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. Author manuscript; available in PMC: 2014 Jun 3.

Published in final edited form as: Hypertens Res. 2011 May 12;34(7):869–875. doi: 10.1038/hr.2011.44

Effect of hCRP and rosuvastatin on endothelial function. (A) Representative immunoblot analysis for eNOS, PI3K and Akt. (B) Densitometric quantification shows eNOS expression, PI3K expression and Akt phosphorylation were suppressed by AAV-hCRP but normalized by rosuvastatin treatment (p<0.05); (C) Immunoblot and relative densitometric analysis (Control group = 1) show that myosin binding substrate (MBS) phosphorylation was increased by AAV-hCRP injection, but normalized by rosuvastatin treatment (p<0.05). (D) AAV-hCRP injection induced a decrease in serum nitrate/nitrite concentration, an effect that was attenuated by rosuvastatin treatment (p<0.05). Data represent mean ± SEM. * p<0.05 vs. control group. # p<0.05 vs. AAV-hCRP group.

Effect of hCRP and rosuvastatin on endothelial function. (A) Representative immunoblot analysis for eNOS, PI3K and Akt. (B) Densitometric quantification shows eNOS expression, PI3K expression and Akt phosphorylation were suppressed by AAV-hCRP but normalized by rosuvastatin treatment (p<0.05); (C) Immunoblot and relative densitometric analysis (Control group = 1) show that myosin binding substrate (MBS) phosphorylation was increased by AAV-hCRP injection, but normalized by rosuvastatin treatment (p<0.05). (D) AAV-hCRP injection induced a decrease in serum nitrate/nitrite concentration, an effect that was attenuated by rosuvastatin treatment (p<0.05). Data represent mean ± SEM. * p<0.05 vs. control group. # p<0.05 vs. AAV-hCRP group.