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Study On The Mechanism Of The Protective Effect Of Glabridin On The Function Of The Testis Of Atherosclerosis Model Rabbit

Posted on:2019-03-05Degree:MasterType:Thesis
Country:ChinaCandidate:W W WeiFull Text:PDF
GTID:2394330545464433Subject:Human Anatomy and Embryology
Abstract/Summary:PDF Full Text Request
Background Metabolic syndrome is a set of related diseases,and obesity related metabolic abnormality is an important cause of male infertility.Atherosclerosis is the pathological basis of such diseases.Clinical studies have shown that obesity is associated with a decrease in the level of serum testosterone in men with hypogonadism.Glabridin is a unique isoflavone component in glycyrrhiza glabra,which has the effect of antioxidation and anti-inflammation.This study mainly studies whether the glabridin can protect the testosterone synthesis disorder caused by obesity related metabolic diseases caused by the high fat diet.Objective To explore the mechanism of obesity caused by testosterone levels decrease,and the effects of oxidative stress and endoplasmic reticulum stress on the testosterone synthesis function of Leydig cells,and the mechanism of the effect of glabridin on the protection of atherosclerosis model rabbit testis function.Methods New Zealand big ear white rabbit purchased by Anhui Medical University animal center was randomly divided into three groups: N group: normal control group;Group H: high-fat diet model group;G group: glabridin treatment group.N group normal feed feeding;Group H and G group were fed for 12 weeks with high-fat diet.Analysis of changes in blood lipids(triglycerides,total cholesterol,low density lipoprotein);On one side of the testicular tissue,paraffin sections were made and immunohistochemical method was used to observe the expression of 3?-HSD of Leydig cells and the infiltration of macrophages with F4/80 markers.Western blotting respectively detected synthetic testosterone related proteins/enzymes P450 scc,St AR express,SIRT1 and antioxidants Mn SOD GPx4 protein expression,and the change of molecular GRP78 expression of endoplasmic reticulum stress in testicular tissue;The MDA and ABTS methods were used to detect the oxidation-reduction level of testicular tissue and the total antioxidant capacity.Results1.After 12 weeks,compared with the normal control group,TCH,TG and LDL increased in the high-fat model group(p<0.05).Compared with the high-fat diet model group,TG and LDL decreased in the serum of the glabridin treatment group,but the difference was not significant(p>0.05).2.The results showed that the positive expression of the high-fat diet model group was significantly weaker than that in the normal control group by using the anti-tri ?-HSD monoclonal antibody labeled Leydig cell immunohistochemical staining.Compared with the higher fat diet model group,the positive expression of glabridin treatment group was enhanced.The results of immunohistochemical staining of the macrophages with specific antibody F4/80 indicated that the positive expression of the high-fat diet model group was higher than that of the normal control group.Compared with the high-fat model group,the positive expression of the glabridin treatment group decreased.3.Testosterone synthesis of proteins/enzymes related to obesity reduces: in testicular tissue,compared with normal control group,St AR and P450 scc expression level of rabbit testis in the glabridin treatment group decreased significantly(p < 0.05),continuous declining in high-fat diet model group(p < 0.05)4.The antioxidant system function of rabbit testicular tissue of a high-fat diet model group and glabridin treatment group decreased : compared with normal control group,the SIRT1 protein expression in rabbit testicular tissue in high fat model group and glabridin treatment group decrease(p < 0.05).Compared with the high-fat diet model group,the expression of SIRT1 protein in glabridin treatment group increased(P<0.05).Mn SOD and GPx4 protein expression in high-fat diet model group and glabridin treatment group are lower than normal control group(p < 0.05)in testicular tissue,and the glabridin treatment group compared with model group on high-fat diets,Mn SOD and GPx4 protein expression increased(p < 0.05).5.The endoplasmic reticulum stress expression signs of rabbit testicular tissue in high-fat diet model group and glabridin treatment group rise: the expression of GRP78 protein of high-fat model group and glabridin treatment group go higher than normal control group,and compared with high fat model group the glabridin treatment group decreased,with no statistical significance(p > 0.05).6.The results of high fat diet in the testicular tissue causing the tissue REDOX level with MDA detection showed that: MDA level in the high-fat diet model group was higher than that in the control group,but the difference was not obvious.When Gla was administered,the MDA level of glabridin treatment group was significantly lower than even that of the normal control group compared with the high-fat diet model group,with no statistical significance(p > 0.05).7.ABTS was used to determine the total antioxidant capacity of glabridin,and the results showed that the ABTS level of the high-fat diet model group was lower than that in the control group,but the difference was not obvious.When Gla was administered,ABTS of glabridin treatment group was significantly higher compared with that of the high-fat diet model group,with no statistical significance(p > 0.05).Conclusion The results of this study showed that the decreased expression of the protein/enzyme in the testes of atherosclerosis model rabbit testis was associated with decreased testosterone levels.In addition,oxidative stress and endoplasmic reticulum stress in testicular tissue may be an important factor in the reduction of testosterone synthesis ability of testicular Leydig cells in the abnormal metabolism of obesity.As an antioxidant,glabridin can improve Leydig cell's testosterone synthesis ability to a certain extent,and it can protect the testis.
Keywords/Search Tags:Obesity, metabolic syndrome, testis, glabridin, oxidative stress, endoplasmic reticulum stress
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