本文選題：低劑量輻射 + 阿霉素　； 參考：《吉林大學(xué)》2012年碩士論文

【摘要】：低劑量輻射與大劑量輻射對(duì)生物體產(chǎn)生的生物學(xué)效應(yīng)是截然不同的，目前研究主要集中在低劑量輻射誘導(dǎo)生物體產(chǎn)生的興奮性效應(yīng)和適應(yīng)性反應(yīng)。興奮性效應(yīng)主要表現(xiàn)為增強(qiáng)機(jī)體免疫功能、促進(jìn)機(jī)體正常細(xì)胞增殖等。適應(yīng)性反應(yīng)是指機(jī)體對(duì)后續(xù)的大劑量輻射引起的損傷產(chǎn)生耐受，從而減輕大劑量輻射引起的損傷。目前研究已證實(shí)低劑量輻射不能誘導(dǎo)腫瘤細(xì)胞產(chǎn)生興奮性效應(yīng)、適應(yīng)性反應(yīng)，而且對(duì)部分腫瘤細(xì)胞還具有協(xié)同放、化療殺傷作用。但是否能將LDR應(yīng)用于抗腫瘤藥物心肌損傷的保護(hù)，目前國(guó)內(nèi)外尚未見報(bào)道。本研究旨在論證低劑量輻射對(duì)化療藥物阿霉素引起的心肌損傷是否產(chǎn)生保護(hù)作用，并探討其作用機(jī)制。 本實(shí)驗(yàn)設(shè)6個(gè)試驗(yàn)組，包括對(duì)照組及荷瘤鼠組。荷瘤鼠組隨機(jī)分為5組，具體分組為：假照組；低劑量輻射組；阿霉素組；低劑量輻射聯(lián)合阿霉素組，此組分2個(gè)亞組：低劑量輻射后間隔6小時(shí)給予阿霉素組；低劑量輻射后間隔12小時(shí)給予阿霉素組。 通過觀察記錄各組裸鼠的飲食、活動(dòng)和體重變化，并測(cè)量記錄移植瘤生長(zhǎng)情況，稱瘤重，計(jì)算抑瘤率，探討低劑量輻射聯(lián)合阿霉素對(duì)乳腺癌裸鼠的抑瘤作用。結(jié)果發(fā)現(xiàn)單獨(dú)阿霉素組裸鼠一般狀態(tài)極差，消瘦明顯，，活動(dòng)遲緩，飲食、飲水明顯減少，與低劑量輻射聯(lián)合阿霉素組比，體重減低明顯。此外，單獨(dú)低劑量輻射組較假照組比抑瘤率沒有明顯增加，聯(lián)合阿霉素組抑瘤率較單獨(dú)阿霉素組稍增高。此結(jié)果說明低劑量輻射可以改善阿霉素化療后乳腺癌荷瘤鼠的一般狀態(tài)，并且不能誘導(dǎo)乳腺癌荷瘤鼠腫瘤組織產(chǎn)生興奮性效應(yīng)及適應(yīng)性適應(yīng)，而且可以一定程度上協(xié)同阿霉素抑制腫瘤生長(zhǎng)。 通過觀察荷瘤鼠新鮮心肌組織抗氧化酶SOD、GSH-Px活力及脂質(zhì)過化產(chǎn)物MDA含量變化，論證低劑量輻射對(duì)阿霉素誘導(dǎo)的心肌損傷是否保護(hù)作用。結(jié)果顯示阿霉素組心肌抗氧化酶SOD、GSH-Px活力明顯降，而脂質(zhì)過氧化產(chǎn)物MDA含量明顯增高，與低劑量輻射聯(lián)合阿霉素組，差異明顯，結(jié)果表明低劑量輻射可以通過增強(qiáng)心肌抗氧化酶活性，減脂質(zhì)過氧化產(chǎn)物生成，從而減輕阿霉素誘導(dǎo)的心肌損傷。 通過免疫組化方法檢測(cè)心肌組織VEGF、HIF-1α、SOD蛋白及腫瘤組VEGF、HIF-1α蛋白表達(dá)，探討低劑量輻射對(duì)心肌及腫瘤組織血管形成影響，此外，進(jìn)一步論證低劑量輻射對(duì)心肌抗氧化酶的作用，結(jié)果顯示劑量輻射可以一定程度上抑制腫瘤組織VEGF、HIF-1α蛋白表達(dá)，同時(shí)進(jìn)心肌組織HIF-1α、SOD蛋白的表達(dá)。綜上，低劑量輻射可以用于阿霉所致心肌損傷的保護(hù)，一方面可以協(xié)同抑瘤，一方面可以增強(qiáng)心肌抗氧酶活性，降低及防治阿霉素所致心肌損傷，以上實(shí)驗(yàn)結(jié)果分析為低劑量射應(yīng)用于阿霉素誘導(dǎo)心肌損傷的保護(hù)提供了充實(shí)的證據(jù)。
[Abstract]:The biological effects of low dose radiation and large dose radiation are very different. The current research mainly focuses on the excitatory and adaptive responses produced by low dose radiation induced organisms. The excitatory effects are mainly manifested in enhancing the immune function of the body and promoting the normal cell proliferation. The body is tolerant to subsequent damage caused by large dose radiation, thus reducing the damage caused by large doses of radiation. Current studies have shown that low dose radiation can not induce excitability, adaptive response and synergistic radiation to some tumor cells, but whether LDR can be applied to the anti tumor cells. The protection of myocardial injury of tumor drugs has not been reported at home and abroad. The purpose of this study is to demonstrate the protective effect of low dose radiation on the myocardial injury induced by doxorubicin, and to explore the mechanism of its action.
The experiment set up 6 experimental groups, including the control group and the tumor bearing rat group. The mice group was randomly divided into 5 groups, which were divided into three groups: the fake group, the low dose radiation group, the adriamycin group, the low dose radiation combined with adriamycin group, 2 subgroups: the low dose radiation interval was given to the amycomycin group for 6 hours, and the low dose radiation interval was given 12 hours. Adriamycin group.
