icaritin and Adenocarcinoma

We aimed to investigate whether icaritin (ICT) would inhibit serum proinflammatory cytokines and postpone prostate cancer (PCa) development and progression in both normal diet and high-fat diet (HFD) transgenic adenocarcinoma mouse prostate (TRAMP) mice.. TRAMP mice were randomly divided into four groups: normal diet with/without ICT group and HFD with/without ICT group. Each TRAMP mouse received intraperitoneal injection of ICT solution at the dose of 30 mg/kg 5 times per week.. ICT treatment could significantly increase the survival when compared with those in normal diet group (P = 0.015, log-rank test) and HFD group (P = 0.009, log-rank test). Proinflammatory cytokine levels, including IL-1α, IL-1β, IL-6, and TNF-α, were decreased more or less in ICT-treated TRAMP mice. Moreover, significant higher inflammation scores were detected in normal diet group and HFD group compared with their relevant ICT treatment groups (P = 0.026 and P = 0.006, respectively). Meanwhile, the incidences of well-differentiated tumor tissue in two ICT treatment groups (39.13 and 31.82 %) were moderately higher than control groups (29.41 and 20.00 %, respectively), though no significant difference was observed.. Taken together, our findings indicate that ICT could inhibit the development and progression of PCa in TRAMP mice via inhibiting proinflammatory cytokines.

Topics: Adenocarcinoma; Animals; Antineoplastic Agents; Cytokines; Diet, High-Fat; Disease Models, Animal; Disease Progression; Flavonoids; Inflammation; Male; Mice; Mice, Transgenic; Prostatic Neoplasms; Signal Transduction