查詢結果分析
來源資料
相關文獻
- 三黃瀉心湯對心臟缺血再灌流傷害動物模式之療效評估
- Effect of Trilinolein on Superoxide Dismutase Activity in Isolated Rat Cardiomyocytes Subjected to Hypoxia and Normoxic Perfusion
- Antioxidant and Myocardial Ischemia: Reperfusion Injuries
- 自由基與抗氧化物在心臟血管疾病所扮演的角色
- Effects of the Addition of Free Radical Initiators on the Waterresistance of Heat-Setting PVAc Emulsion Adhesives
- 從認識體內的自由基探討適度運動與健康的正確理念
- 缺氧缺血性腦病變的探討--文獻回顧
- 蘿蔔嬰萃取物於模式系統之抗氧化性
- 亞麻油酸存在下膽固醇受熱時自氧化動力學模式
- 維生素C、E與自由基對運動表現的交互影響
頁籤選單縮合
題 名 | 三黃瀉心湯對心臟缺血再灌流傷害動物模式之療效評估=Study the Cardioprotection of San-Huang- Xie-Xin-Tang in Ischemia-reperfusion Injury Rat Model |
---|---|
作 者 | 葉竹來; | 書刊名 | 中醫藥年報 |
卷 期 | 28:6 2010.09[民99.09] |
頁 次 | 頁1-38 |
分類號 | 413.95 |
關鍵詞 | 缺血再灌流; 細胞程式凋亡; 缺氧; 自由基; 心臟保護作用; Ischemia-reperfusion; Apoptosis; Hypoxia; Reactive oxygen species; Cardioprotection; |
語 文 | 中文(Chinese) |
中文摘要 | 三黃瀉心湯是一種包含大黃、黃蓮、黃芩的傳統中藥複方,它已經被用 於治療胃發炎相關的疾病。然而三黃瀉心湯是否具有對抗缺血再灌流的心臟 保護作用,目前並無相關文獻報導。本實驗的目的就是同時利用缺血再灌流 造成心肌自我凋亡的動物模式和缺氧再給氧誘發心肌細胞自我凋亡的體外模 式去研究探討三黃瀉心湯的心臟保護作用。 麻醉的大鼠將其冠狀動脈結紮維持45分鐘,接著再灌流2小時。將大鼠 隨機分成7大組:(1)控制組(Sham group);(2)溶媒組(Solvent-surgry group); (3)靜脈注射三黃瀉心湯萃取液SHXT (10mg/kg)組;(4)靜脈注射三黃瀉心湯 SHXT (30mg/kg)組;(5)口服投予三黃瀉心湯SHXT(10 mg/kg)組;(6)口服投 予三黃瀉心湯SHXT (30mg/kg);(7)口服投予長效型鈣離子拮抗劑amlodipine (150μg/kg)。監測各組的血液動力學和測量各組切片的梗塞面積,並且分別 進行血漿中Lactate dehydrogenase (LDH)、CK-MB和troponin-I的測定。在體外模式,H9c2細胞在進行缺氧(1% O2)24小時及再給氧8小時前先給予三黃瀉心 湯反應1小時。我們將測定H9c2細胞中NO的含量,並且同時利用annexin-V/PI 染色後進行流式細胞儀分析、Hoechst染色觀察、caspase-3活性測量來測定缺 氧再給氧誘發心肌細胞的自我凋亡現象。為了知道是否在缺氧時會產生自由 基,我們利用兩種螢光染劑(H2DCF-DA和hydroethidine)染色進行流式細胞儀 分析。此外,我們也利用西方墨點法去分析Bcl-2/Bax、eNOS、MAPK等蛋白 質的表現。 在體內和體外模式的研究,我們的結果顯示三黃瀉心湯可減少缺血再 灌流造成心肌的自我凋亡現象。在缺血再灌流所誘發急性心肌梗塞的動物模 式下,三黃瀉心湯可改善心臟功能、血液動力學的參數和減少心肌的梗塞面 積。三黃瀉心湯也能減少降低血漿中的LDH、CK-MB和troponin-I的含量。更進ㄧ步,在細胞模式下,藉由MTT的分析可得知给予三黃瀉心湯可提升細胞 在缺氧再給氧時的存活率。而由annexin-V/PI染色後進行流式細胞儀分析、 Hoechst染色觀察、caspase-3活性測量可得知三黃瀉心湯可抑制缺氧再給氧所 誘發心肌細胞的自我凋亡現象。此外,三黃瀉心湯也能減少缺氧和缺氧再給 氧所產生的自由基。三黃瀉心湯的這些作用可能和增加心肌細胞中Bcl-2/Bax 的分率表現有關。我們得到的結論是三黃瀉心湯可能是透過調節caspase-3和 Bcl-2家族的蛋白表現來達到保護心肌細胞避免缺血再灌流造成的自我凋亡現 象。因此,在臨床上將可被用於預防急性心肌梗塞。 |
英文摘要 | Aim: San-Huang-Xie-Xin-Tang (SHXT) is a traditional Chinese medicinal formula containing Coptidis rhizoma, Scutellariae radix and Rhei rhizome, has been used to treat gastric inflammatory diseases. However, whether SHXT has a cardioprotective effect against ischemia and reperfusion (I/R) injury remains unknown. The aim of this study was to investigate cardioprotective effects of SHXT both in an in vivo model of I/R-induced myocardial apoptosis