Ginkgolide B Mediated Alleviation of Inflammatory Cascades and Altered Lipid Metabolism in HUVECs via Targeting PCSK-9 Expression and Functionality
Figure 3
(a) Ox-LDL treatment induces the ROS generation in HUVECs. The cultured HUVECs cells were either treated with native LDL or Ox-LDL (25, 50, 75, and 100 μg/ml) for determination of ROS generation in terms of % DCFDA fluorescence. Significantly different from native LDL at <0.001. (b) Ginkgolide B suppresses ROS generation in Ox-LDL-treated HUVECs. ROS level in terms of %DCFDA fluorescence was quantified by the pretreatment of HUVECs with different concentrations of Ginkgolide B (20-100μg/ml) for 24 h followed by the treatment of Ox-LDL (75μg/ml) for another 6 h. Significantly different from control HUVECs at <0.001. Significantly different from control HUVECs at <0.01. Nonsignificantly different from control HUVECs at >0.05. Significantly different from Ox-LDL at <0.001. Significantly different from Ox-LDL at <0.01. (c) Ox-LDL treatment upregulates the expression of ICAM-1 and VCAM-1 in HUVECs. The cultured HUVECs cells were either treated with native LDL or Ox-LDL (25, 50, 75, and 100 μg/ml) for the ICAM-1 and VCAM-1 expression analysis. Significantly different from native LDL at <0.001. Significantly different from native LDL at <0.01. (d) Ginkgolide B ameliorates endothelial dysfunction by suppressing expression of ICAM-1 and VCAM-1 in Ox-LDL-treated HUVECs. Cells were pretreated with 20, 40, 80, and 100 μg/ml of Ginkgolide B for 24 h and then exposed to Ox-LDL (75μg/ml) for another 24 h. The cells were harvested and transcript levels of ICAM-1 and VCAM-1 were examined by qRT-PCR. Significantly different from control HUVECs at <0.001. Significantly different from control HUVECs at <0.01. Nonsignificantly different from control HUVECs at >0.05. Significantly different from Ox-LDL at <0.001. All the values in (a), (b), (c), and (d) have been expressed as mean ± SEM of three independent experiments.