Skip to main content
. 2020 Jun 12;11:885. doi: 10.3389/fphar.2020.00885

Figure 5.

Figure 5

Blocking of phosphatase and tensin homolog on chromosome ten (PTEN) activity suppresses PR-957–mediated inhibitory effect on cardiac hypertrophy in mice. (A) The structure of VO-Ohpic. (B) Western blot analysis of PTEN, phospho-AKT, AKT, phospho-mTOR, mTOR, and GAPDH in LV tissues from mice after Ang II infusion in the presence or absence of PR-957 (12 mg/kg BW) together with VO-OHpic (10 mg/kg BW) (left) and quantification of each protein band (left, n = 5). (C) Representative echocardiography images of left ventricular chamber (top), and measurement of left ventricular ejection fraction (LV EF%, bottom). (D) Representative images of heart size (top) and ratios of heart weight/body weight (HW/BW) and heart weight/tibial length (HW/TL) (bottom, n = 5). (E) LV sections were stained with WGA to demarcate cell boundaries (left). Quantification of the relative myocyte cross-sectional area (200 cells counted per heart) (right, n = 5). (F) Quantitative real-time polymerase chain reaction analysis of the mRNA expression of ANF (right, n = 5). Data are expressed as mean ± SEM, and n represents the number of animals per group. *P < 0.05, **P < 0.01 vs. Ang II; #P < 0.05, ##P < 0.01 vs. Ang II + PR-957.