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Objective: To investigate allicin apolipoprotein E gene knockout mouse small intestine and Caco-2 cell cholesterol transport related genes affect the clear allicin anti-atherosclerosis mechanism of action. Methods: 48 6-week-old male apoE-/ - mice, weight (20.1 ± 1.6) g were randomly divided into four groups, each group 12: I normal diet group (normal diet, PBS 0.1ml/2d, intraperitoneal injection) II high fat and high cholesterol group (hypercholesterolemic diet feeding, the PBS 0.1ml/2d, intraperitoneal injection), Ⅲ high fat and high cholesterol allicin group (hypercholesterolemic diet feeding, allicin 0.1ml/2d , intraperitoneal injection), the allicin group IV normal diet (normal diet, allicin 0.1ml/2d, intraperitoneal injection), high-fat diet for the normal diet plus 2% cholesterol and 10% lard. After 12 weeks, all the mice by 20% of urethane of 0.2 to 0.3 ml of intraperitoneal anesthesia, removal of the eye blood oxidase method determination of ApoE-/ - mouse serum triacylglycerol (triglyceride, TG), total cholesterol (total cholesterol, TC), high density lipoprotein cholesterol (high density lipoprotein cholesterol, HDL-C) and low-density lipoprotein cholesterol (low density lipoprotein cholesterol, LDL-C) content. Paraffin HE staining detection apoE-/ - mouse aortic root cross-section of atherosclerotic lesions. Immunofluorescence small intestine of mice ABCG5 and ABCG8 expression of,. RT-PCR detection of mouse intestinal tissue ABCG5 and ABCG8 mRNA expression. Caco-2 cells by culture passage is divided into four groups: I Caco-2 cell control group II Caco-2 cell model group, Caco-2 cell model allicin group IV Caco-2 cells allicin group. Plus processing factors processing, high performance liquid chromatographic method for the measurement of intracellular cholesterol content, oil red O staining of intracellular lipid droplets, RT-PCR and Western blot were used to detect cell ABCG5 and ABCG8 mRNA and protein expression. : Hypercholesterolemic mice serum TC, TG, HDL-C, LDL-C water were higher than the normal diet group, high fat and high cholesterol allicin group TC, TG, and LDL-C levels were significantly low hypercholesterolemic group (p lt; 0.05), HDL-C tended to increase, but not statistically significant; the normal diet allicin group TC, TG, LDL-C were lower than the normal diet group, and the difference significant (p lt; 0.05). Hypercholesterolemic allicin group, normal diet allicin group hypercholesterolemic group, respectively, between the normal diet group compared mouse aortic sinus plaque area of ??the former is lower than the latter, and there are significant differences sex (p lt; 0.05 or p LT; 0.01). Organization immunofluorescence and RT-PCR showed apolipoprotein E gene knock addition to the mouse hypercholesterolemic allicin group, normal diet allicin group ABCG5 and ABCG8 protein and mRNA expression were higher than the high-fat high-cholesterol group and normal diet group , the allicin group of Caco-2 cell model and Caco-2 cells allicin group of ABCG5 and ABCG8 protein and mRNA were significantly higher than the Caco-2 cell model group and Caco-2 cells in the control group (p lt; 0.05 or p lt; 0.01), Caco-2 cells by oil red O staining display allicin treated to increase the lipid deposition are less than the corresponding None increase allicin group treated further by HPLC results showed increase allicin processing cells in total cholesterol decreased significantly (p lt; 0.05 or p LT; 0.01). Conclusion: ① allicin can reduce the apolipoprotein E knockout mice artery atherosclerotic lesions; ② allicin to increase the apolipoprotein E gene knock in addition to the small intestine of mice adenosine triphosphate-binding cassette transporter G5 and G8 expression; (3) allicin can increase human colon adenocarcinoma cells (Caco-2), adenosine triphosphate-binding cassette transporter G5 and G8 expression, and promote the discharge of intracellular cholesterol.
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