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Objective To investigate the effect of hydrogen sulfide (H2S) on the cholesterol efflux and ATP-binding cassette transporter A1 (ABCA1) expression in foam cells .Methods RAW 264 .7 macrophages were incubated with oxidized low density lipoprotein to induce foam cells .Foam cells were incubated with H2S donor sodium hydrosulfide .Cholesterol efflux from macropha-ges was tested by labed cholesterol .The cellular levels of free cholesterol (FC) ,cholesterol ester (CE) and total cholesterol (TC) were measured by high performance liquid chromatography assays .The mRNA and protein expressions of ABCA1 were detected by Real-time PCR and Western blot .Results Compared with the foam cells ,the rates of cholesterol efflux were significantly in-creased ,the levels of TC ,FC ,CE and CE/TC ratio were significantly decreased(P<0 .05) and expression of ABCA1 was signifi-cantly increased by treatment with H2S in dose-and time-dependent manner(P<0 .05) .Conclusion H2S up-regulates of expres-sion ABCA1 and promotes cholesterol efflux in RAW 264 .7 macrophage-derived foam cells .
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Objective To investigate the effect of 17β-estradiol on insulin resistance and the expression of insulin receptor-α in skeletal muscle of ovariectomized rats with insulin resistance induced by high fructose.Methods Forty-eight mature female Sprague-Dawley (SD) rats were randomly divided into four groups: the normal control group (NC, n= 12) rats were fed with the normal diet for 8 weeks; the model group (M, n= 12)rats were ovariectomized and fed with the high fructose diet for 8 weeks, meanwhile the physiological-dose of 17βestradiol (30 μg · kg-1 · d-1 ) was injected subcutaneously every day; the vehicle control group (VC, n= 12) rats were ovariectomized and fed with the high fructose diet for eight weeks, meanwhile equivalent alcohol was injected subcutaneously every day. Systolic blood pressure (SBP), fasting blood sugar (FBS), and fasting serum insulin (FSI) were measured and insulin sensitivity index (ISI) was calculated. The expressions of mRNA and protein of insulin receptor-α in quadriceps femoris were measured by RT-PCR and Western-blot. Results Compared with the normal control group, SBP (P<0.05), FBS (P<0.05) and FSI (P<0.01) were increased significantly while ISI was decreased significantly (P < 0. 05) in the model group. The expressions of mRNA and protein of insulin receptor-α and phosphorylated Akt were decreased significantly in quadriceps femoris in the model group (P<0.05), compared with the normal control group. However, these effects were reversed by 17β-estradiol in the 17βestradiol replacement group. Conclusions 17β-Estradiol inhibits insulin resistance, and up-regulates the expression of insulin receptor-α and the level of phosphorylated Akt in ovariectomized rats with insulin resistance induced by high fructose diet.
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Aim To investigate the effects of arecoline on glucose and lipid metabolism in type 2 diabetic rats and its mechanisms in glucose metabolism.Methods A type 2 diabetic rat model was established by fed with high fructose-high fat diet.The animals were randomly divided into 7 groups: control group,high fructose-high fat diet group(HF)and high fructose-high fat diet+arecoline(1 mg?kg-1,5 mg?kg-1,10 mg?kg-1,20 mg?kg-1,50 mg?kg-1)groups.The blood glucose,lipid level,hepatic function and liver histology were measured.The mRNA expression of liver glucose-6-phosphatase(G6Pase),phosphoenolpyruvate carboxykinase(PEPCK),Forkhead Box O1(FoxO1)and peroxisome proliferator-activated receptor-? coactlvator-1? (PGC-1?)were observed through RT-PCR.Results In comparison with the high fructose-high fat diet group,the fasting blood glucose and TC of the rats were significantly decreased by arecoline in a dose-dependment manner in high fructose-high fat diet+arecoline group.But hepatic function was damaged by 10 mg?kg-1,20 mg?kg-1 and 50 mg?kg-1 arecoline.The mRNA expression of hepatic G6Pase,PEPCK,FoxO1 and PGC-1? was decreased by treatment with 1 mg?kg-1 and 5 mg?kg-1 arecoline compared with the high fructose-high fat diet group.Conclusions Low dose arecoline can decrease fasting blood glucose and TC in type 2 diabettic rats,and the mechanism in glucose metabolism may be related to its effect on the inhibition of hepatic gluconeogenesis.
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AIM To investigate the action of rosiglitazone on blood glucose,blood lipid,and the vascular remodeling in rats fed with high-fructose diet. METHODS After fed with high-fructose diet for one month,rats were randomly divided into two groups:High-fructose diet group that continued feeding with high-fructose diet for another month; High-fructose diet+rosiglitazone group fed with high-fructose diet and rosiglitazone (5 mg?kg -1?d -1, dissolved in water) for one month. At last,one half of each group were anesthetized,and the fasting blood, obtained from heart,was used to detect blood glucose,blood lipid,blood insulin. The aorta and mesenteric artery were gotten from the other half of each group, fixed in formalin,sliced and HE dyed. Pathology analysis system was used to measure the remodeling indexes of aorta and mesenteric artery:Lumen ,media,media/lumen,media cross-section area. RESULTS Comparing high-fructose diet+rosiglitazone group with high-fructose diet group, rosiglitazone decreased blood pressure(16.0 kPa vs 18.0 kPa, P
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Insulin resistant rats induced by fructose were treated with rosiglitazone (RSG), and the effect of RSG on the endocrine function of vascular endothelial cells were investigated. The results showed that RSG can improve the endocrine function of endothelia by enhancing aortic NO synthase activity and the ability of anti-oxidative stress.