蘆丁對(duì)大鼠心肌缺血再灌注損傷的保護(hù)作用及機(jī)制研究
發(fā)布時(shí)間：2018-11-09 08:40
【摘要】：目的探討蘆丁對(duì)大鼠心肌缺血再灌注損傷保護(hù)作用及機(jī)制。方法雄性SD大鼠隨機(jī)分為5組:假手術(shù)組(sham組)、缺血再灌注損傷模型組(MI/RI組)、蘆丁高劑量組(RH組80mg/kg)、蘆丁中劑量組(RM組40mg/kg)、蘆丁低劑量組(RL組20mg/kg),每組10只,建立心肌缺血再灌注損傷模型,蘆丁治療組于術(shù)前30分鐘灌胃給藥。心肌缺血再灌注后超聲心動(dòng)圖評(píng)估心功能:FS%、EF%;導(dǎo)管法測(cè)定血流動(dòng)力學(xué)指標(biāo):心率(HR)、左心室舒張末壓(LVEDP)、左心室收縮壓(LVSP)、左心室舒張最大上升/下降速率(±LVd P/dtmax);染色法測(cè)定心肌梗死面積及計(jì)算心肌梗死程度;酶標(biāo)儀檢測(cè)血清及組織心肌酶生成量(CK-MB、LDH、AST)和氧化指標(biāo)活性(ROS、SOD、還原型GSH、MDA);HE染色觀察組織細(xì)胞形態(tài);免疫印跡法(Western Blot)檢測(cè)Prx II及凋亡相關(guān)蛋白Bcl-2、Bax、Caspase-3和Caspase-9的表達(dá)。結(jié)果與假手術(shù)組比較,模型組EF%、FS%顯著降低、LVEDP顯著升高、LVSP及±LVd P/dtmax顯著降低,差異均具有統(tǒng)計(jì)學(xué)意義(P0.01);心肌酶顯著升高(P0.01);ROS與MDA生成量顯著升高、SOD與GSH活力/濃度顯著降低(P0.01);凋亡蛋白表達(dá)增高及抗凋亡蛋白表達(dá)降低(P0.01);Prx II表達(dá)顯著降低(P0.01)。與模型組比較,蘆丁治療組EF%、FS%顯著升高、LVEDP顯著降低、LVSP及±LVd P/dtmax顯著升高,差異均具有統(tǒng)計(jì)學(xué)意義(P0.01,0.05),呈劑量依賴性;心肌梗死面積顯著縮小,心肌梗死程度降低(P0.01,0.05,呈量依賴性;血清心肌酶譜異常變化得到不同程度改善,呈劑量依賴性;ROS與MDA生成量降低、SOD與GSH活力/濃度升高(P0.05,0.01),呈劑量依賴性;凋亡蛋白表達(dá)減少及抗凋亡蛋白表達(dá)增多(P0.01),Prx II表達(dá)顯著升高(P0.01),呈劑量依賴性。結(jié)論蘆丁可以劑量依賴性的減少心肌缺血再灌注損傷模型大鼠的心肌梗死面積、改善心功能,對(duì)缺血后復(fù)灌的心肌發(fā)揮保護(hù)作用,其機(jī)制可能與蘆丁促進(jìn)心肌內(nèi)Prx II的表達(dá),提高SOD活力,發(fā)揮抗氧化作用,進(jìn)而抑制心肌細(xì)胞凋亡相關(guān)。
[Abstract]:Objective to investigate the protective effect and mechanism of rutin on myocardial ischemia reperfusion injury in rats. Methods male SD rats were randomly divided into five groups: sham-operated group (sham group), ischemia-reperfusion injury model group (MI/RI group), rutin high dose group (80mg/kg), and RM group (40mg/kg). Low dose of rutin (20mg/kg) group (10 rats in each group) was used to establish myocardial ischemia-reperfusion injury model. Rutin treatment group was administered intragastrically 30 minutes before operation. Echocardiographic Evaluation of Cardiac function after Myocardial Ischemia reperfusion: FS%,EF%; Left ventricular end-diastolic pressure (HR), left ventricular systolic pressure (LVEDP), left ventricular systolic pressure (LVSP), left ventricular diastolic maximum ascending / descending rate (鹵LVd P/dtmax); The myocardial infarction size was measured by staining and the myocardial infarction degree was calculated. The serum and tissue myocardial enzyme production (CK-MB,LDH,AST) and the activity of oxidation index (ROS,SOD, reduced GSH,MDA) were detected by enzyme marker. The expression of Prx II and apoptosis-related proteins (Bcl-2,Bax,Caspase-3 and Caspase-9) were detected by HE staining and Western blot (Western Blot). Results compared with the sham-operated group, the EF%,FS%, LVEDP, LVSP and 鹵LVd P/dtmax in the model group were significantly lower than those in the sham-operated group (P0.01), the difference was statistically significant (P0.01), the myocardial enzyme was significantly increased (P0.01). The production of ROS and MDA increased significantly, the activity / concentration of SOD and GSH decreased significantly (P0.01), the expression of apoptotic protein increased and the expression of anti-apoptotic protein decreased (P0.01); Prx II). Compared with the model group, the EF%,FS%, LVEDP, LVSP and 鹵LVd P/dtmax in the rutin treatment group were significantly higher than those in the model group. The difference was significant in a dose-dependent manner. The area of myocardial infarction decreased significantly (P 0.01) and the degree of myocardial infarction decreased in a dose-dependent manner, and the abnormal changes of serum myocardial enzymes were improved in a dose-dependent manner. The production of ROS and MDA decreased, and the activity / concentration of SOD and GSH increased in a dose-dependent manner. The expression of apoptotic protein decreased and the expression of anti-apoptotic protein increased (P0.01), Prx II increased significantly (P0.01) in a dose-dependent manner. Conclusion Rutin can decrease myocardial infarction size, improve cardiac function and protect myocardium from reperfusion injury in a dose-dependent manner. The mechanism of rutin may promote the expression of Prx II in myocardium. Increasing the activity of SOD, exerting antioxidant effect, and then inhibiting cardiomyocyte apoptosis.
