探討腦部外傷病人腦脊髓液中細胞激素的變化

探討腦部外傷病人腦脊髓液中細胞激素的變化

 腦部外傷是一項嚴重的臨床問題，不僅有較高死亡率，易引起長期性的神經 行為障礙，並且常造成家庭；社會經濟的負擔，特別是那些遭受嚴重腦部外 傷的病患。腦部外傷的病理生理機轉是複雜且互有關聯的。雖然在動物實驗 及臨床上對腦部外傷的研究使我們對腦部外傷的病理生理學有較多的認識，

但目前仍未有一神經保護製劑在減輕或預防因腦部外傷引起的腦部損傷方面 有明顯的效果。本研究著力於腦部外傷發生後，病人腦脊髓液中各種細胞激 素的變化情形。此實驗結合了抗體微陣列檢測分析 (Antibody microarray) 還 有酵素連結免疫吸附分析法 (Enzyme linked immunosorbent assay, ELISA) ， 用以分析腦部外傷發生後不同時間點所收集到的病人腦脊髓液中細胞激素的 變化。觀察到了 interleukin 8 (IL-8) 、 macrophage-derived chemokine (MDC)

、 neutrophil activating protein-2 (NAP-2) 、 monocyte chemoattractant protein-1 (MCP-1) 、 interleukin 6 (IL-6) 、 soluble interleukin 6 receptor (sIL-6R) 、 interc ellular adhesion molecule-1 (ICAM-1) 、 soluble Fas (sFas) 、 tissue inhibitor of metalloprotease-1 (TIMP-1) 在腦部外傷初期病人的腦脊髓液中有濃度增加；

matrix metalloproteinase-9 (MMP-9) 及 matrix metalloproteinase-2 (MMP-2) 活 性增加的表現。在本研究中所觀察的這些細胞激素多和發炎反應，細胞凋亡 有關，雖然這結果受限於本篇研究檢體數目，是需要更多的實驗再加以觀察 佐證的，但仍希望此一實驗，在未來對於腦部外傷的研究上能有些微的貢獻

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Cytokine profile in cerebrospinal fluid from patient with traumatic brain injury

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Traumatic brain injury is a serious clinical problem connected with high mortality rate, long-te

rm neurobehavioral disabilities, familial and socio-economic burden, in particular patients wit

h severe neurotrauma. It should be realized that pathophysiology processes involved in trauma

tic brain damage are complex and interrelated. Although more is known about the pathophysio

logy of traumatic brain injury, deriving from mechanistic studies in experimental models and c

linical head injury, none of the neuroprotective drugs that have been tested to reduce or preven

t brain damage have been shown clear benefit. This study focused on cytokine concentration i

n cerebrospinal fluid from patient with traumatic brain injury. This study used enzyme linked i

mmunosorbent assay (ELISA) and antibody microarray to analyze cytokine variance in conce

ntration in cerebrospinal fluid collected in different point of time from patient with traumatic b

rain injury. This study found interleukin 8 (IL-8); macrophage-derived chemokine (MDC); ne

utrophil activating protein-2 (NAP-2); monocyte chemoattractant protein-1 (MCP-1); interleu

kin 6 (IL-6); soluble interleukin 6 receptor (sIL-6R); intercellular adhesion molecule-1 (ICA

M-1); soluble Fas (sFas); tissue inhibitor of metalloprotease-1 (TIMP-1), matrix metalloprotei

nase-9 (MMP-9), and matrix metalloproteinase-2 (MMP-2) increased their expression in the v

ery beginning of brain trauma. In this study all cytokines used are associated with inflammator

y response and apoptosis. Although in this study the sample number is limited and this finding

need more experiments to prove it, I still hope this finding can offer some contribution toward

traumatic brain injury.