探討黃耆皂苷對於液柱撞擊誘導腦損傷之神經保護效果評估

Protective Effects of Astragaloside in Fluid Percussion Induced Brain Injury Rat Model

腦損傷在全世界是個發生率極高且致死率高的一種意外傷害。據估計，發生率(新發病例數)是每年每10萬個人中就有300例(是人口比例的0.3%)，腦損傷可能影響生理、認知、社會行為、情緒等功能障礙，嚴重可能導致死亡，因此研究有效治療頭部外傷的藥物是迫切需要的。本實驗利用液柱撞擊方式模擬頭部外傷(Traumatic brain injury, TBI)，探討傳統中草藥黃耆皂苷(Astragaloside, AST)之治療效果，實驗分為三組進行，假手術組(Sham)，黃耆皂苷安慰劑合併頭部外傷組(AST vehicle/ TBI)，黃耆皂苷合併頭部外傷組(AST/ TBI)。利用2,3,5-氯化三苯基四唑(2,3,5 triphenyltetrazolium chloride, TTC)染色法定量損傷區域、免疫螢光染色法觀察細胞凋亡情形、行為測試評估大鼠損傷後之行為功能改變。基本生理參數的結果中我們確立動物模式的成立， TTC染色中發現大鼠腦部損傷的體積在經過頭部外傷後有明顯的增加，經過AST治療後具有顯著的減輕效果。而免疫螢光染色結果顯示，神經元細胞經損傷後呈現大量凋亡狀態，經AST治療後有效的降低細胞凋亡之情形。利用行為測試檢視大鼠治療後行為之恢復狀況，結果也證實AST能有效幫助大鼠頭部外傷損傷後醒為功能之恢復。以上結果說明，利用AST藥物的治療，都有效地降低大鼠經頭部外傷後的腦損傷，並有效改善損傷後行為功能之恢復。此結果未來將可以應用於臨床頭部外傷病患治療藥物之選擇。

Brain injury is a major cause of death and disability worldwide. According to statistics, 0.3% of the population suffer brain injury per year. Traumatic brain injury (TBI) causes a host of physical, cognitive, social, emotional, and behavioral effects, which can range from complete recovery to permanent disability or death. For this reason, developing novel therapeutic strategies or finding new effective therapeutic drugs are very important. The aim of this study was to assess whether Astragaloside (AST) processes neuroprotection effect in TBI induced by fluid percussion injury (FPI) in rats. Animals were separated into five groups: (1) sham operation group (Sham), (2) AST vehicle with TBI group (AST vehicle/ TBI), (3) AST with TBI group (AST/ TBI). Cell morphological changes such as size of infarction volume and extent of neuronal apoptosis were evaluated by triphenyltetrazolium chloride staining and double immunofluoresence staining with TUNEL / Neu. The functional outcome of treatment such as sensation, motor and behavior were evaluated by incline plane. Compared to those of the sham operated controls, the animals with FPI had higher values of infarction area, cell morphology change, neuron apoptosis and gliosis in the cortex and hippocampus, which could be attenuated by AST IV adopted immediately after FPI. Our conclusion is that AST IV may be an effective therapeutic drug for clinical TBI patients.