School of Food and Biological Engineering, Yantai Institute of Technology, Yantai, 264003, China.
Department of College of Biological Science and Technology, Yangzhou University, Yangzhou, 225009, China.
Reprod Sci. 2024 Aug;31(8):2261-2272. doi: 10.1007/s43032-024-01543-6. Epub 2024 Apr 17.
Tannic acid (TA) is a polyphenol with antioxidant properties present in various plants. In this study, we explored the protective effect of TA against ovarian oxidative stress in Brandt's voles and its underlying mechanism. At various doses, 3-nitropropionic acid (3-NPA) was intraperitoneally injected into Brandt's voles to simulate ovarian oxidative stress. Thereafter, various doses of TA were intragastrically administered to examine the protective effect of TA against 3-NPA-induced ovarian damage. Changes in inflammation, autophagy, apoptosis, and oxidative stress-related factors were investigated through various biochemical and histological techniques. Ovarian oxidative stress was successfully induced by the intraperitoneal administration of 12.5 mg/kg 3-NPA for 18 days. As a result, the ovarian coefficient decreased and ovarian tissue fibrosis was induced. TA treatment effectively alleviated the increase in luteinizing hormone and follicle-stimulating hormone levels; the decrease in estradiol, progesterone, and anti-Müllerian hormone levels; and the decline in fertility induced by 3-NPA. Compared to that in the 3-NPA group, TA decreased the expression of autophagy-related proteins beclin-1 and LC3, as well as the level of apoptosis. It also activated the AKT/mTOR signaling pathway, downregulated PTEN and p-NF-κB expression, and upregulated Nrf2 expression. In conclusion, our findings indicate that TA could inhibit autophagy via the regulation of AKT/mTOR signaling, suppressing oxidative damage and inflammatory responses through Nrf2 to alleviate 3-NPA-induced ovarian damage. Collectively, the current findings highlight the protective effects of TA in Brandt's vole, where it promotes the maintenance of normal ovarian function.
鞣酸（TA）是一种具有抗氧化特性的多酚，存在于各种植物中。在这项研究中，我们探讨了 TA 对布氏田鼠卵巢氧化应激的保护作用及其潜在机制。用不同剂量的 3-硝基丙酸（3-NPA）腹腔注射布氏田鼠以模拟卵巢氧化应激。此后，用不同剂量的 TA 灌胃，以观察 TA 对 3-NPA 诱导的卵巢损伤的保护作用。通过各种生化和组织学技术研究炎症、自噬、细胞凋亡和氧化应激相关因素的变化。用 12.5mg/kg 的 3-NPA 连续腹腔注射 18 天成功诱导卵巢氧化应激。结果导致卵巢系数降低和卵巢组织纤维化。TA 处理可有效缓解 3-NPA 引起的促黄体生成素和卵泡刺激素水平升高、雌二醇、孕酮和抗苗勒管激素水平降低以及生育力下降。与 3-NPA 组相比，TA 降低了自噬相关蛋白 beclin-1 和 LC3 的表达以及细胞凋亡水平。它还激活了 AKT/mTOR 信号通路，下调了 PTEN 和 p-NF-κB 的表达，上调了 Nrf2 的表达。总之，我们的研究结果表明，TA 可以通过调节 AKT/mTOR 信号抑制自噬，通过 Nrf2 抑制氧化损伤和炎症反应，从而减轻 3-NPA 诱导的卵巢损伤。综上所述，本研究结果强调了 TA 对布氏田鼠的保护作用，可促进其正常卵巢功能的维持。
