DC Field | Value | Language |
---|---|---|
dc.contributor.author | E B Baek | - |
dc.contributor.author | Y H Hwang | - |
dc.contributor.author | S Park | - |
dc.contributor.author | E J Hong | - |
dc.contributor.author | Young Suk Won | - |
dc.contributor.author | H J Kwun | - |
dc.date.accessioned | 2022-10-04T16:32:25Z | - |
dc.date.available | 2022-10-04T16:32:25Z | - |
dc.date.issued | 2022 | - |
dc.identifier.issn | 2253-2447 | - |
dc.identifier.uri | https://oak.kribb.re.kr/handle/201005/30419 | - |
dc.description.abstract | Introduction: Benign prostatic hyperplasia (BPH) is a non-neoplastic proliferative disease of the prostate. Eriochloa villosa (EV) reportedly possesses various pharmacological activities, including anti-lipase activity and modulation of various antioxidative enzymes. In this study, we investigate the therapeutic potential of EV against BPH in a testosterone-induced BPH rat model. Methods: Rats were subjected to a daily subcutaneous injection of testosterone (3 mg kg-1) for 4 weeks to induce BPH. Along with testosterone, rats in the treatment group were administered finasteride (10 mg kg-1) or EV (150 mg kg-1) via oral gavage. Prostatic cancer (LNCaP) cell line was used to examine the effect of EV. Results: Finasteride and EV significantly decrease the relative prostate weight, serum levels of dihydrotestosterone and testosterone, and prostate epithelial thickness. Testosterone injection induced prostatic hyperplasia and proliferating cell nuclear antigen expression; however, EV treatment significantly attenuated these effects. Moreover, finasteride- and EV-treated rats exhibit an increase in the number of TUNEL-positive cells and reduced Bcl-2 expression in the prostate tissues compared with the testosterone-treated animals. Furthermore, EV suppresses inflammatory cytokines, including interleukin (IL)-6 and IL-8, in the prostate tissues. Meanwhile, the expression of inflammatory mediator cyclooxygenase-2 is consistently upregulated in testosterone-treated rats, whereas EV treatment significantly reverses this effect. Notably, EV treatment suppresses malondialdehyde (MDA) levels and upregulates testosterone-induced catalase (CAT) expression. In addition, EV suppresses expression of androgen receptor (AR) and prostate-specific antigen (PSA) induced by testosterone in LNCaP cells. Conclusion: The present study results suggest that EV regulates prostatic proliferation, apoptosis, response to inflammation, and oxidative stress in the BPH rat model, and may, therefore, serve as a useful therapeutic agent for BPH. | - |
dc.publisher | Dovepress | - |
dc.title | Eriochloa villosa alleviates progression of benign prostatic hyperplasia in vitro and in vivo | - |
dc.title.alternative | Eriochloa villosa alleviates progression of benign prostatic hyperplasia in vitro and in vivo | - |
dc.type | Article | - |
dc.citation.title | Research and Reports in Urology | - |
dc.citation.number | 0 | - |
dc.citation.endPage | 326 | - |
dc.citation.startPage | 313 | - |
dc.citation.volume | 14 | - |
dc.contributor.affiliatedAuthor | Young Suk Won | - |
dc.contributor.alternativeName | 백은복 | - |
dc.contributor.alternativeName | 황연환 | - |
dc.contributor.alternativeName | 박수영 | - |
dc.contributor.alternativeName | 홍은주 | - |
dc.contributor.alternativeName | 원영석 | - |
dc.contributor.alternativeName | 권효정 | - |
dc.identifier.bibliographicCitation | Research and Reports in Urology, vol. 14, pp. 313-326 | - |
dc.identifier.doi | 10.2147/RRU.S381713 | - |
dc.subject.keyword | Benign prostatic hyperplasia | - |
dc.subject.keyword | Eriochloa villosa | - |
dc.subject.keyword | Proliferation | - |
dc.subject.keyword | Apoptosis | - |
dc.subject.keyword | Inflammation | - |
dc.subject.keyword | Oxidative stress | - |
dc.subject.local | Benign prostatic hyperplasia | - |
dc.subject.local | benign prostatic hyperplasia | - |
dc.subject.local | Eriochloa villosa | - |
dc.subject.local | Proliferation | - |
dc.subject.local | proliferation | - |
dc.subject.local | Apoptosis | - |
dc.subject.local | apoptosis | - |
dc.subject.local | Inflammation | - |
dc.subject.local | inflammation | - |
dc.subject.local | nflammation | - |
dc.subject.local | OXIDATIVE STRESS | - |
dc.subject.local | Oxidative Stress | - |
dc.subject.local | Oxidative stre | - |
dc.subject.local | Oxidative stress | - |
dc.subject.local | oxidative stress | - |
dc.description.journalClass | N | - |
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