Mid-Taiwan Journal of Medicine>13卷1期
頁數:11 需求點數:44 電子全文:
篇 名Gui-Zhi-Fu-Ling-Wan Reduces Cerebral Infarction Area via the Anti-inflammatory Effects in Ischemia-reperfusion Injured Rats
作 者謝慶良(Ching-Liang Hsieh);侯庭鏞(Tin-Yun Ho);蘇珊玉(Shan-Yu Su);程錦宜(Chin-Yi Cheng);徐維聰(Wei-Tsung Hsu);謝慶竇(Ching-Tou Hsieh);蒲曉韻(Hsiao-Yun Pu);唐娜櫻(Nou-Ying Tang)
刊 名Mid-Taiwan Journal of Medicine
卷期/出版年月13卷1期 (2008/03)
摘要背景/目的 血瘀是傳統中醫的病理概念,許多研究已顯示血瘀伴隨著中風的發展,而桂枝茯苓丸能改善嚴重血瘀狀態,因此本研究的目的是觀察桂枝茯苓丸對腦梗塞的效用。 方法 將Sprague-Dawley大鼠兩側總頸動脈和右側中大腦動脈的血流阻斷90分鐘,隨後再灌流24小時建立一個腦梗塞的大鼠動物模型。以大鼠的神經缺損程度和腦梗塞面積與該片腦切片總腦面積的百分率做爲桂枝茯苓丸和MK801的療效指標。同時也計算梗塞區域的ED1(mouse anti rat CD68)、interleukin-1β(IL-1β、tumor necrosis factor-α (TNF-α)、intercellular adhesion molecule-1 (ICAM-1)、myeloperoxidase (MPO)免疫反應細胞和凋亡細胞(apoptotic cell)。另外,也利用西方點墨(western blotting)法偵察mitogen activated protein (MAP) kinase的磷酸化(phosphorylation)。 結果 桂枝茯苓丸0.6g/kg、0.8g/kg、MK801(非競爭性N-methyl-D-asparate受體拮抗劑)1.0mg/kg前治療,以及桂枝茯苓丸0.6g/kg後治療減少腦梗塞面積:桂枝茯苓丸0.6g/kg和MK801 1.0mg/kg前治療減少神經神經缺損程度,以及減少ED1,11-lβ、TNF-α、ICAM-1、MPO免疫反應細胞和凋亡細胞的數目。桂枝茯苓丸0.6g/kg減少腦缺血所誘發的c-jun N-terminal kinase (JNK)的磷酸化路徑。 結論 桂枝茯苓丸減少大鼠的腦梗塞面積和神經缺損,推測桂枝茯苓丸可能減少人類的腦梗塞。桂枝茯苓丸也能抑制microglia的活化、TNF-α、IL-1β、ICAM-1的表現,以及嗜中性白血球的浸潤(neurotrophil infiltration),推測桂枝茯苓丸有抗發炎作用。進而,我們的資料顯示桂枝茯苓丸的抗發炎作用是經由腦缺血的JNK信息傳導路徑。

Background/Purpose. Blood stasis, a pathological concept of blood circulation disturbance in Traditional Chinese Medicine, has been demonstrated to be associated with the process of stroke. Gui-Zhi-Fu-Ling-Wan (GZFLW) is known to improve the status of severe blood stasis. The purpose of this study is to investigate the effects of GZFLW on cerebral infarct. Methods. A rat model of cerebral infarct was established by blocking both common carotid arteries and the right middle cerebral artery for 90 min, followed by reperfusion for 24 h. Neurodeficit score and the percentage of cerebral infarction area to total brain area were used as a therapeutic effect index of GZFLW, (a Chinece Medicine formula), and MK801(a non-competitive N-methyl-D-asparate receptor antagonist) treatment. The numbers of ED1 (mouse anti rat CD68)-, interleukin-1β (IL-1β)-, tumor necrosis factor-α (TNF-α)-, intercellular adhesion molecule-1 (ICAM-1)-, myeloperoxidase (MPO)-immunoreactive cells, and apoptotic cells in the cerebral infarction region were counted under light microscope. In addition, the phosphorylation of mitogen-activated protein (MAP) kinases was detected by Western blotting 90 min after blocking the blood flow. Results. Pre-treatment with GZFLW 0.6 g/kg, GZFLW 0.8 g/kg, MK801 1.0 mg/kg and post-treatment with GZFLW 0.6 g/kg reduced the cerebral infarction area; pre-treatment with GZFLW 0.6 g/kg and MK8011.0 mg/kg reduced the neuro-deficit score and also reduced the numbers of ED1-, IL-1β-, TNF-α-, ICAM-1-, MPO-immunoreactive and apoptotic cells in the cerebral infarction region. GZFLW 0.6 g/kg reduced the cerebral ischemia-induced phosphorylation of c-Jun N-terminal kinases (JNKs). Conclusion. GZFLW reduced the cerebral infarction area and neuro-deficit in rats, suggesting that GZFLW has the potential to reduce cerebral infarction size in humans. GZFLW also inhibited microglia activation, neutrophil infiltration, and TNF-α, IL-1β, ICAM-1 expression, suggesting that GZFLW has an anti-inflammatory effect. Moreover, our data indicate that the anti-inflammatory effect of GZFLW might be associated with the JNK signaling pathway in cerebral ischemia.

關鍵詞腦梗塞,c-Jun N-terminal kinases,ED1,桂枝茯苓丸,intercellular adhesion molecule-1,神經缺損;cerebral infarct,c-Jun N-terminal kinases,ED1,Gui-Zhi-Fu-Ling-Wan,intercellular adhesion molecule-1,neurologic deficit

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