Combination of Total Astragalus Extract and Total Panax Notoginseng Saponins Strengthened the Protective Effects on Brain Damage through Improving Energy Metabolism and Inhibiting Apoptosis after Cerebral Ischemia-Reperfusion in Mice
Combination of Total Astragalus Extract and Total Panax Notoginseng Saponins Strengthened the Protective Effects on Brain Damage through Improving Energy Metabolism and Inhibiting Apoptosis after Cerebral Ischemia-Reperfusion in Mice
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DOI：
10.1007/s11655-015-1965-0
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发表时间：
2017-06-01
影响因子：
2.9
通讯作者：
Deng Chang-qing
中科院分区：
文献类型：
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作者：
Huang Xiao-ping;Tan Hua;Deng Chang-qing
目的：探讨黄芪总提取物（TAE）与三七总皂苷（TPNS）联合抗脑缺血再灌注损伤的作用及其分子机制。方法：将C57BL/6小鼠随机分为假手术组、模型组、TAE （110 mg/kg）组、TPNS （115 mg/kg）组、TAE-TPNS联合组、依达拉奉（4 mg/kg）组，治疗4 d，结扎双侧颈总动脉（CCA） 20 min，再灌注1、24 h。再灌注1 h后，TAE与TAE-TPNS联用可提高三磷酸腺苷（ATP）水平，增加ATP、二磷酸腺苷（ADP）含量和Na+-K+-ATP酶活性，且TAE-TPNS联用的作用强于TAE或TPNS单用。TPNS与TAE-TPNS联合使用可显著提高神经细胞存活率，降低细胞凋亡率，下调磷酸化C - 6 n端激酶1/2 （p-JNK1/2）、细胞色素C （Cyt C）、半胱氨酸天冬氨酸特异性蛋白酶(Caspase)-9、Caspase-3的表达。此外，TAE-TPNS联合治疗的效果优于TAE或TPNS单独治疗。结论：TAE 110 mg/kg联合TPNS 115 mg/kg可增强对脑缺血损伤的保护作用，其机制可能与联合改善早期能量代谢，通过抑制JNK信号转导的线粒体凋亡途径缓解延迟性凋亡有关。
Objective: To explore the effects and molecular mechanisms of the combination between total Astragalus extract (TAE) and total Panax notoginseng saponins (TPNS) against cerebral ischemia-reperfusion injury. Methods: C57BL/6 mice were randomly divided into sham-operated group, model group, TAE (110 mg/kg) group, TPNS (115 mg/kg) group, TAE-TPNS combination group and Edaravone (4 mg/kg) group, treated for 4 days, then, cerebral ischemia-reperfusion injury was established by bilateral common carotid artery (CCA) ligation for 20 min followed by reperfusion for 1 and 24 h. Results: TPNS could increase adenosine triphosphate (ATP) level, TAE and TAE-TPNS combination increased ATP, adenosine diphosphate (ADP) contents and Na+-K+-ATPase activity, and the effects of TAE-TPNS combination were stronger than those of TAE or TPNS alone after reperfusion for 1 h. After reperfusion for 24 h, TAE, TPNS and TAE-TPNS combination significantly increased neurocyte survival rate and decreased the apoptosis rate as well as down-regulated the expression of phosphorylated c-June N-terminal kinase1/2 (p-JNK1/2), cytochrome C (Cyt C), cysteine aspartic acid-specific protease (Caspase)-9 and Caspase-3. Furthermore, the effects in TAE-TPNS combination were better than those in TAE or TPNS alone. Conclusion: The combination of TAE 110 mg/kg and TPNS 115 mg/kg could strengthen protective effects on cerebral ischemia injury, the mechanism underlying might be related to improving jointly the early energy metabolism, and relieving the delayed apoptosis via inhibiting the mitochondrial apoptosis pathway of JNK signal transduction.