Chinese Skullcap (Scutellaria baicalensis Georgi) inhibits inflammation and proliferation on benign prostatic hyperplasia in rats.

ETHNOPHARMACOLOGICAL RELEVANCE

Chinese Skullcap (Scutellaria baicalensis Georgi), which is part of the 50 fundamental herbs of Traditional Chinese Medicine, has been extensively used in the several East Asian countries to treat pyrexia, micturition disorder and inflammation. Although skullcap has effective properties on various diseases, the effects and molecular mechanism of Chinese Skullcap on BPH are still needed for better understanding.

AIM OF THE STUDY

In present study, we aimed to demonstrate the efficacy of Chinese Skullcap root extract (SRE) in testosterone-induced BPH rats and investigate the exact regulatory mechanism involved.

MATERIALS AND METHODS

We followed a protocol of testosterone-induced BPH. Rats were allocated into five groups: Group 1, control; Group 2, BPH-induced rats; Group 3, BPH-induced rats administrated with finasteride; Group 4, BPH-induced rats administrated with SRE 100 mg/kg/day; Group 5 - BPH-induced rats administrated with SRE 200 mg/kg/day. We measured the weight of prostate, and thickness of prostate using H&E staining. Western blotting, immunostaining and real-time PCR were used to measure proliferation- and inflammation-relative markers. To confirm the effects of SRE on apoptotic events in BPH-induced tissues, we performed the TUNEL assay.

RESULTS

Compared with the untreated group, the SRE administration group suppressed pathological alterations, such as prostate growth and increase in serum DHT and 5α-reductase levels. Furthermore, SRE significantly obliterated the expression of AR and PCNA. SRE also restored Bax/Bcl-2 balance, inducing apoptosis in rats with BPH. These effect of SRE was more prevalent than commercial 5α-reductase inhibitor, finasteride.

CONCLUSIONS

Taken together, we propose that SRE suppresses abnormal androgen events in prostate tissue and inhibits the development of BPH by targeting inflammation- and apoptosis-related markers. These finding strengthens that SRE could be used as plant-based 5α-reductase inhibitory alternative.