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. 2017 Jan 25;114(6):1359–1364. doi: 10.1073/pnas.1620884114

Fig. 1.

Fig. 1.

GHRH antagonists MIA-690 and JV-I-38 reduce prostate enlargement in EAP. (A) GHRH and GHRHRs are localized mainly in the epithelial cells of the ventral prostate of Balb/C mice, as shown by immunohistochemistry. (Scale bar: 100 µm.) (B) Representative images showing volumetric changes in the ventral prostate detected by VEVO 1100 US imaging system. EAP was induced by two immunizations with a homogenate of rat male tissue injected 2 wk apart. Ultrasound images were recorded before the first injection (baseline) and 2 and 8 wk after the second injection. (C) Average volume of ventral prostates in EAP and control animals before and 2, 4, and 8 wk after the induction. (D) H&E staining shows leukocyte infiltrate in the ventral prostate of the EAP model (arrow) and no signs of inflammation in the control tissue. (Scale bar: 100 µm.) (E and F) GHRH antagonists reduce inflammation-induced enlargement of the ventral prostate in EAP. As depicted by the scheme, mice were treated with GHRH antagonists MIA-690 or JV-I-38 at 5 µg/d for 4 wk starting 8 wk after the induction of EAP and compared with vehicle-treated animals. Representative ultrasound images (E) and average volumes of the ventral prostates (F) are shown 8 and 12 wk after the induction of EAP. (G) Western blot analysis of the expression of phospho-NF-κβ p65, NF-κβ p65, and prepro-GHRH in ventral prostates from control, EAP, and EAP treated with MIA-690. GAPDH or β-actin were used as standard genes (*P < 0.05, **P < 0.01, and ***P < 0.01 by Student’s t test).