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Effect Of Melatonin On Blood Lipids, TLR4Pathway, Inflammatory Cytokines And The Development Of Experimental Atherosclerosis In Rabbits

Posted on:2014-10-13Degree:MasterType:Thesis
Country:ChinaCandidate:N FangFull Text:PDF
GTID:2254330401468983Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Objective To investigate the influence of melatonin on the expression of toll-likereceptor4(TLR4), Nuclear transcription factor-κB(NF-κB), Myeloid differentiationfactor88(MyD88), blood lipids, Inflammatory cytokines and the development ofexperimental atherosclerosis in rabbits.Methods36New Zealand white rabbits were randomly assigned to three groups,including control group, Model group, and MLT group. The control group was givenordinary forage, the model group was given high-fat food based on ordinary forage, andthe MLT group was given MLT daily on the basis of food in-take like high-fat group.Serum total cholesterol(TC), low density lipoprotein cholesterol(LDL-c), high densitylipoprotein cholesterol (HDL-c), triglyceride (TG), tumor necrosis factor-α(TNF-α), andhigh-sensitivity C-reactive protein(hs-CRP) were detected on the twelfth week ofexperiment. The change of morphology of artery wall in model rabbits was watched byHE staining. TLR4, NF-κB, MyD88expression was detected by Immunohistochemistryand Western blot.Results The atherosclerosis model was established successfully. Serum TC, LDL-c,HDL-c, TG, TNF-α, hs-CRP and arterial TLR4, NF-κB, MyD88levels as well as thearterial intima and intima-to-media thickness ratio of the model group were significantlyhigher than those of control group(p<0.05). Serum TC, LDL-c, HDL-c, TG, TNF-α,hs-CRP and arterial TLR4, NF-κB, MyD88levels as well as the arterial intima and intima-to-media thickness ratio of the MLT group were significantly lower than modelgroup(p<0.05).Conclusion Melatonin might suppress the development of experimental atherosclerosisin rabbits by decreasing toll-like receptor4pathway and Inflammatory cytokines...
Keywords/Search Tags:melatonin, atherosclerosis, TLR4, Inflammatory Cytokines
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