Astragalus Extract Alleviates Nerve Injury after Cerebral Ischemia by Improving Energy Metabolism and Inhibiting Apoptosis

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  • Huang Xiao-Ping
    Pathophysiology Laboratory, Hunan University of Chinese Medicine
  • Tan Hua
    Pathophysiology Laboratory, Hunan University of Chinese Medicine
  • Chen Bei-Yang
    Department of Histology and Embryology, Hunan University of Chinese Medicine
  • Deng Chang-Qing
    Pathophysiology Laboratory, Hunan University of Chinese Medicine

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  • <i>Astragalus</i> Extract Alleviates Nerve Injury after Cerebral Ischemia by Improving Energy Metabolism and Inhibiting Apoptosis

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This aim of this study was to explore the effects and molecular mechanisms of Astragalus extract against cerebral ischemia injury through the energy metabolism and apoptosis pathways of c‑Jun N-terminal kinase (JNK) signal transduction. After the bilateral common carotid artery of C57BL/6 mice was occluded for 20 min followed by 1-h reperfusion, the ATP content, total adenine nucleotides (TAN), energy charge (EC), and sodium potassium ATPase (Na+–K+‑ATPase) activity were decreased markedly in brain tissues. Astragalus extract markedly increased the ATP and ADP levels, EC value, and Na+–K+-ATPase activity. Twenty-four and 48 h after reperfusion, the neurocyte survival rate decreased and apoptosis rate increased, while the expression of phosphorylated JNK1/2, cytochrome c (Cyt C), and cysteine aspartic acid-specific protease (caspase)-9 and -3 were significantly enhanced in brain tissues. Astragalus extract significantly increased neurocyte survival and decreased the apoptosis rate as well as down-regulated the expression of p-JNK1/2, Cyt C, caspase-9, and caspase-3. These results suggest that Astragalus extract has neuroprotective effects against nerve injury after cerebral ischemia-reperfusion, and the underlying mechanism may be associated with improved cellular energy metabolism, inhibition of JNK signal transduction pathway activation, and then suppression of the mitochondrial apoptosis pathway.

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