Objective To test the hypothesis that increased plasma levels of Lp(a)may enhance the development of atherosclerosis in the setting of hypercholesterolemia.Methods The plasma Lp(a)was analyzed by SDS-PAGE Western blot...Objective To test the hypothesis that increased plasma levels of Lp(a)may enhance the development of atherosclerosis in the setting of hypercholesterolemia.Methods The plasma Lp(a)was analyzed by SDS-PAGE Western blotting and quantitated using specific ELISA kits.Plasma total cholesterol,triglycerides and HDL-cholesterol were determined using Wako assay kits.The left coronary artery was used for the evaluation of coronary atherosclerosis(stenosis %).For quantitative study of the lesions in coronary atherosclerosis,hematoxylin-eosin and Elastica-van Gieson staining were used.To study cellular components(SMC vs.macrophages)and Lp(a)deposits in the lesions,immunohistochemical staining was performed and then image analysis system was used.Results Plasma total cholesterol,triglycerides,or HDL-C were not significantly different between transgenic(Trg)and nontransgenic(nonTrg)rabbits.Trg rabbits had 200% increase in coronary stenosis caused by atherosclerosis.The lesions of Trg WHHL rabbits contained more SMCs and less macrophage than those of nonTrg WHHL rabbits.Conclusions The results suggest that increased plasma levels of Lp(a)enhance the development of coronary atherosclerosis.展开更多
Effect of antiatherogenic high density lipoprotein (HDL) and apolipoprotein AI (apo AI) on production of prostaglandin E2 (PGE2 ) by human m onocyte- derived macrophages was investigated.Macrophages were loaded with...Effect of antiatherogenic high density lipoprotein (HDL) and apolipoprotein AI (apo AI) on production of prostaglandin E2 (PGE2 ) by human m onocyte- derived macrophages was investigated.Macrophages were loaded with acetylated low density lipoprotein followed by incuba- tion with HDL3or apo AI.PGE2 produced and secreted in culture supernatant was quantified by en- zyme im munoassay.HDL3induced production of PGE2 by m acrophages in a time- dependent m an- ner.2 4 h after incubation,PGE2 production by HDL3- treated macrophages increased 3.7- fold of that by control cells.Apo AI also induced PGE2 secretion to 2 .1- fold,which was significantly less than HDL3.The data indicate that both HDL3and lipid- free apo AI enhance PGE2 synthesis and se- cretion by hum an m acrophages and this may further contribute to the protection from atheroscle- rosis.展开更多
文摘Objective To test the hypothesis that increased plasma levels of Lp(a)may enhance the development of atherosclerosis in the setting of hypercholesterolemia.Methods The plasma Lp(a)was analyzed by SDS-PAGE Western blotting and quantitated using specific ELISA kits.Plasma total cholesterol,triglycerides and HDL-cholesterol were determined using Wako assay kits.The left coronary artery was used for the evaluation of coronary atherosclerosis(stenosis %).For quantitative study of the lesions in coronary atherosclerosis,hematoxylin-eosin and Elastica-van Gieson staining were used.To study cellular components(SMC vs.macrophages)and Lp(a)deposits in the lesions,immunohistochemical staining was performed and then image analysis system was used.Results Plasma total cholesterol,triglycerides,or HDL-C were not significantly different between transgenic(Trg)and nontransgenic(nonTrg)rabbits.Trg rabbits had 200% increase in coronary stenosis caused by atherosclerosis.The lesions of Trg WHHL rabbits contained more SMCs and less macrophage than those of nonTrg WHHL rabbits.Conclusions The results suggest that increased plasma levels of Lp(a)enhance the development of coronary atherosclerosis.
文摘Effect of antiatherogenic high density lipoprotein (HDL) and apolipoprotein AI (apo AI) on production of prostaglandin E2 (PGE2 ) by human m onocyte- derived macrophages was investigated.Macrophages were loaded with acetylated low density lipoprotein followed by incuba- tion with HDL3or apo AI.PGE2 produced and secreted in culture supernatant was quantified by en- zyme im munoassay.HDL3induced production of PGE2 by m acrophages in a time- dependent m an- ner.2 4 h after incubation,PGE2 production by HDL3- treated macrophages increased 3.7- fold of that by control cells.Apo AI also induced PGE2 secretion to 2 .1- fold,which was significantly less than HDL3.The data indicate that both HDL3and lipid- free apo AI enhance PGE2 synthesis and se- cretion by hum an m acrophages and this may further contribute to the protection from atheroscle- rosis.
