ArticleExperimental and therapeutic medicine2018
Roles of autophagy in androgen-induced benign prostatic hyperplasia in castrated rats.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 16 citations in OpenAlex.
- Review
- Identifying hub genes and common biological pathways between COVID-19 and benign prostatic hyperplasia by machine learning algorithms.Frontiers in immunology · 2023Article
- Ameliorative effect ofNutrition research and practice · 2022Article
- Effect of Beclin-1 gene silencing on autophagy and apoptosis of the prostatic hyperplasia epithelial cells.Clinics (Sao Paulo, Brazil) · 2022Article
- Chemerin regulates autophagy to participate in polycystic ovary syndrome.The Journal of international medical research · 2021Article
- Oral exposure of sulpiride promotes the proliferation of Brown-Norway rat prostates.Experimental and therapeutic medicine · 2020Article
- Rapamycin‑induced autophagy attenuates hormone‑imbalance‑induced chronic non‑bacterial prostatitis in rats via the inhibition of NLRP3 inflammasome‑mediated inflammation.Molecular medicine reports · 2019Article
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
The present study investigated the role of androgen in the process of androgen-induced prostate hyperplasia in castrated rats and assessed the role of the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR) pathway in this process. Furthermore, the extent to which autophagy may affect the level of androgen-induced benign prostatic hyperplasia was also explored. A total of 40 Sprague Dawley rats were randomly divided into four groups: Testosterone group, rapamycin group, 3-methyladenine (3-MA) group, and control group. The extent of hyperplasia in prostate tissue the apoptosis and autophagy were assayed. The prostate wet weight, volume and index in the testosterone group were significantly higher compared with the control group (P<0.05) and these factors were significantly lower in the rapamycin group compared with the testosterone group (P<0.05). HE staining demonstrated that prostate hyperplasia was obvious in the testosterone group. Western blotting revealed that caspase-3 levels were higher in the 3-MA group compared with the control group and Bcl-2 was higher in the testosterone group compared with the control group (P<0.05). Furthermore, in the rapamycin group, Bcl-2 protein expression levels were significantly lower than those in the testosterone group (P<0.05). The prostate tissue was analyzed using electron microscopy and autophagy bodies were identified in the rapamycin group. In the process of androgen-induced prostatic hyperplasia in castrated rats, the role of androgen may be related to the PI3K/Akt/mTOR signaling pathway. Rapamycin was able to inhibit the effect of testosterone and promoted prostate tissue hyperplasia by inhibiting the PI3K/Akt pathway. In addition to inhibiting apoptosis in prostate cells, androgen was able to induce rat prostate hyperplasia and may also be related to the promotion of the proliferation of prostate cells.
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