A Study Of Effects Of Chitosan On Experimental Rabbit Atherosclerosis

It is well known that atherosclerosis(AS) is the principal cause of death in the world and hyperlipidemia is the major risk factor for AS. Chitosan has been proved to be able to low serum lipid level, which might affect the genesis and development of AS. Because both the ligand and receptor of platelet-derived growth factor(PDGF) were involved in the process of AS, we observed the changes of PDGFR-βin primary cultured rat vascular smooth muscle cells(RVSMC), primary cultured human vascular fibroblasts(HVFB) and rabbits in vivo to elucidate the mechanism for effects of chitosan.Main procedure1 The effects of chitosan on RVSMC induced by oxLDL,TNF-α, PDGFR-β expression were studied by MTT method and immunoblotting method, respectively.2 The effects of chitosan on HVFB induced by PDGF-BB,TNF-α, PDGFR-β expression were studied by MTT method and immunoblotting method, respectively.3 A rabbit AS model was established by a high fat diet. The effects of chitosan on serum lipids, AS plaque in rabbits by means of serum index, immunohistochemistry and immunoblotting were studied to find out potential mechanisms for the effects of chitosan on AS.Main results1 Chitosan inhibited the proliferation of RVSMC in time-dependent and dose-dependent manners, and chitosan downregulated PDGFR-β expression in RVSMC.2 Chitosan inhibited the proliferation of HVFB in time-dependent and dose-dependent manners, and chitosan downregulated PDGFR-β expression in HVFB.3 Chitosan decreased serum lipid concentration and reduced aorta AS plaque area in rabbits fed on a high fat diet. There were no changes in serum lipid concentration and liver function in rabbits fed on common and chitosan diet. Chitosan downregulated PDGFR-βexpression in rabbits aorta fed on a high fat diet with immunohisto-chemistry and immunoblotting.The results suggested that chitosan reduce AS degree in rabbits fed on a high fat diet and the effect might be related to the decrease of serum lipid, the inhibition of VSMC as well as FB proliferation and the downregulation of PDGFR-β.