[Inhibitory effect of cocoomyxa gloeobotrydifomis on benign prostate hyperplasia in aged rats and its action mechanism].

Objective: To investigate the inhibitory effect of cocoomyxa gloeobotrydifomis (CGD) on benign prostate hyperplasia (BPH) in aged rats and its underlying mechanism.

Methods: Thirty SD male rats aged 21 months were equally randomized to three groups, aged control, low-dose CGD and high-dose CGD, the latter two groups fed on a diet with CGD at 50 and 100 mg per kg per d for 3 months, while the aged controls on normal laboratory chow. Another 10 3-month-old male rats were included in a young control group and fed on the same diet as the aged control rats. At the end of 3 months of CGD treatment, the prostates of all the rats were harvested and weighed. The histomorphological and interstitial changes of the prostatic tissue were observed by HE staining and Masson staining, respectively. The expressions of phosphorylated phosphoinositide-dependent kinase 1 (PDK1), phosphorylated Akt (Ser 473) and phosphorylated PTEN in the rat prostate were determined by Western blotting.

Results: The wet weight and index of the prostate were significantly higher in the aged controls than in the young controls ([1 220 +/- 140] vs [550 +/- 60] mg, P < 0.01; 2.08 +/- 0.17 vs 1.94 +/- 0.10, P < 0.05). High-dose CGD significantly inhibited the increase in the prostatic wet weight and index of the aged rats ([1 080 +/- 97] mg and 1.85 +/- 0.16) as compared with the aged controls (P < 0.01 and P < 0.05). The epithelium and interstitium, particularly the latter, were evidently thicker in the aged control than in the CGD-treated rats. The protein levels of phosphorylated PDK1 and Akt were significantly enhanced, while that of phosphorylated PTEN remarkably down-regulated in the aged rats as compared with the young ones. The expressions of phosphorylated PDK1 and Akt were significantly decreased, whereas that of phosphorylated PTEN markedly increased in both the low-dose and high-dose CGD groups.

Conclusion: CGD can significantly inhibit BPH in aged rats through down-regulating the PI3K/Akt pathway.