Scholarlink

Objective <p>This study aimed to evaluate the protective effect of taxifolin on methotrexate (MTX)-induced ovarian toxicity in a rat model. Given the increasing clinical use of MTX and its known detrimental effects on ovarian function, identifying effective protective strategies is crucial for fertility preservation. Taxifolin, a potent natural antioxidant, was investigated for its potential to mitigate oxidative damage and maintain follicular integrity.</p> Materials and methods <p>Thirty adult female Wistar albino rats were randomly assigned to three groups (<i>n</i> = 10 each): Control, MTX, and MTX + Taxifolin. Ovarian injury was induced via a single intraperitoneal injection of MTX (20&#xa0;mg/kg). The Taxifolin group received 50&#xa0;mg/kg/day of taxifolin by oral gavage for 21 days post-MTX administration. Plasma malondialdehyde (MDA), anti-Müllerian hormone (AMH), and tumor necrosis factor-alpha (TNF-α) levels were assessed by ELISA. Ovarian tissue levels of bone morphogenetic protein-7 (BMP-7) and transforming growth factor-beta (TGF-β) were measured, and histopathological evaluations of follicle counts and stromal fibrosis were performed.</p> Results <p>Primordial (<i>p</i> &lt; 0.001), primary (<i>p</i> = 0.001), secondary (<i>p</i> &lt; 0.001), and tertiary (<i>p</i> &lt; 0.001) follicle counts were significantly reduced in the MTX group compared to controls but improved with taxifolin treatment (<i>p</i> &lt; 0.01 or <i>p</i> &lt; 0.001). Ovarian fibrosis significantly increased with MTX (<i>p</i> &lt; 0.001) and was attenuated by taxifolin (<i>p</i> &lt; 0.001). Biochemically, MTX elevated plasma MDA (<i>p</i> &lt; 0.001) and TNF-α (<i>p</i> &lt; 0.001) levels and reduced AMH (<i>p</i> &lt; 0.001) and BMP-7 (<i>p</i> &lt; 0.001) while increasing TGF-β (<i>p</i> &lt; 0.001). Taxifolin significantly reversed these biochemical alterations (<i>p</i> &lt; 0.01 or <i>p</i> &lt; 0.001).</p> Conclusion <p>Taxifolin mitigates MTX-induced ovarian damage by reducing oxidative stress, inflammation, and fibrosis while preserving follicular development. These findings suggest taxifolin as a potential therapeutic agent for protecting ovarian function during MTX therapy.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Taxifolin protects ovarian tissue from methotrexate-induced injury by targeting TGF-β/BMP-7 pathways

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月12日

查看全文
  • Bakiye Akbaş,
  • Gülseren Dinç,
  • Ahmet Akbaş,
  • Gulcin Ercan,
  • Hatice Aygün,
  • Oytun Erbas

摘要

Objective

This study aimed to evaluate the protective effect of taxifolin on methotrexate (MTX)-induced ovarian toxicity in a rat model. Given the increasing clinical use of MTX and its known detrimental effects on ovarian function, identifying effective protective strategies is crucial for fertility preservation. Taxifolin, a potent natural antioxidant, was investigated for its potential to mitigate oxidative damage and maintain follicular integrity.

Materials and methods

Thirty adult female Wistar albino rats were randomly assigned to three groups (n = 10 each): Control, MTX, and MTX + Taxifolin. Ovarian injury was induced via a single intraperitoneal injection of MTX (20 mg/kg). The Taxifolin group received 50 mg/kg/day of taxifolin by oral gavage for 21 days post-MTX administration. Plasma malondialdehyde (MDA), anti-Müllerian hormone (AMH), and tumor necrosis factor-alpha (TNF-α) levels were assessed by ELISA. Ovarian tissue levels of bone morphogenetic protein-7 (BMP-7) and transforming growth factor-beta (TGF-β) were measured, and histopathological evaluations of follicle counts and stromal fibrosis were performed.

Results

Primordial (p < 0.001), primary (p = 0.001), secondary (p < 0.001), and tertiary (p < 0.001) follicle counts were significantly reduced in the MTX group compared to controls but improved with taxifolin treatment (p < 0.01 or p < 0.001). Ovarian fibrosis significantly increased with MTX (p < 0.001) and was attenuated by taxifolin (p < 0.001). Biochemically, MTX elevated plasma MDA (p < 0.001) and TNF-α (p < 0.001) levels and reduced AMH (p < 0.001) and BMP-7 (p < 0.001) while increasing TGF-β (p < 0.001). Taxifolin significantly reversed these biochemical alterations (p < 0.01 or p < 0.001).

Conclusion

Taxifolin mitigates MTX-induced ovarian damage by reducing oxidative stress, inflammation, and fibrosis while preserving follicular development. These findings suggest taxifolin as a potential therapeutic agent for protecting ovarian function during MTX therapy.