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Inflammatory pathway employed by Red Maca to treat induced benign prostatic hyperplasia in rats

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dc.contributor.author Vásquez-Velásquez, C.
dc.contributor.author Gasco, M.
dc.contributor.author Fano-Sizgorich, D.
dc.contributor.author Gonzales, G.F.
dc.date.accessioned 2020-12-14T16:11:07Z
dc.date.available 2020-12-14T16:11:07Z
dc.date.issued 2020
dc.identifier.uri https://hdl.handle.net/20.500.12866/8845
dc.description.abstract Benign prostatic hyperplasia (BPH) is a pathology characterised by an increase in prostate size associated with low urinary tract symptoms. Finasteride (F), a 5a-reductase inhibitor, is the standard treatment for BPH reducing prostate weight but also sexual desire. The Peruvian plant known as Red Maca (RM) (Lepidium meyenii) inhibits BPH in rats and mice. The aim of the study was to assess the inflammatory effect of RM and finasteride in rats with testosterone enanthate (TE)-induced BPH. Thirty rats were divided into 5 groups: Control, TE (50 mg/rat), TE + F (0.6 mg/kg), and two groups of TE + RM 40/80 (40 or 80 mg). After treatments, tumour necrosis factor alpha (TNFa), interleukin 4 (IL4) and interferon gamma (INFg) as well as testosterone and oestradiol were evaluated and inflammatory cells (neutrophils, mast cells and lymphocytes) in prostate were quantified. Red Maca and finasteride treatments decreased inflammatory cells counts in prostate, inhibiting TNFa by different pathways. Finasteride increased IL4 whereas Red Maca increased INFg. In conclusion, data suggest that finasteride acts on Th2 response by increasing IL4 in prostate, while Red Maca acts on Th1 response mediated by INFg. en_US
dc.language.iso eng
dc.publisher Wiley
dc.relation.ispartof urn:issn:1439-0272
dc.rights info:eu-repo/semantics/restrictedAccess
dc.rights.uri https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
dc.subject UNAVAILABLE en_US
dc.title Inflammatory pathway employed by Red Maca to treat induced benign prostatic hyperplasia in rats en_US
dc.type info:eu-repo/semantics/article
dc.identifier.doi https://doi.org/10.1111/and.13516
dc.subject.ocde https://purl.org/pe-repo/ocde/ford#3.02.00 es_PE
dc.subject.ocde https://purl.org/pe-repo/ocde/ford#3.02.01


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