| Hyperlipidemia(HLP)is a common disorder of lipid metabolism characterized by high levels of total cholesterol(TC),triglyceride(TG)and low-density lipoprotein cholesterol(LDL-C),or low levels of high-density lipoprotein cholesterol(HDL-C),and is an independent risk factor for atherosclerotic cardiovascular disease.Hyperlipidemia and obesity are positively correlated,and that changes in eating habits,particularly increases in high-fat and high-sugar diets,are important cause of hyperlipidemia.Long-term chronic hyperlipidemia,as a kind of chronic low-grade inflammation,can lead to the imbalance of oxidation and anti-oxidation in the body,lead to the increase of reactive oxygen species(ROS)in the body,the enhancement of the peroxide reaction,and the decline of the enzyme activity of scavenging oxygen free radicals.Statins,which are widely used at present,can cause liver and kidney toxicity and other side effects when taken for a long time.The research and development of natural fat regulating products with non-toxic and low side effects are the focus of attention of all sectors of society.when hyperlipidemia occurs,adjusting lifestyle and changing diet habits on the basis of rational use of natural fat regulating products is an effective adjunct way to treat hyperlipidemia.Lifeceramics(LC)is a mineral element complex made from oyster shells and natural zeolites at high temperature and pressure,in vitro studies have shown that LC has anti-oxidative stress effects.ObjectiveTo study the effect and possible mechanism of LC on lipid regulation?antioxidant function and anti-inflammatory factor in hyperlipidemia rats by establishing hyperlipidemia rat model.Method1 Sixty SPF-Grade healthy male SD rats were randomly divided into five groups,every group 12 rats included: blank control group(control),hyperlipidemia model group(model),low-dose LC group(LC 1),high-dose LC group(LC 2),and positive drug control group(Atorvastatin).The animals were kept in separate cages in animal houses with a temperature of 22±1?,a relative humidity of 50-60%,and a light and dark cycle of 12 hours.Adaptive feeding for one week before the experiment.Control group: normal diet(basic feed for commercially sold rats),free drinking of tap water;Model group: high-fat and high-sugar diet(63.6% basic diet,20% sucrose,15% lard,1.2% cholesterol,0.2% sodium deoxycholate),free drinking of tap water.LC 1 group: high fat and high sugar diet,free drinking of tap water;LC 2 group: high fat and high sugar diet,free drinking of tap water;Atorvastatin group: high fat and high sugar diet,free drinking of tap water;control group and model group were given distilled water daily at a dose of 5ml/kg·d.The LC 1 group and LC 2 group were given different doses of LC daily by intragastric administration,respectively 50mg/kg·d and 100mg/kg·d.Atorvastatin calcium tablets were administered daily to the Atorvastatin group at a dose of 2mg/kg·d.At the end of the 20 th week,abdominal aorta blood collection was completed and the model was made.2 The body weight and blood pressure of the rats were measured.3 Organ index(liver weight/body weight,epididymal fat/body weight),four items of blood lipid(serum total cholesterol TC,serum triglyceride TG,serum low-density lipoprotein cholesterol LDL-C,serum high-density lipoprotein cholesterol HDL-C)and AI were measured.4 The morphology of rat liver was observed by naked eyes,HE staining and oil red O staining were used to observe the steatosis of rat live.5 Indexes of antioxidant capacity of rat serum and liver were detected,including glutathione(GSH),superoxide dismutase(SOD),catalase(CAT)and malondialdehyde(MDA).6 Serum inflammatory factors including tumor necrosis factor(TNF-?)and adiponectin(ADPN)were measured.7 HMG-Co A activity in rat liver was determined.8 SPSS 21.0 statistical software was used for statistical analysis to draw experimental conclusions.Result1 Changes in rat weight and blood pressure: the weight of the model group increased significantly compared with that of the control group(P<0.01),the weight of the LC 2 group decreased compared with that of the model group(P<0.05),while the weight of others two groups decreased slightly compared with that of the model group,but there was no significant difference.Systolic blood pressure and diastolic blood pressure in the model group were higher than those in the control group(P<0.05),systolic blood pressure and diastolic blood pressure in the LC 1 group were lower than those in the model group(P<0.05),and systolic blood pressure and diastolic blood pressure in the other two groups were not significantly higher than those in the model group.2 Changes of serum lipid,AI and viscera index in rats: TC?TG and LDL-C in the model group were significantly higher than those in the control group(all P<0.01);AI,liver weight/body weight and epididymal fat/body weight in the model group were