Abstract：
Purpose: This study aimed to investigate the protective effects of gallic acid (GA) against ovarian damage induced by bisphenol A (BPA) exposure in female rats. We evaluated whether GA can mitigate the adverse effects of BPA on ovarian structure, inflammatory markers, oxidative stress, apoptosis, and reproductive hormone levels. Methods: Thirty-two female rats were categorized into four groups: control, GA, BPA, and GA+BPA. Histopathological evaluations of ovarian tissue were performed using hematoxylin-eosin staining. The immunohistochemical analysis was conducted for inflammatory, oxidative DNA damage, and apoptotic markers (Tumor necrosis factor alpha [TNFα], cyclooxygenase-2 [COX2], interleukin-1 beta [IL-1β], 8-hydroxydeoxyguanosine [8-OHdG], and caspase 3). Oxidative stress was assessed by measuring malondialdehyde and superoxide dismutase levels. Furthermore, follicle-stimulating hormone (FSH), luteinizing hormone (LH), estrogen, and progesterone levels were quantified using enzyme-linked immunosorbent assay. Results: Histopathological outcomes revealed that BPA significantly induced follicular degeneration, which was effectively mitigated by GA treatment (P < 0.05). Immunohistochemical analysis highlighted the exacerbation of inflammatory responses and oxidative DNA damage and apoptosis (TNFα, COX-2, IL-1β, 8-OHdG, and caspase 3) in BPA-exposed tissues, which were reduced in the presence of GA (P < 0.05). The assessment of oxidative stress demonstrated that GA could significantly decrease lipid peroxidation and partially restore antioxidant defense mechanisms disrupted by BPA (P < 0.05). Hormonal profiling indicated that BPA exposure altered the levels of FSH, LH, estrogen, and progesterone, with GA treatment showing a capacity to modulate these changes, especially in progesterone levels (P < 0.05). Conclusions: The findings suggest that GA exhibits protective properties against BPA-induced ovarian damage through its antioxidative and anti-inflammatory activities, alongside its ability to modulate hormonal imbalances. This research underscores the therapeutic potential of GA in safeguarding reproductive health against environmental toxicants.
摘要：
目的:探讨没食子酸(GA)对双酚A(BPA)暴露所致雌性大鼠卵巢损伤的保护作用。我们评估了GA是否可以减轻BPA对卵巢结构的不利影响，炎症标志物，氧化应激，凋亡，和生殖激素水平。方法:将32只雌性大鼠分为4组:对照组,GA,BPA,GA+BPA使用苏木精-伊红染色进行卵巢组织的组织病理学评估。对炎症进行了免疫组织化学分析，氧化性DNA损伤，和凋亡标志物(肿瘤坏死因子α[TNFα]，环氧合酶-2[COX2]，白细胞介素-1β[IL-1β]，8-羟基脱氧鸟苷[8-OHdG]，和胱天蛋白酶3）。通过测量丙二醛和超氧化物歧化酶水平来评估氧化应激。此外，卵泡刺激素（FSH），黄体生成素(LH),雌激素,和孕酮水平使用酶联免疫吸附测定进行定量。结果：组织病理学结果显示BPA显著诱导卵泡变性，GA治疗有效缓解(P<0.05)。免疫组织化学分析强调了炎症反应和氧化DNA损伤和细胞凋亡的加剧（TNFα，COX-2，IL-1β，8-OHdG,和半胱天冬酶3）在BPA暴露的组织中，在GA存在下降低(P<0.05)。氧化应激评估表明，GA可以显着降低脂质过氧化并部分恢复BPA破坏的抗氧化防御机制（P<0.05）。激素谱分析表明，BPA暴露改变了FSH的水平，LH,雌激素,和黄体酮,GA治疗显示出调节这些变化的能力，尤其是孕酮水平(P<0.05)。结论：研究结果表明，GA通过其抗氧化和抗炎活性对BPA诱导的卵巢损伤具有保护作用。以及它调节荷尔蒙失衡的能力。这项研究强调了GA在保护生殖健康免受环境毒物侵害方面的治疗潜力。
