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<p>The present study explored the neuroprotective potential of luteolin using a Cecal ligation and puncture (CLP)-subjected rat model of SAE. CLP significantly impaired cognitive and motor functions through impaired performance in the open field test, novel object recognition test, and Morris water maze, indicating impairment in locomotion, recognition memory, and spatial learning. CLP markedly increased S100β, NSE, TNF-α, and IL-1β levels, indicating substantial neuronal damage and systemic inflammation. Further, oxidative stress was also found to be increased in CLP-subjected rats as evidenced by increased MDA levels and decreased antioxidant defense (SOD and GSH) in brain homogenates. In addition, CLP increased neuronal apoptosis, as indicated by upregulated caspase-3 and downregulated expression of Bcl-2, along with increased brain water content, indicative of cerebral edema. Cresyl violet staining and immunohistochemistry revealed neuronal damage and elevated p-p38 MAPK expression, indicating neuroinflammation. Pharmacological treatment with luteolin at doses of 25, 50, and 100&#xa0;mg/kg significantly attenuates sepsis-associated effects. Luteolin treatment dose dependently enhanced behavioral performance, lowered neuroinflammation, regulated apoptosis and oxidative stress markers, maintained neuronal integrity by lowering brain edema, and reduced histopathological changes and activation of p-p38 MAPK. Therefore, the neuroprotective effects of luteolin against SAE through inhibition of neuroinflammation, oxidative stress, and neuronal apoptosis might be attributed to suppression of TNF-α-mediated p-p38 MAPK activation.</p> Graphical Abstract <p></p>

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Protective Effect of luteolin on CLP-induced Sepsis-associated Encephalopathy via Inhibiting p38 MAPK Signalling in a Rat Model

  • 期刊论文

  • 发表日期：

    2026年1月6日

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  • Raunak Kumar,
  • Harshita Singh,
  • Mohd. Hanifa,
  • Manisha Suri,
  • Bivek Bajgai,
  • Anjana Bali

摘要

The present study explored the neuroprotective potential of luteolin using a Cecal ligation and puncture (CLP)-subjected rat model of SAE. CLP significantly impaired cognitive and motor functions through impaired performance in the open field test, novel object recognition test, and Morris water maze, indicating impairment in locomotion, recognition memory, and spatial learning. CLP markedly increased S100β, NSE, TNF-α, and IL-1β levels, indicating substantial neuronal damage and systemic inflammation. Further, oxidative stress was also found to be increased in CLP-subjected rats as evidenced by increased MDA levels and decreased antioxidant defense (SOD and GSH) in brain homogenates. In addition, CLP increased neuronal apoptosis, as indicated by upregulated caspase-3 and downregulated expression of Bcl-2, along with increased brain water content, indicative of cerebral edema. Cresyl violet staining and immunohistochemistry revealed neuronal damage and elevated p-p38 MAPK expression, indicating neuroinflammation. Pharmacological treatment with luteolin at doses of 25, 50, and 100 mg/kg significantly attenuates sepsis-associated effects. Luteolin treatment dose dependently enhanced behavioral performance, lowered neuroinflammation, regulated apoptosis and oxidative stress markers, maintained neuronal integrity by lowering brain edema, and reduced histopathological changes and activation of p-p38 MAPK. Therefore, the neuroprotective effects of luteolin against SAE through inhibition of neuroinflammation, oxidative stress, and neuronal apoptosis might be attributed to suppression of TNF-α-mediated p-p38 MAPK activation.

Graphical Abstract