Tolouei Azar Javad, Habibi Maleki Aref, Moshari Sana, Razi Mazdak
Department of Exercise Physiology and Corrective Exercises, Faculty of Sport Sciences, Urmia University, Urmia, Iran.
Department of Exercise Physiology and Corrective Exercises, Faculty of Sport Sciences, Urmia University, Urmia, Iran.
Gene. 2020 Sep 5;754:144850. doi: 10.1016/j.gene.2020.144850. Epub 2020 Jun 4.
Obesity is associated with germ cell apoptosis, spermatogenesis arrest, and testicular endocrine suppression. The aim of the present study was to investigate the crosstalk between germ cell apoptosis and cell cycle machinery in sedentary and obese rats after moderate-intensity continuous (MICT), high-intensity continuous (HICT) and High-intensity interval (HIIT) exercise trainings. Male Wistar rats (n = 30) were randomly divided into 5 groups; the control, sedentary high-fat diet (HFD)-received (HFD-sole), MICT, HICT and HIIT-induced HFD-received groups. The serum levels of LDL-C, HDL-C, triglyceride, and testosterone, mRNA and protein levels of Cyclin D1, Cdk4, p21, apoptotic cell number/mm of testicular tissue and testicular DNA fragmentation ratio were investigated. The obese animals in HFD-sole group represented a significant (p < 0.05) reduction in serum HDL-C and testosterone levels, Cyclin D1, Cdk4 expressions, and exhibited a remarkable (p < 0.05) increment in LDL-C, triglyceride, p21 expression, apoptotic cell number and DNA fragmentation ratio versus control animals. However, the animals in MICT, HICT, HIIT groups exhibited a significant (p < 0.05) increment in serum HDL-C and testosterone, Cyclin D1 and Cdk4 expressions and showed a significant (p < 0.05) reduction in serum LDL-C and triglyceride, p21 expression, apoptotic cell number and DNA fragmentation versus the HFD-sole group. In conclusion, a crosslink between cell cycle machinery and apoptosis of germ cells was revealed in the testicles of HFD-sole animals, and MICT, HICT and HIIT could ameliorate the obesity-induced impairments, respectively. This effect may be attributed to the effect of exercise training protocols on maintaining Cyclin D1 and Cdk4 and suppressing p21 expression levels in the testicles.
肥胖与生殖细胞凋亡、精子发生停滞以及睾丸内分泌抑制有关。本研究的目的是调查在中等强度持续运动（MICT）、高强度持续运动（HICT）和高强度间歇运动（HIIT）训练后，久坐不动和肥胖大鼠生殖细胞凋亡与细胞周期机制之间的相互作用。将30只雄性Wistar大鼠随机分为5组：对照组、久坐不动接受高脂饮食（HFD）组（仅HFD组）、MICT组、HICT组和HIIT诱导接受HFD组。检测血清低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）、甘油三酯和睾酮水平，细胞周期蛋白D1（Cyclin D1）、细胞周期蛋白依赖性激酶4（Cdk4）、p21的mRNA和蛋白水平，睾丸组织中每毫米的凋亡细胞数以及睾丸DNA片段化率。仅HFD组的肥胖动物血清HDL-C和睾酮水平、Cyclin D1和Cdk4表达显著降低（p < 0.05），与对照动物相比，LDL-C、甘油三酯、p21表达、凋亡细胞数和DNA片段化率显著升高（p < 0.05）。然而，MICT组、HICT组、HIIT组动物血清HDL-C和睾酮、Cyclin D1和Cdk4表达显著升高（p < 0.05），与仅HFD组相比，血清LDL-C和甘油三酯、p21表达、凋亡细胞数和DNA片段化显著降低（p < 0.05）。总之，在仅HFD组动物的睾丸中揭示了细胞周期机制与生殖细胞凋亡之间的交联，MICT、HICT和HIIT可分别改善肥胖引起的损伤。这种作用可能归因于运动训练方案对维持睾丸中Cyclin D1和Cdk4以及抑制p21表达水平的影响。
