OBJECTIVE: Chronic @entity888 ( @entity7865 ) abuse could induce @entity2359 due to reactive @entity26 species generation and sympathetic activation. Both factors are associated with @entity731 , so we tested the hypothesis that chronic @entity7865 administration might also promote @entity731 formation in @entity6970 -/- knockout @entity19 fed normal diet. METHODS AND RESULTS: Male @entity6970 -/- @entity19 (6 weeks-old) were treated with saline (NS) or @entity7865 [4 mg/kg/day (M4) or 8 mg/kg/day (M8) through intraperitoneal injection] for 24 weeks. @entity731 area on oil red O stained en face aorta was dose-dependently increased in M4 and M8 groups compared to NS group. Percentage of @entity731 area was significantly higher in M8 group compared to NS and M4 groups. Plasma CRP was increased and inflammatory cytokine ( @entity8024 , @entity6580 , @entity637 , and INF-y) expression on aortic root was upregulated in @entity7865 groups compared to NS group. @entity32327 ( @entity32327 ) protein and mRNA expressions in aortic root and myocardial tissue were determined by Western blot and real time PCR, which were significantly upregulated in M4 and M8 groups. Moreover, mRNA expressions of @entity33530 , @entity36888 and @entity64380 in aortic and myocardial tissue were also significantly upregulated in M4 and M8 groups. Raw264.7 cells were treated with @entity32327 , @entity32327 receptor antagonists, @entity7865 (10  M or 100  M) with or without lipopolysaccharide (LPS), and the expressions of @entity637 , CRP, @entity8929 and reactive @entity26 species (ROS) production were significantly increased in @entity7865 and LPS + @entity7865 groups compared to control and LPS groups. Co-treatment with @entity33530 antagonist decreased the expressions of @entity637 , CRP and @entity8929 in @entity32327 and @entity7865 treated cells. CONCLUSIONS: Chronic @entity7865 administration can promote @entity32 and @entity731 plague formation in @entity6970 -/- @entity19 fed normal chow. @entity32327 might be involved in the pathogenesis of @entity7865 -induced atherogenic effects through @entity32327 Y1 receptor pathway.

Chronic administration of @entity888 promotes @entity731 formation in XXXX -/- knockout @entity19 fed normal diet.

@entity32327 :: ('109648(Tax:10090)', 'Gene') :: ['NPY', 'Neuropeptide Y'] @entity32 :: ('MESH:D007249', 'Disease') :: ['inflammation'] @entity6970 :: ('11816(Tax:10090)', 'Gene') :: ['Apo E', 'ApoE'] @entity8929 :: ('17224(Tax:10090)', 'Gene') :: ['MCP-1'] @entity7865 :: ('D008694', 'Chemical') :: ['METH'] @entity888 :: ('MESH:D008694', 'Chemical') :: ['methamphetamine'] @entity19 :: ('10090', 'Species') :: ['mice'] @entity26 :: ('MESH:D010100', 'Chemical') :: ['oxygen'] @entity36888 :: ('18167(Tax:10090)', 'Gene') :: ['NPY2R'] @entity64380 :: ('18168(Tax:10090)', 'Gene') :: ['NPY5R'] @entity6580 :: ('22329(Tax:10090)', 'Gene') :: ['VCAM-1'] @entity33530 :: ('18166(Tax:10090)', 'Gene') :: ['NPY1R'] @entity8024 :: ('15894(Tax:10090)', 'Gene') :: ['ICAM-1'] @entity731 :: ('MESH:D050197', 'Disease') :: ['atherosclerotic', 'Atherosclerotic lesion', 'atherosclerosis', 'atherosclerotic lesion'] @entity637 :: ('21926(Tax:10090)', 'Gene') :: ['TNF-a'] @entity2359 :: ('MESH:D020258', 'Disease') :: ['neurotoxicity']
@entity6970 :: (11816(Tax:10090),Gene) :: ['ApoE']
