Fig 1: Effects of Rb1 and Rg3 on blood pressure, CWI and RAS activity in the serum. (A) SBP, (B) DBP and (C) PP of rats prior to and following 6 weeks treatment. (D) Body and (E) heart weights and (F) CWI. Serum (G) ACE and (H) Ang II levels. Data are presented as the mean ± standard deviation, n=8 (A-F) or n=6 (G-H) for each group. *P<0.05 vs. WKY group prior to treatment; #P<0.05 vs. WKY group following treatment; $P<0.05 vs. SHR group following treatment. Rb1, ginsenoside Rb1; Rg3, ginsenoside Rg3; CWI, cardiac weight index; RAS, renin angiotensin system; SBP, systolic blood pressure; DBP, diastolic blood pressure; PP, pulse pressure; ACE, angiotensin converting enzyme; Ang II, angiotensin II; WKY, Wistar-Kyoto; SHR, spontaneously hypertensive rats.
Fig 2: Effects of Rb1 and Rg3 on RAS and TGF-β1 levels in the myocardium. (A) Representative IHC staining photomicrographs of myocardium tissue. (Magnification, ×400). Antibodies against ACE, Ang II, AT1 and TGF-β1 were used as the primary antibodies. (B-E) Quantitative results of IHC staining, which were presented as IOD/Area and were proportional to the levels of ACE, Ang II, AT1 and TGF-β1. Data are presented as the mean ± standard deviation, n=4. #P<0.05 vs. the WKY group following treatment; $P<0.05 vs. the SHR group following treatment. Rb1, ginsenoside Rb1; Rg3, ginsenoside Rg3; RAS, renin angiotensin system; TGF-β1, transforming growth factor β1; IHC, immunohistochemistry; ACE, angiotensin converting enzyme; Ang II, angiotensin II; AT1, Ang II receptor type 1; IOD, integrated optical density; WKY, Wistar-Kyoto; SHR, spontaneously hypertensive rats.
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