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目的:探讨内质网应激途径在高脂血症大鼠睾丸生殖细胞损伤中的作用。方法:42只雄性Wistar大鼠于鼠龄4周末随机化分为两组:对照组(12只)和高脂组(30只),分别给予普通饲料和高脂高热量饲料喂养建立高脂血症大鼠模型。第10周末(即鼠龄14周)全自动生化分析仪检测外周血甘油三酯(TG)和总胆固醇(TC)含量,TUNEL法检测睾丸组织中凋亡生殖细胞,免疫组化法检测睾丸组织中葡萄糖调节蛋白78(GRP78)及caspase-12蛋白表达,RT-PCR法检测睾丸组织GRP78及caspase-12 mRNA的表达。结果:高脂组大鼠血清TG、TC[(3.00±0.92)mmol/L、(3.04±0.39)mmol/L]较对照组[(1.43±0.41)mmol/L、(1.55±0.23)mmol/L]显著升高(P<0.01),睾丸生殖细胞凋亡指数[(37.17±2.74)%]较对照组[(5.16±0.81)%]显著升高(P<0.01);以精原细胞和精母细胞凋亡为主。高脂组睾丸组织中GRP78蛋白(0.32±0.03)及caspase-12蛋白(0.34±0.02)表达较对照组(0.19±0.01、0.12±0.01)明显升高(P<0.01),GRP78 mRNA及caspase-12 mRNA(0.86±0.05、0.87±0.01)较对照组(0.37±0.03、0.34±0.03)明显增加(P<0.01)。结论:高脂血症大鼠睾丸生殖细胞凋亡增多;内质网应激可能是高脂血症大鼠睾丸生殖细胞凋亡的主要途径之一。
Objective: To investigate the role of endoplasmic reticulum (ER) stress pathways in the germ cell damage of testis in hyperlipidemic rats. Methods: Forty-two male Wistar rats were randomly divided into two groups: control group (12 rats) and high-fat diet group (30 rats). Rats were fed with normal diet and high-fat and high-calorie diet respectively to establish hyperlipemia Symptomatic rat model. Peripheral blood triglyceride (TG) and total cholesterol (TC) levels were detected by automated biochemical analyzer at week 10 (week 14). Apoptotic germ cells were detected by TUNEL assay and testicular tissue was detected by immunohistochemistry The expressions of GRP78 and caspase-12 were detected by RT-PCR. The expressions of GRP78 and caspase-12 mRNA in testis were detected by RT-PCR. Results Compared with control group [(1.43 ± 0.41) mmol / L, (1.55 ± 0.23) mmol / L, TG, TC [(3.00 ± 0.92) mmol / L, (P <0.01). The apoptotic index of testicular germ cells [(37.17 ± 2.74)%] was significantly higher than that of control group [(5.16 ± 0.81)%] Spermatogenic cell apoptosis. The expression of GRP78 protein (0.32 ± 0.03) and caspase-12 protein (0.34 ± 0.02) in testis tissue of high fat diet group were significantly higher than those in control group (0.19 ± 0.01, 0.12 ± 0.01), GRP78 mRNA and caspase- 12 mRNA (0.86 ± 0.05,0.87 ± 0.01) was significantly higher than that of the control group (0.37 ± 0.03,0.34 ± 0.03) (P <0.01). Conclusion: The apoptosis of testicular germ cells in hyperlipidemic rats is increased. Endoplasmic reticulum stress may be one of the main pathways of testicular germ cell apoptosis in hyperlipidemic rats.