Fig 2: RvD1 attenuates CCs-induced NF?B activation, ICAM1 and VCAM1 expression and EC-monocyte interactions by protecting PP2A from H2O2-mediated inhibition. A & B. Quiescent HAECs were treated with and without CCs (200 µg/ml) in the presence and absence of RvD1 (200 ng/ml) for 10 min or 30 min and assayed for H2O2 production (A) or PP2A activity (B), respectively. C-E. Quiescent HAECs were treated with and without CCs (200 µg/ml) in the presence and absence of RvD1 (200 ng/ml) for 30 min or 1 h and cell extracts were prepared and analyzed by Western blotting for pPP2A-C(a/ß), pI?Ba, pIKKa/ß and pNF?B levels (30 min samples) and ICAM1 and VCAM1 expression (1 h samples) and the blots were normalized for their total levels or a-tubulin. F & G. Quiescent HAEC monolayer was treated with and without CCs (200 µg/ml) in the presence and absence of RvD1 (200 ng/ml) for 2 h and subjected to THP1 cell adhesion (F) and transmigration (G) assays. The bar graphs represent quantitative analysis of three experiments. The values are expressed as Mean ± SD. *p < 0.05 vs control; **p < 0.05 vs CCs or vehicle + CCs.

Fig 3: RvD1 inhibits CRD-induced XO expression and its activity, PP2A inactivation, NF?B activation and ICAM1 and VCAM1 expression. A, C & E. Eight weeks old C57BL/6 mice were fed with CRD in combination with and without RvD1 (10 µg/kg body weight, every 3 days by IP) or left on CD for 12 weeks, aortas were isolated and either tissue extracts were prepared and assayed for H2O2 production (A) or XO and PP2A activities (C & E). B, D, F & G. An equal amount of protein from aortic tissue extracts prepared as in panel A were analyzed by Western blotting for XO, pPP2A-C(a/ß), pI?Ba, pIKKa/ß and pNF?B, ICAM1 and VCAM1 levels and the blots were normalized for a-tubulin or their total levels. The bar graphs represent quantitative analysis of three experiments. The values are expressed as Mean ± SD. *p < 0.05 vs CD; **p < 0.05 vs CRD.