| 摘要: | 熱中風好發於高溫環境下的工作者，會造成發燒、腦缺血缺氧等情形，並併發多重器官衰竭，最終導致神經細胞損傷或死亡，有文獻指出其造成損傷之可能的病理機制與心血管疾病所導致的傷害之作用機制類似，且心血管疾病患者較正常人容易罹患熱中風。研究發現川芎因具有某些特定的活性物質，被廣泛應用於抗發炎與治療心血管疾病及神經損傷之相關疾病。然而卻鮮少有研究探討川芎之有效成分 (Active compound of Ligusticum chuanxiong Hort., 以下簡稱ACL) 對於熱中風生成的預防與保護效果。本研究藉由大鼠熱中風動物模式來探討在不同時間點給予不同濃度之 ACL 是否會影響熱中風的生成或減少其損傷程度。大鼠麻醉後，給予 42℃ 之高溫環境誘發大鼠生成熱中風，並在熱暴露期間分別於熱暴露起始點後第 40 分鐘、第 60 分鐘、第 70 分鐘 (此時間點為熱中風控制組之熱中風生成點) 給予靜脈注射 ( Intravenous injection, iv.) 1 ml不同濃度之 ACL 溶液 (0、50、80 mg/kg body weight)，過程中連續記錄大鼠生理參數並觀察其影響情況。結果顯示，大鼠的平均動脈壓 (MAP)、心跳速率 (HR)、直腸溫度 (Tco) 會隨著誘發時間的增加而顯著升高，並大約在熱暴露起始點後第 70 分鐘被誘發生成熱中風，但若在熱暴露起始點後第 60 分鐘給予前處理 ACL (80 mg/kg body weight) 則可顯著增加熱中風生成時間及熱中風發病後的存活時間，並藉由測得血漿中麩草酸轉氨基脢 (Glutamate oxaloacetate transaminase, GOT)、磷酸肌酸激酶 (Creatine phosphokinase, CPK)、乳酸去氫酶 (Lactate dehydrogenase, LDH) 等器官功能性生化指標及細胞激素 (Cytokines) 與觀察腦組織切片發現 ACL 能顯著減少因熱中風所造成之發炎反應、器官損傷及神經損傷，具有保護的效果。
Many studies indicated that the active compound of Ligusticum chuanxiong Hort. (ACL) have been used to treat cardiovascular diseases and neuronal injury widely. Workers in high temperature and humidity were easy to induce heat stroke formation. Studies found that the heat stroke patients and animals all displayed the central ischemia, hypoxia, multi-organ system failure, neuronal damage and high mortality. Many literatures suggested that the patients of cardiovascular diseases might be easier to evoke heat stroke induction. However, there was less attention to investigate the effects of ACL on heat stroke. The main purpose of this study was to observe the effects of ACL on heat stroke by a rat model. Rats under anesthesia were exposed to an ambient temperature (42℃) to induced heat stroke. This study observed the effects of pretreatment with the vehicle and two doses of ACL solution (50、80 mg/kg body weight, iv.) at 40th minute, 60th minute or 70th minute (the onset of heat stroke) after heat exposure start. Recorded and observed the physiological parameters of rats continuously. The results showed that the mean arterial pressure (MAP), heart rate (HR), colonic temperature (TCO) were significantly increased with the time of heat exposure. Pretreatment with 1 ml ACL solution (80 mg/kg body weight, iv.) at 60th minute after heat exposure start was significantly increased the duration time and survival time. On the other hand, it significantly decreased the inflammation, organ damage and neural injury due to heat stroke by histological examination and analyzing glutamate oxaloacetate transaminase (GOT), creatine phosphokinase (CPK), lactate dehydrogenase (LDH). Pretreatment with 1 ml ACL solution (80 mg/kg body weight, iv.) at 60th minute after heat exposure start could possess protective effects on heat stroke rats. |
