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Objective <p>To investigate the mechanisms by which butylphthalide (NBP) alleviates cerebral edema after intracerebral hemorrhage (ICH) through the regulation of miR-7-5p expression.</p> Methods <p>An ICH model was generated in CTX-TNA2 rat astrocyte cell lines using hemin intervention. An in vivo ICH model was created by injecting type IV collagenase into the basal ganglia of Sprague–Dawley (SD) rats. The cell/rat models were treated with NBP and/or stattic. The expression of STAT3, miR-7-5p, EGFR, PI3K, AKT, p-AKT, AKT2, AKT3, and AQP4 were assessed using qRT-PCR, Western blotting, and immunofluorescence. Brain water content was measured using the wet-to-dry weight method, and neurological deficits were evaluated using the NSS (neurological severity score).</p> Results <p>In both the CTX-TNA2 ICH model and the rat ICH model, miR-7-5p expression was significantly reduced, while STAT3, EGFR, AKT, p-AKT, AKT2, AKT3, and AQP4 expression were elevated compared to the blank/sham-operated group. NBP increased the expression of STAT3 and miR-7-5p, while reducing the expression of EGFR, AKT, p-AKT, AKT2, AKT3, and AQP4. NBP also decreased brain water content and improved NSS scores. STAT3 inhibition significantly reduced STAT3 and miR-7-5p expression, increased the expression of EGFR, PI3K, AKT, p-AKT, AKT2, AKT3, and AQP4, and elevated brain water content. NBP can reverse the downregulation of STAT3 and miR-7-5p expression, the upregulation of EGFR/PI3K/AKT axis and AQP4 expression, and the increase in brain water content induced by STAT3 inhibition.</p> Conclusion <p>NBP alleviates cerebral edema after ICH by upregulating STAT3 expression, thereby increasing miR-7-5p levels and inhibiting the EGFR/PI3K/AKT axis and AQP4 expression.</p> Graphical Abstract <p></p>

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Mechanistic study of butylphthalide in alleviating cerebral Edema after intracerebral Hemorrhage by regulating miR-7-5p expression

  • 期刊论文

  • 发表日期：

    2025年7月1日

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  • Xiqian Chen,
  • Shige Wang,
  • Qiang Lei,
  • Jia Liu,
  • Wei Lu

摘要

Objective

To investigate the mechanisms by which butylphthalide (NBP) alleviates cerebral edema after intracerebral hemorrhage (ICH) through the regulation of miR-7-5p expression.

Methods

An ICH model was generated in CTX-TNA2 rat astrocyte cell lines using hemin intervention. An in vivo ICH model was created by injecting type IV collagenase into the basal ganglia of Sprague–Dawley (SD) rats. The cell/rat models were treated with NBP and/or stattic. The expression of STAT3, miR-7-5p, EGFR, PI3K, AKT, p-AKT, AKT2, AKT3, and AQP4 were assessed using qRT-PCR, Western blotting, and immunofluorescence. Brain water content was measured using the wet-to-dry weight method, and neurological deficits were evaluated using the NSS (neurological severity score).

Results

In both the CTX-TNA2 ICH model and the rat ICH model, miR-7-5p expression was significantly reduced, while STAT3, EGFR, AKT, p-AKT, AKT2, AKT3, and AQP4 expression were elevated compared to the blank/sham-operated group. NBP increased the expression of STAT3 and miR-7-5p, while reducing the expression of EGFR, AKT, p-AKT, AKT2, AKT3, and AQP4. NBP also decreased brain water content and improved NSS scores. STAT3 inhibition significantly reduced STAT3 and miR-7-5p expression, increased the expression of EGFR, PI3K, AKT, p-AKT, AKT2, AKT3, and AQP4, and elevated brain water content. NBP can reverse the downregulation of STAT3 and miR-7-5p expression, the upregulation of EGFR/PI3K/AKT axis and AQP4 expression, and the increase in brain water content induced by STAT3 inhibition.

Conclusion

NBP alleviates cerebral edema after ICH by upregulating STAT3 expression, thereby increasing miR-7-5p levels and inhibiting the EGFR/PI3K/AKT axis and AQP4 expression.

Graphical Abstract