Fig. 4.
Atorvastatin prevents oxidized low-density lipoprotein (oxLDL)-induced macrophage adhesion to endothelial cells. (A) Atorvastatin coincubation of oxLDL-activated endothelial cells prevented increased macrophage adhesion in an in vitro assay (n = 6; P < 0.01). (B) Characterization of viability by propidium iodine revealed that while viability decreased over time († P < 0.001; n = 5) neither dosage of atorvastatin affected this process (vehicle vs. 1 nm atorvastatin, § P > 0.99, n = 5; vehicle vs. 10 nm atorvastatin, ‡ P > 0.99, n = 5). (C) Within 4 days of culture the amount of macrophages per well increased due to proliferation (day 4 vs. day 0; # P < 0.001; n = 5). However, the effect of atorvastatin on proliferation only became obvious at day 7 (vehicle vs. atorvastatin; * P < 0.02; n = 5) whereas no relevant difference was observed until day 4. nLDL = native low-density lipoprotein; nm = nanomolar.

Atorvastatin prevents oxidized low-density lipoprotein (oxLDL)-induced macrophage adhesion to endothelial cells. (A) Atorvastatin coincubation of oxLDL-activated endothelial cells prevented increased macrophage adhesion in an in vitro assay (n = 6; P < 0.01). (B) Characterization of viability by propidium iodine revealed that while viability decreased over time († P < 0.001; n = 5) neither dosage of atorvastatin affected this process (vehicle vs. 1 nm atorvastatin, § P > 0.99, n = 5; vehicle vs. 10 nm atorvastatin, ‡ P > 0.99, n = 5). (C) Within 4 days of culture the amount of macrophages per well increased due to proliferation (day 4 vs. day 0; # P < 0.001; n = 5). However, the effect of atorvastatin on proliferation only became obvious at day 7 (vehicle vs. atorvastatin; * P < 0.02; n = 5) whereas no relevant difference was observed until day 4. nLDL = native low-density lipoprotein; nm = nanomolar.

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