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The Effect Of Huayu Qutan Recipe On The Regulation Of AMPK/PGC-1? Pathway On Liver Lipid Deposition In AS Rabbits And Its Mechanism

Posted on:2020-10-16Degree:MasterType:Thesis
Country:ChinaCandidate:Y F GaoFull Text:PDF
GTID:2434330599976852Subject:Integrative basis
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Purpose:By observing the effect of Huayu Qutan Recipe on AMPK/PGC-1? pathway and its downstream molecule-mediated lipid metabolism in the liver of AS rabbits,the possible mechanism of Huayu Qutan Recipe in preventing and treating AS disease was discussed.Material and method:Sixty healthy male New Zealand rabbits were fed with common diet for two weeks.They were randomly divided into normal group,model group,Huayu Qutan Recipe group and simvastatin group.Fifteen rabbits in each group.The model of AS was established by immune endothelial injury combined with high fat diet compound method.The normal group continues to feed the general feed,and the other groups are fed with high-fat feed.After 8 weeks,The group of removing stasis and expelling phlegm was given16 g/(kg·d)Huayu Qutan recipe,the group of simvastatin was given 1.4 mg/(kg·d)simvastatin,the normal group and the model group were given the same dose of normal saline once a day,continuous administration for 4 weeks.After 4 weeks,the abdominal aorta was collected and the liver was taken.The changes of serum lipid levels were detected by automatic biochemical analyzer.The pathological changes and lipid deposition were observed by HE staining and oil red O staining.The expression levels of AMPK,p-AMPK,CTP-1,PPAR-? and PGC-1? proteins were detected by Western Blot technique.The expressions of AMPK,CTP-1,PPAR-? and PGC-1? m RNA were detected by Realtime RT-PCR.Results:1.Serum TC,TG and LDL levels in model group were significantly higher than those in normal group(P<0.01),while HDL levels were significantly lower(P<0.05);Compared with model group,serum TC,TG and LDL levels in Huayu Qutan group and simvastatin group were significantly lower(P<0.05 or P<0.01),and HDL levels were significantly higher(P<0.05 or P<0.01).2.HE staining results showed that compared with the normal group,the liver morphology of the model group was significantly abnormal,the arrangement of hepatocytes was loose,and the swelling became round,and there were more fat vacuoles.Compared with the model group,the liver cells of the Huayu Qutan group and the simvastatin group were closely arranged,the swelling was significantly reduced,and the fat vacuoles were significantly reduced.3.Oil red O staining results showed that the normal group had clear hepatocyte strands,normal sinuses and no lipid droplets accumulation in the cytoplasm;compared with the normal group,the lipid droplets accumulation in the cytoplasm of the model group was obvious;compared with the model group,the lipid droplets deposition in the liver tissue of the rabbits in the Huayu Qutan group and simvastatin group was significantly reduced.4.The results of Realtime RT-PCR showed that the expression levels of CPT-1,PPAR-?,PGC-1? and AMPK in liver of model group were significantly lower than those of normal group(P<0.05 or P<0.01);compared with model group,the expression levels of CPT-1,PPAR-a,PGC-1a and AMPK in liver of model group and simvastatin group were significantly higher(P<0.05 or P<0.01).5.Western blot showed that the expression levels of CPT-1,PPAR-?,PGC-1? and p-AMPK in liver of model group were significantly lower than those of normal group(P<0.05 or P<0.01).Compared with model group,the expression levels of CPT-1,PPAR-?,PGC-1? and p-AMPK in liver of model group and simvastatin group were significantly higher(P<0.05 or P<0.01).Conclusion:1.Huayu Qutan Decoction can correct the dyslipidemia of AS rabbits to some extent and reduce liver lipid deposition.2.The mechanism of Huayu Qutan Decoction improving lipid metabolism disorder in AS rabbits may be related to regulating and controling the expression of AMPK/PGC-1?signaling pathway.
Keywords/Search Tags:Dyslipidemia, Huatan Quyu Recipe, Fatty acid beta oxidation, Adenosine-activated protein kinase, Carnitine palmitoyltransferase I, Peroxisome proliferator-activated receptor ?, Peroxisome proliferator-activated receptor gamma co-activator
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