頁籤選單縮合
題 名 | Possibly of Angiotesin Ⅱ-induced Brain Microvascular Endothelial Cell Injury through Oxidative Stress=血管緊張素Ⅱ可能透過氧化應激機制損傷腦微血管內皮細胞 |
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作 者 | 劉慧青; 魏欣冰; 孫茹; 張斌; 王姿穎; 孫霞; 張岫美; | 書刊名 | 藥物食品分析 |
卷 期 | 14:2 2006.06[民95.06] |
頁 次 | 頁147-152+220 |
分類號 | 418.22 |
關鍵詞 | 腦微血管內皮細胞; 血管緊張素Ⅱ; AT[feb5]受體; 氯沙坦; 氧化應激反應; Brain microvascular endothelial cell; Angiotensin Ⅱ; AT[feb5] receptor; Losartan; Oxidative stress; |
語 文 | 英文(English) |
中文摘要 | 血管緊張素II (angiotensinII,AngII) 作為腎素-血管緊張素系統重要的生物活性肽,可能透過損傷腦微血管內皮細胞 (brain microvascularendothelial cells,BMEC) 參與腦血管疾病的發生發展,但是目前AngII損傷BMEC的機制還不是很清楚。最近研究提示AngII誘導氧自由基的產生與內皮細胞損傷密切相關,因此本研究利用體外培養的大鼠BMEC模型,探討AngII損傷BMEC的氧化應激機制。以MTT法檢測BMEC存活率,通過比色法測定乳酸脫氫酶 (lactate dehydrogenase,LDH) 漏出量反映細胞損傷的程度。生物化學法測定細胞培養液中及細胞內丙二醛 (malondialdelyde,MDA) 含量及細胞內超氧化物歧化酶 (superoxide dismutase,SOD) 和谷胱甘肽過氧化物酶 (glutathione peroxidase,G8H-Px) 活性,檢測BMEC的氧化應激損傷水準。結果顯示,10-6mol/LAngII明顯增加BMEC的LDH漏出量,並呈時間依賴性降低BMEC的存活率;此外,10-6mol/LAngII孵育48hr可明顯增加BMEC培養基中和細胞內MDA含量,降低BMEC內SOD、G8H-Px活性。10-5mol/L選擇性AT1受體拮抗劑氯沙坦能明顯抑制AngII誘導的上述效應,而10-5mol/L選擇性AT2受體拮抗劑PD123319對AngII誘導的上述效應則無明顯影響;氯沙坦和PD123319同時應用也可明顯抑制AngII誘導的上述效應,但與單獨應用氯沙坦組相比,無明顯差異。研究結果顯示,AngII可能透過激動AT1受體誘導氧化應激反應損傷BMEC,從而參與腦血管疾病的發生發展。 |
英文摘要 | An increasing number of studies suggest that angiotensin (Ang) II contributes to the pathology of cerebrovascular disease possibly through injuring of the brain microvascular endothelial cells (BMEC), but the mechanisms involved are not well elucidated. Recent studies reveal the importance of Ang II in reactive oxygen species induction and endothelial injury. Hence, the present study investigated the involvement of oxidative stress in Ang II-induced BMEC injury. Our results showed that 10-6 mol/L Ang II increased lactate dehydrogenase (LDH) leakage and inhibited the viability of primary cultured BMEC. Incubation with 10-6 mol/L of Ang II for 48 hr increased the extracellular and intracellular malondialdehyde (MDA) content and decreased the activities of intracellular glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) significantly. These effects were abolished by pretreatment with the selective AT1 receptor antagonist losartan, but not with the AT2 selective antagonist PD123319. Combining Losartan with PD123319 neither diminished nor promoted the effect of losartan alone. These findings indicated that Ang II induced injury of BMEC may result from oxidative stress by activating AT1 receptors. This injury may in turn lead to the development of cerebrovascular disease. |
本系統中英文摘要資訊取自各篇刊載內容。