The Study On Germ Cell Apotosis In Testis Of Both Hyperlipidemic And Diabetic Rats

Objective To investigate the changes of apoptosis and Bcl-2,Bax in hyperlipidemia and diabetic rats testis.Methods 60 male SD rats of SPF grade were randomly divided into three groups:control group (n=14),high-fat group (n=16) and diabetes group(n=30) . control group fed with normal feed;high-fat group and diabetes group fed with lipid rich food for 24 weeks,and then the formor were given containing 0.2% oxygen pyrimidine lipid rich food to keep feeding , while the later were given 20mg/kg STZ by intraperitoneal injection. At the end of 36w,Fasting Blood glucose, serum TG,QTC,LDL-C,HDL-C and Fasting insulin levels were measured. The testis was embedded in paraffin, sectioned, and stained with hematoxylin and eosin (HE). Germ cell apoptosis was detected by means of the teminal deoxynucleotidyl transferase-mediateddUTP nick end labeling(TUNEL)method. Expressions of Bcl-2 and Bax proteins in thetestis were detected by Strept avidin-biotin-complex (SABC) immunohistochemical staining and computerized image analysis.Results The results of fasting blood glucose,fasting insulin and blood lipid showed that the rat model was established successfully. The testis of hyperlipidemia and diabetic rats exhibited obvious pathological change:basement membrane of seminiferous tubule was not complete; the layers of spermatogenic cells decreased, and the gap increased. Germ cell apoptosis was detected in the testis of all groups. There was significant increase of germ cell apoptosis rate in hyperlipidemia and diabetic rats compared with control group.Bcl-2 and Bax expressed in the testis of all group. The expressions of Bcl-2 was significantly down-regulated and Bax up-regulated in hyperlipidemia and diabetic group compared with control group. The decreased Bcl-2 expressions and increased Bax expressions were observed in the testis of diabetic group compared with hyperlipidemic group.Conclusion the number of apoptotic about spermatogenic cells were significantly increased in male rats with Hyperlipemia and diabetes, which is probably through down-regulation of anti apoptotic factor Bcl-2, up-regulation of proapoptotic Bax, and then promote apoptosis of spermatogenic cells.