Department of Pathobiology, Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran.
Department of Basic Sciences, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran; RASTA Specialized Research Institute (RSRI), West Azerbaijan Science and Technology Park (WASTP), Urmia, Iran.
Life Sci. 2021 Aug 15;279:119633. doi: 10.1016/j.lfs.2021.119633. Epub 2021 May 19.
Current study was conducted to uncover the effect of high-fat diet (HFD)-induced obesity on heat shock proteins 70-2a and 90 expression levels and to investigate the network between these proteins with PCNA expression, endocrine status of testicular tissue and nucleotide backbone damages.
For this purpose, 20 mature male Wistar rats were divided into two groups of control and HFD-received obese animals (n = 10/group). After 8 weeks from obesity approval, the animals were euthanized. The expression levels of Hsp70-2a, Hsp90 and PCNA were analyzed by qRT-PCR and immunohistochemical staining techniques. The Leydig cell distribution/mm of interstitial tissue, serum level of testosterone, testicular total antioxidant capacity (TAC), and mRNA and DNA damage were investigated.
The obese (HFD-received) animals represented a remarkable (p < 0.05) increment in the mRNA levels of hsp70-2a and Hsp90, and the percentages of Hsp70-2a and Hsp90 cells/seminiferous tubules with the same criteria. The PCNA mRNA level and the percentage of PCNA cells were decreased in the obese (HFD-received) group. The obesity, significantly decreased testicular TAC and with no effect on the Leydig cell distribution, but by reducing their steroidogenic activity resulted in a remarkable (p < 0.05) reduction in serum testosterone level. Finally, severe mRNA and DNA damage were revealed in the obese (HFD-received) group.
Therefore, considering massive testicular DNA damage in the obese (HFD-received) animals, we can conclude that an increased expression of Hsp70-2a and Hsp90 with no harmony with PCNA could not properly maintain the cellular DNA integrity and/or appropriately finalize the DNA repair process.
本研究旨在揭示高脂肪饮食(HFD)诱导的肥胖对热休克蛋白 70-2a 和 90 表达水平的影响,并研究这些蛋白质与 PCNA 表达、睾丸组织内分泌状态和核苷酸骨架损伤之间的网络关系。
为此,将 20 只成熟雄性 Wistar 大鼠分为对照组和 HFD 肥胖组(n=10/组)。肥胖确认 8 周后,处死动物。采用 qRT-PCR 和免疫组织化学染色技术分析 Hsp70-2a、Hsp90 和 PCNA 的表达水平。研究间质组织 Leydig 细胞分布/mm、血清睾酮水平、睾丸总抗氧化能力(TAC)以及 mRNA 和 DNA 损伤。
肥胖(HFD 接受)动物的 hsp70-2a 和 Hsp90 mRNA 水平显著增加(p<0.05),相同标准下 Hsp70-2a 和 Hsp90 细胞/生精小管的百分比也增加。肥胖组 PCNA mRNA 水平和 PCNA 细胞的百分比降低。肥胖显著降低了睾丸 TAC,对 Leydig 细胞分布没有影响,但通过降低其类固醇生成活性,导致血清睾酮水平显著降低(p<0.05)。最后,肥胖(HFD 接受)组显示出严重的 mRNA 和 DNA 损伤。
因此,考虑到肥胖(HFD 接受)动物睾丸大量 DNA 损伤,我们可以得出结论,Hsp70-2a 和 Hsp90 的表达增加与 PCNA 不和谐,不能很好地维持细胞 DNA 完整性和/或适当完成 DNA 修复过程。