Rahmani Somayyeh, Najdegerami Ebrahim, Razi Mazdak, Nikoo Mehdi
Department of Biology, Faculty of Science, Urmia University, Urmia, Iran.
Division of Comparative Histology and Embryology, Department of Basic Science, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran.
Iran J Basic Med Sci. 2025;28(2):158-169. doi: 10.22038/ijbms.2024.76649.16589.
Nonalcoholic fatty liver disease (NAFLD) is known to disrupt testicular anti-oxidant capacity, leading to oxidative stress (OS) that can negatively affect male fertility by damaging sperm DNA. Heat shock proteins (HSP70 and HSP90), in association with transitional proteins (TP1 and TP2), play crucial roles in protecting sperm DNA integrity in oxidative conditions. Whiteleg shrimp protein hydrolysates (HPs) exhibit anti-oxidant properties, prompting this study to explore the potential of HPs in ameliorating NAFLD-induced testicular damage.
The study divided rats into four groups: control, a group subjected to a high-fat diet (HFD) to induce NAFLD without supplementation, and two HFD-induced NAFLD groups receiving HP doses (20 and 300 mg/kg). After 70 days, the testicular total anti-oxidant capacity (TAC), malondialdehyde (MDA), glutathione (GSH), glutathione disulfide (GSSG), HSP70-2a, HSP90 expression, and TP mRNA levels were assessed.
The results showed that HFD-induced NAFLD significantly increased GSH and MDA levels and disrupted the GSH/GSSG ratio (<0.05) while also reducing HSP70-2a, HSP90, TP1, and TP2 expression (<0.05). However, HP administration effectively restored testicular redox balance, reduced oxidative stress, and enhanced these protective proteins' expression compared to HFD (<0.05).
NAFLD negatively affects the testicular redox system and HSP and TP expression, disrupting male fertility potential. In contrast, HP-treated rats showed a marked effect on NAFLD-induced damage by improving testicular anti-oxidant status and regulating the expression of HSPs and TP proteins. These findings suggest a potential therapeutic role for HP in safeguarding male fertility against the damaging effects of NAFLD.
已知非酒精性脂肪性肝病(NAFLD)会破坏睾丸的抗氧化能力,导致氧化应激(OS),而氧化应激会通过损伤精子DNA对男性生育能力产生负面影响。热休克蛋白(HSP70和HSP90)与过渡蛋白(TP1和TP2)共同作用,在氧化条件下对保护精子DNA完整性起着关键作用。凡纳滨对虾蛋白水解物(HPs)具有抗氧化特性,促使本研究探索HPs改善NAFLD诱导的睾丸损伤的潜力。
本研究将大鼠分为四组:对照组、高脂饮食(HFD)诱导NAFLD且不补充任何物质的组,以及两组接受HP剂量(20和300 mg/kg)的HFD诱导NAFLD组。70天后,评估睾丸总抗氧化能力(TAC)、丙二醛(MDA)、谷胱甘肽(GSH)、谷胱甘肽二硫化物(GSSG)、HSP70-2a、HSP90表达以及TP mRNA水平。
结果表明,HFD诱导的NAFLD显著提高了GSH和MDA水平,破坏了GSH/GSSG比值(<0.05),同时还降低了HSP70-2a、HSP90、TP1和TP2的表达(<0.05)。然而,与HFD组相比,给予HP有效恢复了睾丸氧化还原平衡,降低了氧化应激,并增强了这些保护蛋白的表达(<0.05)。
NAFLD对睾丸氧化还原系统以及HSP和TP的表达产生负面影响,破坏男性生育潜力。相比之下,HP处理的大鼠通过改善睾丸抗氧化状态和调节HSPs和TP蛋白的表达,对NAFLD诱导的损伤显示出显著效果。这些发现表明HP在保护男性生育能力免受NAFLD损害方面具有潜在的治疗作用。