Immediate and prolonged effects of jaboticaba peel extract on prostate cancer progression: chemopreventive potential of continuous treatment in a transgenic mouse model

Prostate cancer (PCa) is the second most common cancer affecting men worldwide. Thus, finding alternative treatments that can act in disease chemoprevention is mandatory. This study evaluated the immediate and prolonged potential therapeutic effects of jabuticaba peel extract (JPE) (Myrciaria jaboticaba) on PCa progression in the Transgenic Adenocarcinoma of Mouse Prostate (TRAMP) model, considering its abundance in antioxidant and anti-inflammatory agents.

Animals were treated with 5.8 g/kg of JPE daily during 8 weeks: in the TJI18 (n=6) group, mice underwent euthanasia immediately after the treatment whereas in the TJP22 group (n=6), the treatment period was followed by a refractory pause of 4 weeks. Two corresponding control groups were established: TCI18 (n=6) and TCP22 (n=6), which received placebo treatment at the same frequency. Ventral prostate was collected for histopathological and immunohistochemical analysis of markers related to oxidative stress and inflammation pathways. 

Morphological analysis indicated that continuous treatment with JPE (TJI18) delayed the progression of prostatic lesions, as evidenced by the higher incidence of healthy epithelium (P<0.001) and low-grade pre-malignant lesions (LGNIP) (P<0.05) with simultaneous decrease of high-grade pre-malignant lesions (HGNIP) (P<0.01) and well-differentiated adenocarcinoma foci (WDAC) (P<0.01) compared to the TCI18 control group. Moreover, qualitative immunohistochemical analysis demonstrated that the TJI18 group showed weaker immunolabeling for iNOS, an enzyme directly related to oxidative stress and inflammation, as well as lower epithelial reactivity (P<0.05) for the androgen receptor (AR). Additionally, no significant changes were observed between TJP22 and its corresponding TCP22 control group (P>0.05). 

Therefore, the results herein indicated a promising role for JPE as a chemopreventive treatment against the progression of PCa, probably by means of its interference in inflammatory and hormonal signaling, but only when applied in a continuous approach.