and an in vitro model of hypoxia/ reoxygenation (H/R)-induced H9c2 rat cardiomyocytes apoptosis. Method: Anesthetized rats were subjected to occlusion of the coronary artery for 45 min followed by reperfusionfor 2 hr. Rats were randomly assigned into 7 groups: Group I: the sham group. Group II: a control group that received vehicle. Group III: SHXT (10 mg/kg) was injected i.v. 15 min prior to ischemia. Group IV: SHXT (30 mg/kg; i.v.). Group V: SHXT (10 mg/kg) was administered by oral, 1 hr prior to ischemia. Group VI: SHXT (30 mg/kg, oral). Group VII: amlodipine (150 g/kg, oral). The changes of hemodynamic and infract area was measured. We will assess the serum level of lactate dehydrogenase (LDH), creatine kinase (CK)-MB, and troponin I levels. In vitro study, H9c2 cells were pretreated 1 hr with SHXT before 24 hr hypoxia (1% O2) and 8 hr reoxygenation (H/R). We will assess myocardial NO content in H9c2 cells. In addition, I/R-induced cardiomyocyte apoptosis was measured by annexin-V/PI labeling flowcytometry, Hoechst staining, and capsape-3 activity measurement. To determinw whether reactive oxygen species (ROS) were generated in response to hypoxia, two fluorescent probes (H2DCF-DA and hydroethidine) were used. In addition, we also measured the proportion of Bcl-2/Bax expression, eNOS protein, and mitogen-activated protein kinases (MAPK) with immunoblotting assay. Results and Discussion: From in vitro and in vivo studies, our results suggested that SHXT attenuated the ischemia-reperfusion-induced cardiac apoptosis. In a rat model of acute myocardial infarction induced by I/R, SHXT improved parameters of cardiac function and hemodynamics and reduced myocardial infarct size. SHXT also reduced the LDH, CK-MB, and troponin I levels in blood. Furthermore, in cultured H9c2 cells, as revealed by MTT assay, treatment with SHXT prior to H/R exposure significantly increased cell viability. SHXT also markedly inhibited H/R-induced cardiomyocyte apoptosis, as detected by annexin-V/PI labeling, Hoechst staining, and activation of caspase-3. Hypoxia SHXT also blocked the accumulation of ROS induced by hypoxia and H/R.These effects of SHXT were associated with an increased ratio of Bcl-2/Bax protein in cardiomyocytes. In conclusion, these results suggest that SHXT may protect cardiomyocytes from I/R-induced apoptosis by regulating caspase-3 and Bcl-2 family and thus will be useful clinically in the prevention of acute myocardial infarction. |
本系統中英文摘要資訊取自各篇刊載內容。