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<p>Inflammation is an important pathological process in ischemic stroke (IS). Astaxanthin (ATX) is a natural product with neuroprotection effects. However, the mechanism of ATX on anti-inflammatory after IS is not clear. The aim of this study was to investigate the mechanism of ATX on anti-inflammatory after IS. Male Sprague–Dawley rats were used to establish a model of middle cerebral artery occlusion (MCAO) on one side and were pre-treated with gavage of ATX for 7&#xa0;days. One day after MCAO, behavioral tests were conducted on the rats, and the brain tissues were subsequently collected. Transcriptomic sequencing (differentially expressed genes with fold change &gt; 1 or &lt; − 1 and FDR <i>P</i> value &lt; 0.05 were selected), flow cytometry, brain water content, Western blot, HE staining, immunohistochemistry and ELISA were analyzed to evaluate the brain damage. ATX treatment has improved the neurological deficits and reduced brain edema, cerebral infarction volume, the expression of tight junction protein occludin, and apoptosis. Also, ATX has reduced inflammation and apoptosis-related proteins such as TLR4, MyD88, NFκB, IL-1β, IL-6, Cyt C, and Caspase-3. The protective effect of ATX was inhibited by the TLR4 agonist RS 09. ATX can improve nerve damage after IS, and these protective effects were realized by anti-inflammatory and anti-apoptosis. ATX alleviates apoptosis and inflammation of IS by inhibiting the TLR4 pathway.</p>

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Transcriptomics and Experiments Verified that Astaxanthin Reduces the Apoptosis of Nerve Cells in Ischemic Stroke by Inhibiting the Toll-like Receptor Signaling Pathway

  • 期刊论文

  • 发表日期：

    2026年1月1日

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  • Shan Gao,
  • Jinjian Li,
  • Yuetong Zhao,
  • Zhen Wei,
  • Chunshu Rong,
  • Kuiyang Zuo,
  • Xu Wang,
  • Dexi Zhao

摘要

Inflammation is an important pathological process in ischemic stroke (IS). Astaxanthin (ATX) is a natural product with neuroprotection effects. However, the mechanism of ATX on anti-inflammatory after IS is not clear. The aim of this study was to investigate the mechanism of ATX on anti-inflammatory after IS. Male Sprague–Dawley rats were used to establish a model of middle cerebral artery occlusion (MCAO) on one side and were pre-treated with gavage of ATX for 7 days. One day after MCAO, behavioral tests were conducted on the rats, and the brain tissues were subsequently collected. Transcriptomic sequencing (differentially expressed genes with fold change > 1 or < − 1 and FDR P value < 0.05 were selected), flow cytometry, brain water content, Western blot, HE staining, immunohistochemistry and ELISA were analyzed to evaluate the brain damage. ATX treatment has improved the neurological deficits and reduced brain edema, cerebral infarction volume, the expression of tight junction protein occludin, and apoptosis. Also, ATX has reduced inflammation and apoptosis-related proteins such as TLR4, MyD88, NFκB, IL-1β, IL-6, Cyt C, and Caspase-3. The protective effect of ATX was inhibited by the TLR4 agonist RS 09. ATX can improve nerve damage after IS, and these protective effects were realized by anti-inflammatory and anti-apoptosis. ATX alleviates apoptosis and inflammation of IS by inhibiting the TLR4 pathway.