Scholarlink

<p>Uteroplacental insufficiency (UPI) disrupts fetal brain development and induces oxidative damage. This study evaluates the neuroprotective effects of ferulic acid (FA) on oxidative stress biomarkers, neuroinflammation, the Akt/GSK-3β signaling pathway, and neuronal density in the medial prefrontal cortex (mPFC) following UPI in rats. Twenty pregnant Wistar rats were randomly assigned to four groups: Control, Sham Surgery, UPI + Vehicle (UPI + normal saline), and UPI + FA (UPI + FA at 100&#xa0;mg/kg). UPI was induced via permanent ligation of the uterine arteries on embryonic day (ED) 18. FA or normal saline was administered orally from ED14 to ED21. On ED21, fetal brain tissue was analyzed for oxidative stress biomarkers (8-hydroxy-2′-deoxyguanosine, protein carbonyl, 4-hydroxy-2-nonenal, and malondialdehyde), inflammatory cytokines (interleukin-6 [IL-6], IL-1β, tumor necrosis factor-alpha [TNF-α], and IL-10), Akt/GSK-3β gene expression, and neuronal density in the mPFC. FA treatment significantly reduced oxidative stress biomarkers and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) while decreasing GSK-3β expression and increasing Akt expression. Additionally, FA enhanced neuronal density in the mPFC and elevated IL-10 levels compared to the UPI + Vehicle group (<i>p</i> &lt; 0.05). Pre-treatment with FA prior to UPI induction mitigated oxidative stress, modulated the Akt/GSK-3β signaling pathway, suppressed neuroinflammation, and preserved cortical integrity in the fetal brain.</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

The Effect of Ferulic Acid on the Akt-GSK3β Signaling Pathway, Neuroinflammation, Oxidative Stress, and Cortical Damage in the Fetal Brain with Uteroplacental Insufficiency

  • 期刊论文

  • 发表日期：

    2025年11月14日

查看全文
  • Habibollah Khodabandeh,
  • Mohammad Amin Edalatmanesh,
  • Mohsen Forouzanfar

摘要

Uteroplacental insufficiency (UPI) disrupts fetal brain development and induces oxidative damage. This study evaluates the neuroprotective effects of ferulic acid (FA) on oxidative stress biomarkers, neuroinflammation, the Akt/GSK-3β signaling pathway, and neuronal density in the medial prefrontal cortex (mPFC) following UPI in rats. Twenty pregnant Wistar rats were randomly assigned to four groups: Control, Sham Surgery, UPI + Vehicle (UPI + normal saline), and UPI + FA (UPI + FA at 100 mg/kg). UPI was induced via permanent ligation of the uterine arteries on embryonic day (ED) 18. FA or normal saline was administered orally from ED14 to ED21. On ED21, fetal brain tissue was analyzed for oxidative stress biomarkers (8-hydroxy-2′-deoxyguanosine, protein carbonyl, 4-hydroxy-2-nonenal, and malondialdehyde), inflammatory cytokines (interleukin-6 [IL-6], IL-1β, tumor necrosis factor-alpha [TNF-α], and IL-10), Akt/GSK-3β gene expression, and neuronal density in the mPFC. FA treatment significantly reduced oxidative stress biomarkers and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) while decreasing GSK-3β expression and increasing Akt expression. Additionally, FA enhanced neuronal density in the mPFC and elevated IL-10 levels compared to the UPI + Vehicle group (p < 0.05). Pre-treatment with FA prior to UPI induction mitigated oxidative stress, modulated the Akt/GSK-3β signaling pathway, suppressed neuroinflammation, and preserved cortical integrity in the fetal brain.