By observing the diet, activity and weight change of the nude mice and measuring the growth of the transplanted tumor, the weight of the tumor was recorded, the tumor suppressor rate was calculated, and the anti tumor effect of doxorubicin combined with adriamycin on the nude mice was investigated. The results showed that low dose radiation could improve the general state of breast cancer rats after doxorubicin chemotherapy, and that the low dose radiation could improve the general state of the breast cancer rats after adriamycin chemotherapy, and the results showed that the low dose radiation could improve the general state of the breast cancer mice after adriamycin chemotherapy, and the results showed that the low dose radiation could improve the general state of the breast cancer rats. It can induce excitatory effect and adaptive adaptation in tumor tissue of breast cancer bearing mice, and can synergy adriamycin to inhibit tumor growth to some extent.
The effects of low dose radiation on adriamycin induced myocardial injury were observed by observing the changes of antioxidant enzyme SOD, GSH-Px activity and the content of MDA in the fresh myocardium of the tumor bearing mice. The results showed that the myocardial antioxidant enzyme SOD, GSH-Px activity of the adriamycin group decreased significantly, and the MDA content of the lipid peroxidation product was significantly higher and lower than that of the lipid peroxidation products. The difference between dose radiation and adriamycin group was obvious. The results showed that low dose radiation could reduce the myocardial injury induced by adriamycin by enhancing the activity of myocardial antioxidant enzymes and the production of lipid peroxidation products.
The expression of VEGF, HIF-1 a, SOD protein and VEGF, HIF-1 alpha protein in the tumor group was detected by immunohistochemical method. The effect of low dose radiation on the angiogenesis of myocardium and tumor tissue was investigated. Furthermore, the effect of low dose radiation on myocardial antioxidant enzyme was further demonstrated. The results showed that dose radiation could inhibit the VEG of tumor tissue to a certain extent. F, HIF-1 alpha protein expression, and the expression of HIF-1 alpha, SOD protein in myocardial tissue. Combined, low dose radiation can be used for the protection of myocardial injury caused by almilion. On one hand, it can synergistically inhibit the tumor. On the one hand, it can enhance the activity of myocardial antioxygenase, reduce and prevent the injury of myocardium caused by adriamycin. The above experimental results are analyzed for low dose injection application. It provides substantial evidence for the protection of adriamycin induced myocardial injury.

【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2012
【分類號(hào)】：R142

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