Rosmarinic Acid Protects against Inflammation and Cardiomyocyte Apoptosis during Myocardial Ischemia/Reperfusion Injury by Activating Peroxisome Proliferator-Activated Receptor Gamma

Figures

• 

  FIGURE 1. The effect of RosA on cardiac function in rat I/R model. The effect of RosA on LVDP (A), dp/dtmax (B), dp/dtmin (C), and CF (D) in rat hearts. Control, healthy control mice; I/R, ischemia/reperfusion model mice; RosA, healthy mice treated with RosA; PIO, healthy mice treated with pioglitazone; GW9662, healthy mice treated with GW9662; T0070907, healthy mice treated with T0070907; RosA+I/R, I/R mice treated with RosA; PIO+I/R, I/R mice treated with PIO; RosA+GW9662+I/R, I/R mice treated with RosA plus GW9662; RosA+T0070907+I/R, I/R mice treated with RosA plus T0070907; PIO+GW9662+I/R, I/R mice treated with PIO plus GW9662; PIO+T0070907+I/R, I/R mice treated with PIO plus T0070907. Values are presented as means with their standard deviation, n = 6. Compared with the control group, #P < 0.05, ##P < 0.01. Compared with the I/R group, ∗P < 0.05, ∗∗P < 0.01. Compared with the I/R+RosA group, $P < 0.05, $$P < 0.01. Compared with the I/R+PIO group, &P < 0.05, &&P < 0.01.

• 

  FIGURE 2. The effect of RosA on the size of I/R-induced infarcts. (A) The infarct size was measured by TTC staining. (B) Statistic analysis of the size of I/R-induced infarcts. ##P < 0.01 compared to the control group; ∗∗P < 0.01 compared to the I/R group. Compared with the I/R+RosA group, $P < 0.05, $$P < 0.01. Compared with the I/R+PIO group, &P < 0.05, &&P < 0.01.

• 

  FIGURE 3. The effect of RosA on inflammatory cytokine production in rat model of cardiac I/R. Values are presented as means with their standard deviation, n = 6. The effect of RosA on TNF-α (A), IL-6 (B), and CRP (C) levels in I/R rat model. ##P < 0.01 compared with control group; ∗∗P < 0.01 compared with I/R group. Compared with the I/R+RosA group, $P < 0.05, $$P < 0.01. Compared with the I/R+PIO group, &P < 0.05, &&P < 0.01.

• 

  FIGURE 4. The suppression of RosA in cardiomyocyte apoptosis induced by I/R (×200). Brown staining of the nucleus is indicative of apoptosis. (A) The cardiomyocyte apoptosis was measured by TUNEL. (B) Percentage of apoptotic cells. ##P < 0.01 compared to the control group; ∗∗P < 0.01 compared to the I/R group. Compared with the I/R+RosA group, $P < 0.05, $$P < 0.01. Compared with the I/R+PIO group, &P < 0.05, &&P < 0.01.

• 

  FIGURE 5. The effect of RosA on the mRNA levels and protein levels of PPARγ and NF-κB p65 in rat cardiac tissue. (A) The effect of RosA on the mRNA levels of PPAR-γ; (B) The effect of RosA on the mRNA levels of NF-κB p65; (C) Quantitative analysis of PPARγ protein levels; (D) Quantitative analysis of NF-κB p65 protein levels. (E) Measurement of PPARγ and NF-κB p65 protein levels in rat hearts by Western blot. (1) Control group; (2) I/R group; (3) RosA group; (4) GW9662 group; (5) RosA+I/R group; (6) RosA+GW9662+I/R group; (7) PIO group; (8) T0070907 group; (9) PIO+I/R group; (10) RosA+T0070907+I/R group; (11) PIO+GW9662+I/R group; (12) PIO+T0070907+I/R group. ##P < 0.01 compared to the control group; ∗∗P < 0.01 compared to the I/R group. Compared with the I/R+RosA group, $P < 0.05, $$P < 0.01. Compared with the I/R+PIO group, &P < 0.05, &&P < 0.01.

• 

  FIGURE 6. Schematic diagram of the role of the RosA in acute I/R-induced myocardial injury in isolated rat heart.