Results: 5

1.
Figure 1

Figure 1. From: Rosuvastatin Attenuates the Elevation in Blood Pressure Induced by Overexpression of Human C-Reactive Protein.

AAV-mediated expression of hCRP. (A) Serum concentrations of hCRP at different times after injection of AAV vectors and rosuvastatin treatment. (B) Representative immunoblot of hCRP expression in liver and aorta four months after gene delivery.

Xuguang Li, et al. Hypertens Res. ;34(7):869-875.
2.
Figure 5

Figure 5. From: Rosuvastatin Attenuates the Elevation in Blood Pressure Induced by Overexpression of Human C-Reactive Protein.

Effect of hCRP and rosuvastatin on vascular MAPK activation. (A) Representative immunoblot of ERK1/2, p38 MAPK and JNK/c-JUN. (B) Vascular p38 MAPK, ERK1/2 and JNK/c-JUN phosphorylation were increased in AAV-hCRP injected rats, an effect that was attenuated by rosuvastatin (p<0.05). Results are expressed as the ratio of phospho-ERK1/2, p38, JNK and c-JUN to total ERK1/2, p38, JNK and c-JUN, respectively. Data represent mean ± SEM. * p< 0.05 vs. control group. # p<0.05 vs. AAV-hCRP group.

Xuguang Li, et al. Hypertens Res. ;34(7):869-875.
3.
Figure 2

Figure 2. From: Rosuvastatin Attenuates the Elevation in Blood Pressure Induced by Overexpression of Human C-Reactive Protein.

Effect of hCRP and rosuvastatin on systolic blood pressure. (A) Systolic blood pressure was monitored from the beginning of the study using the tail-cuff method. Rats injected with AAV-hCRP had significantly increased blood pressure starting one month after gene delivery (p<0.05). Blood pressure was reduced by rosuvastatin treatment (p<0.05). (B) Intra-arterial pressure was measured at the end of the experiment using the Millar catheter. Results were consistent with non-invasive blood pressure measurements (p<0.05). Data represent mean ± SEM. * p<0.05 vs. control group. # p<0.05 vs. AAV-hCRP group.

Xuguang Li, et al. Hypertens Res. ;34(7):869-875.
4.
Figure 4

Figure 4. From: Rosuvastatin Attenuates the Elevation in Blood Pressure Induced by Overexpression of Human C-Reactive Protein.

Effect of hCRP and rosuvastatin on vascular expression of AT1 receptors, NAD(P)H oxidase subunits and SOD-1. (A) Representative immunoblot analysis for AT1 receptor, p22 phox, gp91 phox and SOD-1 expression in vasculature. (B) Densitometric analysis (Control = 1) of immunoblots shows that CRP-induced increases in AT1 receptor, p22 phox and gp91phox expression were abolished by rosuvastatin treatment (p<0.05). SOD-1 was downregulated by AAV-hCRP injection, but normalized by rosuvastatin treatment (p<0.05). (C) Superoxide release is expressed as relative chemiluminescence per milligram of aortic tissue (Control = 100) (p<0.05). Data represent mean ± SEM. * p<0.05 vs. control group. # p<0.05 vs. AAV-hCRP group.

Xuguang Li, et al. Hypertens Res. ;34(7):869-875.
5.

Figure 3. From: Rosuvastatin Attenuates the Elevation in Blood Pressure Induced by Overexpression of Human C-Reactive Protein.

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.

Xuguang Li, et al. Hypertens Res. ;34(7):869-875.

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