significantly higher than those in the control group(all P<0.01);HDL-C in the model group was not significantly different from that in the control group.LC 1 group?LC 2 group?Atorvastatin group rats TC,TG,LDL-C dropped in the model group(P<0.05,P<0.01),LC 1 group?LC 2 group rat liver weight/body weight,epididymal fat/weight dropped compared to the model group(P<0.05,P<0.01),Atorvastatin group rat liver weight/body weight,epididymal fat/weight compare to the model group,there was no significant difference;there was no significant difference in HDL-C and AI among the three groups compare to the model group.3 Pathological changes of rat liver: Compared with the control group,rat livers in the model group are yellow and greasy,which showed no hepatocyte structure and increased lipid droplets content,while those in the LC 1 group,LC 2 group and Atorvastatin group are gray-red,which showed complete liver structure and significantly decreased lipid droplets content in the liver of LC 1 group.4 Changes in antioxidant capacity indicators4.1 serum antioxidant capacity: the model group rats serum CAT and MDA increased compared with those of the control group(P<0.01,P<0.05),LC 1 group? LC 2 group?Atorvastatin group rats serum CAT,MDA decreased compared with those of the model group(P<0.05,P<0.01),and the LC 1 group reduced serum CAT is better than LC 2 group is better than that of Atorvastatin group,Atorvastatin group reduced serum MDA is better than LC 1 group is superior to the LC 2 group;the model group rats serum GSH decreased than that in the control group(P<0.05),the model group rats serum SOD showed a slight downward trend compared with the control group,but no statistical difference,LC 2 group rats serum GSH and SOD increased compared with the model group(all P<0.05),while LC 1 group rats serum GSH,there was a slight upward trend in the model group,but no statistical difference,serum GSH in the Atorvastatin group was significantly higher than that in the model group(P<0.01),and serum SOD in the LC 1 group and LC 2 group were higher than those in the model group(P<0.01,P<0.05).4.2 liver antioxidant capacity: the model group rats liver CAT and MDA increased compared with those of the control group(P<0.01,P<0.05),LC 1 group,Atorvastatin group rats liver CAT dropped significantly compared with the model group(all P<0.01),and the LC 1 group drop liver CAT effect is better than that of Atorvastatin group;there was a slight decrease in MDA in the liver of the LC 1 group and the Atorvastatin group compared with the model group,but there was no statistical difference.The liver MDA in the LC 2 group was lower than that in the model group(P<0.05).Model group rats liver GSH slightly downward trend compared with the control group,but no statistical difference,LC 1 group?LC 2 group rats liver GSH increased compared with the model group(P<0.01,P<0.05),and LC 1 group rats liver GSH is better than LC 2 group,Atorvastatin group rats liver GSH,there was a slight upward trend compared with the model group,but no statistical difference;SOD in the liver of rats in the model group decreased compared with that in the control group(P<0.05),while SOD in the liver of rats in the LC 1 group?LC 2 group and Atorvastatin group compared with those in the model group,there were no statistical differences.5 The change of serum inflammatory factors: the model group rats tumor necrosis factor(TNF-?)increased compared with the control group(P<0.05),LC 2 group of rats tumor necrosis factor(TNF-?)declined compared with the model group(P<0.05),LC 1 group?Atorvastatin group rats tumor necrosis factor(TNF-?),there is a slight downward trend compared with the model group,but no statistical difference;rats adiponectin(ADPN)in the model group significantly decreased compared with the control group(P<0.01),rats adiponectin(ADPN)in the LC 1 group significantly increased compared with the model group(P<0.01),while rats adiponectin(ADPN)in the LC 2 group and Atorvastatin group slightly increased compared with the model group,there were no statistical differences.6 HMG-Co A activity in rat liver: the model group rats HMG-Co A activity significantly increased compared with the control group(P<0.01),LC 1 group?LC 2 group and Atorvastatin group rats HMG-Co A activity declined significantly compared with the model group(all P<0.01),the inhibitory effect of Atorvastatin group rats on HMG-Co A activity was better than LC 2 group was better than that of in LC 1 group.Conclusion:1 LC can significantly reduce TC,TG and LDL-C levels in hyperlipidemia rats induced by high-fat and high-sugar diet,and improve the lipid metabolism disorder in hyperlipidemia rats.2 LC can reduce oxidative stress of the body and reduce inflammatory reaction.3 LC may improve the imbalance of lipid metabolism by inhibiting the activity of HMG-Co A. |
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