依達(dá)拉奉預(yù)處理對(duì)吡喃阿霉素誘導(dǎo)大鼠急性心肌損傷的實(shí)驗(yàn)研究
本文選題:依達(dá)拉奉 切入點(diǎn):吡喃阿霉素 出處:《廣西醫(yī)科大學(xué)》2017年碩士論文
【摘要】:目的:觀察依達(dá)拉奉(EDA)對(duì)吡喃阿霉素(THP)誘導(dǎo)的大鼠急性心肌損傷的影響,探討EDA預(yù)處理對(duì)大鼠急性心肌損傷是否具有保護(hù)作用。方法:取體重230-260克的雌性SD大鼠40只,采用隨機(jī)數(shù)字表法分為四組,每組10只:正常對(duì)照組(GNS組)、吡喃阿霉素組(THP組)、EDA-5mg組(EDA-1)、EDA-10mg組(EDA-2)。GNS組于實(shí)驗(yàn)第1至第7天每天腹腔注射與EDA等量生理鹽水,最后一次注射2h后腹腔注射與THP等量的5%葡萄糖;THP組于實(shí)驗(yàn)第1至第7天腹腔注射與EDA等量生理鹽水,最后一次注射2h后一次性腹腔注射THP 15mg/kg;EDA-1組于實(shí)驗(yàn)第1至第7天腹腔注射低劑量依達(dá)拉奉5mg/kg,最后一次注射2h后一次性腹腔注射THP 15mg/kg;EDA-2于實(shí)驗(yàn)第1至第7天腹腔注射高劑量依達(dá)拉奉10mg/kg,最后一次注射2h后一次性腹腔注射THP 15mg/kg。實(shí)驗(yàn)第10天大鼠麻醉后腹主動(dòng)脈取血,檢測(cè)血清cTnI和NT-proBNP水平。取血后制作頸動(dòng)脈標(biāo)本,光鏡下觀察病理變化;取心室前壁心肌組織光鏡觀察病理改變并評(píng)分。余心肌組織制作成勻漿,測(cè)定·OH、GSH-Px、SOD活性和MDA含量。結(jié)果:(1)THP處理后第3天,THP組大鼠的體重較GNS組、EDA-1組、EDA-2組顯著降低(P0.05),GNS組、EDA-1組、EDA-2組三組之間體重差異無(wú)統(tǒng)計(jì)學(xué)意義(P0.05)。(2)EDA-1組、EDA-2組和THP組的心臟體重指數(shù)比高于GNS組(P0.05),THP組的心臟體重指數(shù)高于EDA-1組、EDA-2組(P0.05),EDA-1組和EDA-2組之間無(wú)統(tǒng)計(jì)學(xué)差異(P0.05)。(3)THP組血清cTnI水平明顯高于其它三組(P0.05),EDA-1組水平高于EDA-2組(P0.05)。THP組血清NT-proBNP水平也明顯高于其它三組(P0.05),兩兩比較GNS組、EDA-1組、EDA-2組之間無(wú)統(tǒng)計(jì)學(xué)差異。(4)THP組、EDA-1組、EDA-2組·OH活性明顯高于GNS組(P0.05),THP組、EDA-1組和EDA-2組兩兩比較后顯示:THP組高于EDA-1組、EDA-2組(P0.05),EDA-1組高于EDA-2組(P0.05)。(5)THP組GSH-Px活性明顯低于其它三組(P0.05),THP組、EDA-1組活性低于GNS組活性(P0.05),EDA-2組與GNS組比較無(wú)統(tǒng)計(jì)學(xué)差異(P0.05)。(6)THP組SOD活性低于其它三組(P0.05),EDA-1組、EDA-2組、GNS組活性兩兩比較差別無(wú)統(tǒng)計(jì)學(xué)意義(P0.05)。THP組MDA含量也明顯低于其它三組(P0.05),EDA-1組MDA含量較EDA-2組高(P0.05)。(7)光鏡下顯示,THP組出現(xiàn)明顯的右頸動(dòng)脈和心肌病理改變,EDA-1組、EDA-2組的病理改變較輕。(8)心肌病理評(píng)分:THP組明顯高于其它三組(P0.05),EDA-1組、EDA-2組心肌病理評(píng)分低于THP組(P0.05),EDA-1組、EDA-2組之間差異無(wú)統(tǒng)計(jì)學(xué)意義(P0.05)。結(jié)論:(1)THP可誘發(fā)大鼠心肌損傷和頸動(dòng)脈損傷;(2)EDA5mg/kg、10mg/kg預(yù)處理對(duì)THP致大鼠心肌急性損傷有一定的保護(hù)作用,10mg/kg預(yù)處理保護(hù)作用更好。
[Abstract]:Objective: to observe the effect of Edaravone on acute myocardial injury induced by pyrrolidine trimethopyranicol (THP) in rats, and to explore whether EDA pretreatment has protective effect on acute myocardial injury in rats. Methods: 40 female SD rats weighing 230 to 260 g were selected. Ten rats in each group were randomly divided into four groups: normal control group (n = 10) and adriamycin group (n = 10). The rats in the control group received intraperitoneal injection of the same amount of normal saline as EDA every day from day 1 to day 7. Two hours after the last injection, 5% glucose was injected intraperitoneally with the same amount of THP as normal saline with EDA on the 1st to 7th day of the experiment. Two hours after the last injection, THP 15mg / kg EDA-1 group was injected intraperitoneally with low dose Edaravone 5mg / kg on the 1st to 7th day, and THP 15mg / kg EDA-2 was injected intraperitoneally at the first to seventh day after the last 2 h injection. The dose of Edaravone