【學(xué)位授予單位】：鄭州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R54
本文編號(hào)：2319911
[Abstract]:Objective to investigate the protective effect and mechanism of rutin on myocardial ischemia reperfusion injury in rats. Methods male SD rats were randomly divided into five groups: sham-operated group (sham group), ischemia-reperfusion injury model group (MI/RI group), rutin high dose group (80mg/kg), and RM group (40mg/kg). Low dose of rutin (20mg/kg) group (10 rats in each group) was used to establish myocardial ischemia-reperfusion injury model. Rutin treatment group was administered intragastrically 30 minutes before operation. Echocardiographic Evaluation of Cardiac function after Myocardial Ischemia reperfusion: FS%,EF%; Left ventricular end-diastolic pressure (HR), left ventricular systolic pressure (LVEDP), left ventricular systolic pressure (LVSP), left ventricular diastolic maximum ascending / descending rate (鹵LVd P/dtmax); The myocardial infarction size was measured by staining and the myocardial infarction degree was calculated. The serum and tissue myocardial enzyme production (CK-MB,LDH,AST) and the activity of oxidation index (ROS,SOD, reduced GSH,MDA) were detected by enzyme marker. The expression of Prx II and apoptosis-related proteins (Bcl-2,Bax,Caspase-3 and Caspase-9) were detected by HE staining and Western blot (Western Blot). Results compared with the sham-operated group, the EF%,FS%, LVEDP, LVSP and 鹵LVd P/dtmax in the model group were significantly lower than those in the sham-operated group (P0.01), the difference was statistically significant (P0.01), the myocardial enzyme was significantly increased (P0.01). The production of ROS and MDA increased significantly, the activity / concentration of SOD and GSH decreased significantly (P0.01), the expression of apoptotic protein increased and the expression of anti-apoptotic protein decreased (P0.01); Prx II). Compared with the model group, the EF%,FS%, LVEDP, LVSP and 鹵LVd P/dtmax in the rutin treatment group were significantly higher than those in the model group. The difference was significant in a dose-dependent manner. The area of myocardial infarction decreased significantly (P 0.01) and the degree of myocardial infarction decreased in a dose-dependent manner, and the abnormal changes of serum myocardial enzymes were improved in a dose-dependent manner. The production of ROS and MDA decreased, and the activity / concentration of SOD and GSH increased in a dose-dependent manner. The expression of apoptotic protein decreased and the expression of anti-apoptotic protein increased (P0.01), Prx II increased significantly (P0.01) in a dose-dependent manner. Conclusion Rutin can decrease myocardial infarction size, improve cardiac function and protect myocardium from reperfusion injury in a dose-dependent manner. The mechanism of rutin may promote the expression of Prx II in myocardium. Increasing the activity of SOD, exerting antioxidant effect, and then inhibiting cardiomyocyte apoptosis.
【學(xué)位授予單位】：鄭州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R54
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