目的：本研究旨在探讨没食子酸（GA）对雌性大鼠双酚A（BPA）暴露引起的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、炎症标志物、氧化应激、细胞凋亡和生殖激素水平的不利影响。方法：32只雌性大鼠分为四组：对照组、GA组、BPA组和GA BPA组。使用苏木精-伊红染色对卵巢组织进行组织病理学评估。对炎症、氧化性 DNA 损伤和凋亡标记物（肿瘤坏死因子 α [TNFα]、环氧合酶-2 [COX2]、白介素-1 β [IL-1β]、8-羟基脱氧鸟苷 [8-OHdG]、和半胱天冬酶 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，使用酶联免疫吸附测定对卵泡刺激素（FSH）、黄体生成素（LH）、雌激素和黄体酮水平进行定量。结果：组织病理学结果显示，BPA 显着诱导毛囊变性，GA 治疗可有效减轻毛囊变性（P < 0.05）。免疫组织化学分析强调了 BPA 暴露组织中炎症反应以及氧化 DNA 损伤和细胞凋亡（TNFα、COX-2、IL-1β、8-OHdG 和 caspase 3）的加剧，而在 GA 存在下，这些反应有所减少（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）。激素分析表明，BPA 暴露改变了 FSH、LH、雌激素和黄体酮的水平，而 GA 治疗显示出调节这些变化的能力，尤其是黄体酮水平（P < 0.05）。结论：研究结果表明，GA 通过其抗氧化和抗炎活性以及调节荷尔蒙失衡的能力，对 BPA 引起的卵巢损伤具有保护作用。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。

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.