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<p>Neonatal hypoxia–ischemia (HI) is a significant cause of lasting disabilities and death in newborns. Salvianolic acid C (SAC), a phenolic compound extracted from <i>Salvia miltiorrhiza</i>, exhibits neuroprotection. However, it is currently uncertain if SAC displays a neuroprotective impact against neonatal hypoxic-ischemic brain damage (HIBD), and if it does, what mechanism is involved. Here, our study found SAC administration (15&#xa0;mg/kg/day, i.p.) improved muscle strength, motor function, and spatial memory impairment in rats with HIBD. The amelioration of these behaviors was attributed to a notable suppression of neuron loss by SAC in the CA1 and CA3 hippocampal zones. Moreover, oxidative stress analysis revealed SAC enhanced anti-oxidants production while reducing pro-oxidants production. Western blot assays revealed SAC downregulated the levels of phospho-c-Jun N-terminal kinase (p-JNK) and jun proto-oncogene (c-JUN). ELISA measurements further showed SAC effectively diminished pro-inflammatory factors, including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). Collectively, these results suggest SAC exhibits a potential neuroprotective impact by attenuating neuronal injury through inhibiting oxidative stress, JNK pathway activation, and inflammation, thereupon then polishes up motor and cognitive deficits caused by HI in the neonatal rats, indicating SAC may be a promising treatment for neonatal hypoxic-ischemic encephalopathy (HIE).</p>

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Neuroprotective Effect of Salvianolic Acid C in Neonatal Rats Following Hypoxic-ischemic Brain Damage

  • 期刊论文

  • 发表日期：

    2025年6月16日

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  • Chunfang Dai,
  • Xiaohuan Li,
  • Zhifang Dong,
  • Boqing Xu,
  • Xi Lai,
  • Jianrui Wei,
  • Dahong Long,
  • Dandan Hu

摘要

Neonatal hypoxia–ischemia (HI) is a significant cause of lasting disabilities and death in newborns. Salvianolic acid C (SAC), a phenolic compound extracted from Salvia miltiorrhiza, exhibits neuroprotection. However, it is currently uncertain if SAC displays a neuroprotective impact against neonatal hypoxic-ischemic brain damage (HIBD), and if it does, what mechanism is involved. Here, our study found SAC administration (15 mg/kg/day, i.p.) improved muscle strength, motor function, and spatial memory impairment in rats with HIBD. The amelioration of these behaviors was attributed to a notable suppression of neuron loss by SAC in the CA1 and CA3 hippocampal zones. Moreover, oxidative stress analysis revealed SAC enhanced anti-oxidants production while reducing pro-oxidants production. Western blot assays revealed SAC downregulated the levels of phospho-c-Jun N-terminal kinase (p-JNK) and jun proto-oncogene (c-JUN). ELISA measurements further showed SAC effectively diminished pro-inflammatory factors, including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). Collectively, these results suggest SAC exhibits a potential neuroprotective impact by attenuating neuronal injury through inhibiting oxidative stress, JNK pathway activation, and inflammation, thereupon then polishes up motor and cognitive deficits caused by HI in the neonatal rats, indicating SAC may be a promising treatment for neonatal hypoxic-ischemic encephalopathy (HIE).