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生长抑素和N-乙酰半胱氨酸对缺血再灌注引发的睾丸损伤的作用:细胞保护和抗氧化作用

Somatostatin and N-acetylcysteine on testicular damage triggered by ischemia reperfusion: cellular protection and antioxidant effects.

作者信息

Ciftel Enver, Mercantepe Tolga, Ciftel Serpil, Karakas Sibel Mataracı, Aktepe Riza, Yilmaz Adnan, Mercantepe Filiz

机构信息

Department of Endocrinology and Metabolism, Sivas Numune Hospital, Sivas, Türkiye.

Department of Histology and Embryology, Faculty of Medicine, Recep Tayyip Erdogan University, Rize, Türkiye.

出版信息

Hormones (Athens). 2025 Apr 12. doi: 10.1007/s42000-025-00650-6.

DOI:10.1007/s42000-025-00650-6
PMID:40220169
Abstract

Ischemia-reperfusion (I/R) injury is a significant cause of testicular damage, leading to infertility and other reproductive dysfunctions. Antioxidant therapies have emerged as a potential intervention to mitigate oxidative stress and cellular damage. This study investigates the effects of somatostatin (SST) and N-acetylcysteine (NAC) on testicular damage induced by I/R, focusing on their antioxidant and cellular protective effects. Twenty-four male rats were divided into four groups, as follows: sham operated, I/R injury, I/R + somatostatin treatment, and I/R + NAC treatment. A testicular I/R injury was induced surgically, followed by either SST or NAC administration. Testicular tissues were assessed histopathologically using hematoxylin and eosin staining and employing Johnson's biopsy scoring. Immunohistochemical analyses were performed for caspase- 3, 8-hydroxy- 2'-deoxyguanosine (8-OHdG), testis-specific histone 2B, and testosterone to evaluate apoptosis, oxidative DNA damage, cellular proliferation, and steroidogenesis, respectively. Serum levels of testosterone and follicle-stimulating hormone (FSH) were measured by biochemical analysis. The results showed that both SST and NAC treatments significantly ameliorated histopathological damage and reduced the levels of caspase- 3 and 8-OHdG, indicating reduced apoptosis and oxidative DNA damage. Furthermore, increased testis-specific histone 2B positivity suggested enhanced cellular proliferation. Notably, administration of SST decreased testosterone positivity in the testis, whereas NAC treatment increased it. However, no significant differences in serum testosterone levels were observed between the NAC and SST groups. In addition, serum FSH levels of the I/R + SST group were found to be significantly higher than those of the control group. SST and NAC exhibit protective effects against testicular damage induced by I/R, as evidenced by their antioxidant and anti-apoptotic properties. The differential impact on testosterone positivity in the testis tissue highlights distinct underlying mechanisms, warranting further investigation. Despite these promising findings, the lack of significant changes in serum hormone levels calls for additional studies to fully elucidate the therapeutic potential and mechanistic pathways of SST and NAC in the context of testicular I/R injury.

摘要

缺血再灌注(I/R)损伤是睾丸损伤的一个重要原因,可导致不育和其他生殖功能障碍。抗氧化疗法已成为减轻氧化应激和细胞损伤的一种潜在干预措施。本研究调查了生长抑素(SST)和N-乙酰半胱氨酸(NAC)对I/R诱导的睾丸损伤的影响,重点关注它们的抗氧化和细胞保护作用。将24只雄性大鼠分为四组,如下:假手术组、I/R损伤组、I/R + 生长抑素治疗组和I/R + NAC治疗组。通过手术诱导睾丸I/R损伤,随后给予SST或NAC。使用苏木精和伊红染色并采用约翰逊活检评分对睾丸组织进行组织病理学评估。分别对caspase-3、8-羟基-2'-脱氧鸟苷(8-OHdG)、睾丸特异性组蛋白2B和睾酮进行免疫组织化学分析,以评估细胞凋亡、氧化性DNA损伤、细胞增殖和类固醇生成。通过生化分析测量血清睾酮和促卵泡激素(FSH)水平。结果表明,SST和NAC治疗均显著改善了组织病理学损伤,并降低了caspase-3和8-OHdG的水平,表明细胞凋亡和氧化性DNA损伤减少。此外,睾丸特异性组蛋白2B阳性增加表明细胞增殖增强。值得注意的是,给予SST会降低睾丸中的睾酮阳性,而NAC治疗则会增加睾酮阳性。然而,NAC组和SST组之间的血清睾酮水平没有显著差异。此外,发现I/R + SST组的血清FSH水平显著高于对照组。SST和NAC对I/R诱导的睾丸损伤具有保护作用,其抗氧化和抗凋亡特性证明了这一点。对睾丸组织中睾酮阳性的不同影响突出了不同的潜在机制,值得进一步研究。尽管有这些有前景的发现,但血清激素水平缺乏显著变化,需要进一步研究以充分阐明SST和NAC在睾丸I/R损伤背景下的治疗潜力和作用机制途径。

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The Effects of Dexmedetomidine on Abdominal Aortic Occlusion-Induced Ovarian Injury via Oxidative Stress and Apoptosis.右美托咪定通过氧化应激和细胞凋亡对腹主动脉阻断所致卵巢损伤的影响
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Chemoprotective effect of vitexin against cisplatin-induced biochemical, spermatological, steroidogenic, hormonal, apoptotic and histopathological damages in the testes of Sprague-Dawley rats.牡荆素对顺铂诱导的Sprague-Dawley大鼠睾丸生化、精子学、类固醇生成、激素、凋亡及组织病理学损伤的化学保护作用。
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