was 10 mg / kg, and THP was injected intraperitoneally once 2 hours after the last injection. Blood was taken from abdominal aorta of rats after anesthesia on the 10th day. The serum levels of cTnI and NT-proBNP were measured, the carotid artery specimens were made after blood extraction, the pathological changes were observed under light microscope, the pathological changes were observed and graded by light microscope in the myocardium of the anterior wall of the ventricle, and the remaining myocardial tissue was made into homogenate. Results the body weight of rats in THP group was significantly lower than that in EDA-1 group in GNS group on the 3rd day after THP treatment. There was no significant difference in body weight between EDA-2 group and EDA-2 group (P0.05) and EDA-2 group (THP group). The body mass index of heart in GNS group was higher than that in EDA-1 EDA-2 group and EDA-2 group. There was no significant difference in serum cTnI level between EDA-1 group and EDA-2 group. The level of serum cTnI in THP group was significantly higher than that in other three groups (P0.05EDA-1 group was higher than that in EDA-2 group P0.05TDA-1 group was also higher than that in EDA-2 group. THP group was also significantly higher than EDA-2 group in serum NT-proBNP level. There was no significant difference between EDA-2 group and EDA-2 group in GNS group. The activity of OH in EDA-2 group was significantly higher than that in GNS group P0.05THP group and EDA-2 group. The results showed that the GSH-Px activity of EDA-1 group was higher than that of EDA-1 group EDA-2 group. The GSH-Px activity of EDA-2 group was higher than that of EDA-2 group. The activity of EDA-1 group was lower than that of GNS group. There was no significant difference in SOD activity between GNS group and GNS group. There was no significant difference in MDA content between EDA-2 group and GNS group. The content of MDA in EDA-1 group was significantly lower than that in EDA-2 group (P 0.05). The pathological changes of right carotid artery and myocardium in EDA-1 group were significantly higher than those in EDA-2 group. The pathological changes of right carotid artery and myocardium in EDA-2 group were significantly lower than those in EDA-2 group (P 0.05) and EDA-1 in other three groups were significantly higher than that in other three groups. There was no significant difference between EDA-2 group and THP group (P 0.05g / kg). Conclusion THP can induce myocardial injury and carotid artery injury in rats. [WT5 "HZ] EDA-2 / 10 mg / kg / kg preconditioning has a protective effect on acute myocardial injury induced by THP in rats (10 mg / kg / kg). The protective effect of pretreatment is better.
【學(xué)位授予單位】:廣西醫(yī)科大學(xué)
【學(xué)位級(jí)別】:碩士
【學(xué)位授予年份】:2017
【分類號(hào)】:R614
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