IMR Press / JOMH / Volume 18 / Issue 2 / DOI: 10.31083/jomh.2021.124
Open Access Original Research
Crocin treatment improves testosterone induced benign prostatic hyperplasia in rats
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1 Department of Biological Sciences, Faculty of Science, Yarmouk University, 211-63 Irbid, Jordan
2 Department of Basic Medical Sciences, Faculty of Medicine, Yarmouk University, 211-63 Irbid, Jordan
3 Faculty of Pharmacy, Department of Pharmaceutics and Pharmaceutical Technology, Yarmouk University, 211-63 Irbid, Jordan
4 Department of Biological Sciences, College of Science and Mathematics, Rowan University, Glassboro, NJ 08028, USA
*Correspondence: (Janti Qar); (Bahaa Al-Trad)
J. Mens. Health 2022, 18(2), 38;
Submitted: 22 April 2021 | Accepted: 21 June 2021 | Published: 9 February 2022
Copyright: © 2022 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

Background and objective: Benign prostatic hyperplasia (BPH) is a typical nonmalignant growth of the prostate in the elderly. Crocin, a bioactive component of Crocus sativus L., commonly known as saffron, is known to have an anti-proliferative activity against numerous types of cancer, including prostate cancer. This study investigated the effects of crocin on testosterone-induced BPH development in rats. Materials and methods: The study sample included three groups of adult male rats (3 months old, weighed 250 g): the control group received corn oil only, the second and the third groups were injected with testosterone (3 mg/kg dissolved in corn oil) subcutaneously. The second group was considered as testosterone-induced BPH (untreated) while the third groups were assigned as testosterone-induced BPH-crocin treated group (100 mg/kg orally for 14 days). Results: After animal sacrifice, histopathological analysis of the prostate tissues was performed in parallel with gene expression of proliferation (PCNA), inflammation (IL-6), and vascularization (VEGF-A) markers, analyzed by qRT-PCR. Crocin treatment significantly reduced prostate index and the thickness of the epithelial layer in rats with BPH. Additionally, the mRNA expression levels of PCNA, a marker of cell proliferation; IL-6, an inflammatory cytokine; and VEGF-A, an angiogenesis marker, were significantly down-regulated in the BPH group that were treated with crocin. Conclusions: The present study indicates that crocin can effectively prevent the development of experimentally induced BPH through inhibition of prostatic cellular proliferation, inflammation, and angiogenesis.

Fig. 1.
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