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Background <p>Cerebral ischemia–reperfusion (CI/R) injury following cardiac arrest (CA) leads to profound neurological dysfunction driven by oxidative stress, inflammation, and apoptosis. Salvianolic acid B (SalB), a polyphenolic compound with reported neuroprotective activity, has not been fully evaluated in CA-related CI/R injury.</p> Methods <p>A rat CA-induced cerebral ischemia–reperfusion (CA-CI/R) model was established. SalB (20&#xa0;mg/kg) was administered after resuscitation. Neurological deficits were assessed at 6, 24, and 48&#xa0;h using the neurological deficit score. Neuronal morphology and survival were examined by hematoxylin–eosin (HE) and Nissl staining. Oxidative stress indices included superoxide dismutase (SOD) activity and malondialdehyde (MDA) content. Inflammatory cytokines measured were interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Neuronal apoptosis was evaluated by TUNEL staining. PC12 cells were subjected to oxygen–glucose deprivation/reperfusion (OGD/R) to assess cell viability, reactive oxygen species (ROS) production, lipid peroxidation, apoptosis, and nuclear factor erythroid 2-related factor 2 (Nrf2) pathway activation.</p> Results <p>SalB significantly improved neurological outcomes and preserved cortical neuronal integrity in CA-CI/R rats. SalB enhanced SOD activity, reduced MDA accumulation, decreased IL-1β and TNF-α levels, and attenuated neuronal apoptosis. In OGD/R-treated PC12 cells, SalB increased viability, reduced ROS and lipid peroxidation, and inhibited apoptosis. Mechanistically, SalB facilitated Nrf2 release from Kelch-like ECH-associated protein 1 (Keap1) and its nuclear translocation, leading to upregulation of heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1). Immunofluorescence confirmed Nrf2 nuclear localization, and the Nrf2 inhibitor ML385 reversed these effects.</p> Conclusions <p>SalB protects against CI/R-induced neurological injury by reducing oxidative stress, inflammation, and apoptosis through Nrf2 activation, supporting its potential as a therapeutic agent for post-CA cerebral injury.</p>

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Salvianolic acid B attenuates post-cardiac arrest cerebral ischemia–reperfusion injury via activation of the Nrf2 signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月9日

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  • Chuanbao Lv,
  • Guangsheng Guo,
  • Bao Feng,
  • Shasha Yu

摘要

Background

Cerebral ischemia–reperfusion (CI/R) injury following cardiac arrest (CA) leads to profound neurological dysfunction driven by oxidative stress, inflammation, and apoptosis. Salvianolic acid B (SalB), a polyphenolic compound with reported neuroprotective activity, has not been fully evaluated in CA-related CI/R injury.

Methods

A rat CA-induced cerebral ischemia–reperfusion (CA-CI/R) model was established. SalB (20 mg/kg) was administered after resuscitation. Neurological deficits were assessed at 6, 24, and 48 h using the neurological deficit score. Neuronal morphology and survival were examined by hematoxylin–eosin (HE) and Nissl staining. Oxidative stress indices included superoxide dismutase (SOD) activity and malondialdehyde (MDA) content. Inflammatory cytokines measured were interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Neuronal apoptosis was evaluated by TUNEL staining. PC12 cells were subjected to oxygen–glucose deprivation/reperfusion (OGD/R) to assess cell viability, reactive oxygen species (ROS) production, lipid peroxidation, apoptosis, and nuclear factor erythroid 2-related factor 2 (Nrf2) pathway activation.

Results

SalB significantly improved neurological outcomes and preserved cortical neuronal integrity in CA-CI/R rats. SalB enhanced SOD activity, reduced MDA accumulation, decreased IL-1β and TNF-α levels, and attenuated neuronal apoptosis. In OGD/R-treated PC12 cells, SalB increased viability, reduced ROS and lipid peroxidation, and inhibited apoptosis. Mechanistically, SalB facilitated Nrf2 release from Kelch-like ECH-associated protein 1 (Keap1) and its nuclear translocation, leading to upregulation of heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1). Immunofluorescence confirmed Nrf2 nuclear localization, and the Nrf2 inhibitor ML385 reversed these effects.

Conclusions

SalB protects against CI/R-induced neurological injury by reducing oxidative stress, inflammation, and apoptosis through Nrf2 activation, supporting its potential as a therapeutic agent for post-CA cerebral injury.