PDF(Pubmed)
Abstract：
UNASSIGNED: This study evaluated the regulatory effect of Tetramethylpyrazine (TMP) on the spinal cord injury (SCI) rat model and clarified the neuroprotective mechanism of TMP on SCI.
UNASSIGNED: An SCI rat model was generated and treated with TMP injections for two weeks. miR-497-5p and EGFL7 expression changes were evaluated, motor function recovery after SCI was assessed by BBB score test and footprint analysis, lesions of rat spinal cord were assessed by HE staining and TUNEL staining; angiogenesis was assessed by immunoblotting for CD31; inflammatory factor levels were detected by ELISA. EGFL7 was verified as a target of miR-497-5p by bioinformatics website analysis and luciferase reporter gene assay. H2O2-injured neurons were cultured in vitro to explore the effect of TMP.
UNASSIGNED: After SCI, miR-497-5p was upregulated while EGFL7 was downregulated in rats. TMP inhibited apoptosis and promoted angiogenesis, nerve regeneration, and repair of nerve defects by reducing miR-497-5p and increasing EGFL7 expression. miR-497-5p targeted EGFL7. In addition, TMP hindered neuronal inflammation and apoptosis induced by H2O2in vitro.
UNASSIGNED: TMP promotes angiogenesis by downregulating miR-497-5p to target EGFL7, and promotes nerve regeneration and repair of nerve defects in rats with SCI.
UNASSIGNED: An SCI rat model was generated and treated with TMP injections for two weeks. miR-497-5p and EGFL7 expression changes were evaluated, motor function recovery after SCI was assessed by BBB score test and footprint analysis, lesions of rat spinal cord were assessed by HE staining and TUNEL staining; angiogenesis was assessed by immunoblotting for CD31; inflammatory factor levels were detected by ELISA. EGFL7 was verified as a target of miR-497-5p by bioinformatics website analysis and luciferase reporter gene assay. H2O2-injured neurons were cultured in vitro to explore the effect of TMP.
UNASSIGNED: After SCI, miR-497-5p was upregulated while EGFL7 was downregulated in rats. TMP inhibited apoptosis and promoted angiogenesis, nerve regeneration, and repair of nerve defects by reducing miR-497-5p and increasing EGFL7 expression. miR-497-5p targeted EGFL7. In addition, TMP hindered neuronal inflammation and apoptosis induced by H2O2in vitro.
UNASSIGNED: TMP promotes angiogenesis by downregulating miR-497-5p to target EGFL7, and promotes nerve regeneration and repair of nerve defects in rats with SCI.
摘要：
■本研究评估了川芎嗪（TMP）对脊髓损伤（SCI）大鼠模型的调节作用，并阐明了TMP对SCI的神经保护机制。
■产生SCI大鼠模型并用TMP注射处理两周。评估miR-497-5p和EGFL7表达变化，通过BBB评分测试和足迹分析评估SCI后的运动功能恢复，HE染色和TUNEL染色评估大鼠脊髓病变；CD31免疫印迹法评估血管生成；ELISA法检测炎症因子水平。通过生物信息学网站分析和荧光素酶报告基因检测,验证EGFL7为miR-497-5p的靶标。体外培养H2O2损伤的神经元以探讨TMP的作用。
■SCI后，大鼠miR-497-5p上调，而EGFL7下调。TMP抑制细胞凋亡，促进血管生成，神经再生,通过减少miR-497-5p和增加EGFL7表达来修复神经缺损。miR-497-5p靶向EGFL7。此外,TMP在体外抑制H2O2诱导的神经元炎症和凋亡。
■TMP通过下调miR-497-5p以靶向EGFL7来促进血管生成，并促进SCI大鼠的神经再生和神经缺损修复。
■产生SCI大鼠模型并用TMP注射处理两周。评估miR-497-5p和EGFL7表达变化，通过BBB评分测试和足迹分析评估SCI后的运动功能恢复，HE染色和TUNEL染色评估大鼠脊髓病变；CD31免疫印迹法评估血管生成；ELISA法检测炎症因子水平。通过生物信息学网站分析和荧光素酶报告基因检测,验证EGFL7为miR-497-5p的靶标。体外培养H2O2损伤的神经元以探讨TMP的作用。
■SCI后，大鼠miR-497-5p上调，而EGFL7下调。TMP抑制细胞凋亡，促进血管生成，神经再生,通过减少miR-497-5p和增加EGFL7表达来修复神经缺损。miR-497-5p靶向EGFL7。此外,TMP在体外抑制H2O2诱导的神经元炎症和凋亡。
■TMP通过下调miR-497-5p以靶向EGFL7来促进血管生成，并促进SCI大鼠的神经再生和神经缺损修复。
