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This study found that cucumber seeds (CS) can mitigate heat stress (HS)-induced testicular injury in mice through multiple pathways: ① Antioxidant stress: Activating antioxidant enzymes such as SOD2 and GPx4, reducing malondialdehyde (MDA) production, and significantly alleviating lipid peroxidation damage; ② Enhanced stress defense: Upregulating heat shock protein HSP70 expression to inhibit protein denaturation and germ cell apoptosis induced by heat stress; ③ Anti-inflammation and anti-hypoxia: Suppressing inflammatory cytokines (TNF-α, IL-6) and hypoxia-related pathways (HIF-1α/TGF-β1) to reduce tissue inflammation and hypoxic damage; ④ Hormonal regulation: Selectively restoring follicle-stimulating hormone (FSH) levels to improve the spermatogenic microenvironment, while showing no significant effect on luteinizing hormone (LH) (possibly due to slower repair of Leydig cell damage). The study for the first time confirms the dose-dependent protective effect of CS against heat stress-induced testicular injury and reveals its mechanism through an "antioxidant-apoptosis-inflammation" regulatory network, providing a new direction for the development of natural functional additives against heat stress.

本研究证实,黄瓜籽(CS)可通过多条通路缓解热应激(HS)诱导的小鼠睾丸损伤:① 抗氧化应激:激活超氧化物歧化酶2(SOD2)、谷胱甘肽过氧化物酶4(GPx4)等抗氧化酶,减少丙二醛(MDA)生成,显著减轻脂质过氧化损伤;② 增强应激防御:上调热休克蛋白70(HSP70)的表达,以抑制热应激引发的蛋白质变性与生殖细胞凋亡;③ 抗炎与抗缺氧:抑制炎症因子肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)以及缺氧相关通路缺氧诱导因子-1α(HIF-1α)/转化生长因子-β1(TGF-β1),从而减轻组织炎症与缺氧损伤;④ 激素调控:选择性恢复促卵泡生成素(FSH)水平以改善生精微环境,而对黄体生成素(LH)无显著影响(推测其原因为莱迪希细胞损伤的修复进程相对缓慢)。本研究首次证实了CS对抗热应激诱导睾丸损伤的剂量依赖性保护作用,并通过“抗氧化-凋亡-炎症”调控网络揭示了其作用机制,为抗热应激天然功能添加剂的开发提供了全新方向。

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