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<p>Derived from Rehmanniae Radix, Rehmannioside A (ReA) appears to provide a defensive effect against diseases. This study was designed to investigate ReA’s role and mechanism in cerebral ischemia-reperfusion injury (CI/RI). A transient middle cerebral artery occlusion (tMCAO) mouse model was developed. tMCAO mice were intraperitoneally injected with different doses of ReA for 3 days, and then underwent neurological function examination. Then, brain histopathology was observed by HE staining, neuronal apoptosis was observed by TUNEL staining, glial fibrillary acidic protein (GFAP) expression was detected by immunofluorescence staining to assess astrocyte activation, and blood-brain barrier (BBB) integrity was assessed by determining hemoglobin content and brain water content. p38 MAPK pathway-related proteins were detected by Western blot. Treatment with ReA in tMCAO mice showed a dose-dependent reduction in BBB damage, improvements in neurological function, decreased neuronal apoptosis, and inhibition of astrocyte activation. ReA inhibited p38 MAPK pathway activation, and the p38 MAPK pathway inhibitor SB203580 potentiated the ameliorative effects of ReA on CI/RI. ReA improves CI/RI by inhibiting astrocyte activation and reducing BBB damage through modulation of the p38 MAPK pathway.</p>

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Rehmannioside A: a therapeutic agent for cerebral ischaemia-reperfusion injury via p38 MAPK pathway modulation

  • 期刊论文

  • 发表日期：

    2025年11月7日

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  • XiaoXia Wang,
  • LiXia Wang,
  • ShengXian Wu,
  • RuiXian Wang

摘要

Derived from Rehmanniae Radix, Rehmannioside A (ReA) appears to provide a defensive effect against diseases. This study was designed to investigate ReA’s role and mechanism in cerebral ischemia-reperfusion injury (CI/RI). A transient middle cerebral artery occlusion (tMCAO) mouse model was developed. tMCAO mice were intraperitoneally injected with different doses of ReA for 3 days, and then underwent neurological function examination. Then, brain histopathology was observed by HE staining, neuronal apoptosis was observed by TUNEL staining, glial fibrillary acidic protein (GFAP) expression was detected by immunofluorescence staining to assess astrocyte activation, and blood-brain barrier (BBB) integrity was assessed by determining hemoglobin content and brain water content. p38 MAPK pathway-related proteins were detected by Western blot. Treatment with ReA in tMCAO mice showed a dose-dependent reduction in BBB damage, improvements in neurological function, decreased neuronal apoptosis, and inhibition of astrocyte activation. ReA inhibited p38 MAPK pathway activation, and the p38 MAPK pathway inhibitor SB203580 potentiated the ameliorative effects of ReA on CI/RI. ReA improves CI/RI by inhibiting astrocyte activation and reducing BBB damage through modulation of the p38 MAPK pathway.