration-dependent manner (P<0.05). The proportion of the G0/G1 phase in the negative control group was significantly lower than that in the blank control group, and the proportions of the S phase and the G2/M phase were significantly higher than that of the blank control group. The proportion of G0/G1 phase in the Ganoderma acid D group was significantly higher than that in the negative control group, and the ratio of S phase and G2/M phase was significantly lower than that of the negative control group in a concentration-dependent manner (P<0.05). The expression levels of Caspase-3, Bad and Bax proteins in the mitochondria of BPH mice in the negative control group were significantly lower than those in the blank control group, and the expression level of Bcl-2 protein was significantly higher than that of the blank control group (P < 0.05). The expression levels of Bad and Bax in the 62.5 μM Ganoderma D group were significantly higher than those in the negative control group (P<0.05). The expression of Bad protein in the 125 μM Ganoderma D group was significantly higher than that in the negative control group (P<0.05). The expression level of Caspase-3 protein in the 250 μM Ganoderma acid D group was significantly higher than that in the negative control group, and the expression level of Bcl-2 protein was significantly lower than that of the negative control group (P<0.05).

Conclusion: Ganoderma acid D can promote mitochondrial apoptosis and ROS release induced by testosterone propionate, block the cell cycle at G0/G1, increase the expression levels of Caspase-3, Bad and Bax proteins, and down-regulate the expression of Bcl-2 protein, and this may promote apoptosis of BHP-1 cells through a mitochondrial apoptosis pathway.