參麥注射液對(duì)術(shù)前阿霉素化療乳腺癌裸鼠模型心肌保護(hù)作用的研究
本文關(guān)鍵詞:參麥注射液對(duì)術(shù)前阿霉素化療乳腺癌裸鼠模型心肌保護(hù)作用的研究 出處:《廣西醫(yī)科大學(xué)》2013年碩士論文 論文類(lèi)型:學(xué)位論文
更多相關(guān)文章: 參麥 阿霉素 心肌損傷 麻醉 NRF-1 能量代謝
【摘要】:目的:研究參麥注射液(SMI)干預(yù)治療對(duì)ADM化療的乳腺癌裸鼠模型在圍術(shù)期心肌保護(hù)的作用及可能機(jī)制。 方法:種植乳腺癌細(xì)胞MCF-7于裸鼠乳房墊,建立乳腺癌裸鼠模型。將制作成功的乳腺癌裸鼠27只,隨機(jī)分成3組:A組(生理鹽水組)、B組(ADM+生理鹽水組)、C組(ADM+SMI組)。在T1(干預(yù)前)、T2(麻醉前)、T3(麻醉后20min)三個(gè)時(shí)點(diǎn)分別取血檢測(cè)血清cTnI水平、SOD活力和MDA含量。麻醉后取心肌組織檢測(cè)NRF-1的表達(dá)水平、腺苷酸池的含量及光、電鏡下觀察結(jié)構(gòu)改變。 結(jié)果:(1)T1、T2時(shí)刻,B、c組的cTnI均顯著高于A組(P0.01);T3時(shí)刻,A、C組的cTnI顯著低于B組(P0.01;P0.05),A組低于C組(P<0.01)。B組在T2及T3時(shí)刻的cTnI均顯著高于T1時(shí)刻(P0.05)。(2)T1時(shí)刻,三組之間的SOD活力無(wú)統(tǒng)計(jì)差異(P>0.05);T2時(shí)刻,B、C組SOD均顯著低于A組(P<0.01),B組低于C組(P0.05);T3時(shí)刻,A、C組的SOD活力均顯著高于B組(P0.01;P0.05),A組高于C組(P0.01)。B組SOD在T2及T3時(shí)刻均顯著低于T1時(shí)刻(P0.01)。(3)三個(gè)時(shí)刻,B、C組的MDA含量均顯著高于A組(P0.05);C組的MDA在T1時(shí)刻顯著高于T2及T3時(shí)刻(P0.05)。(4)A、C組NRF-1mRNA的表達(dá)均顯著高于B組(P0.05),A、C組對(duì)比無(wú)統(tǒng)計(jì)學(xué)差異(P0.05)。(5)A、C組的ATP含量均顯著高于B組(P0.05);B組的AMP含量均顯著高于A、C組(P0.05);A組腺苷酸代謝池總量高于B組(P0.05)。(6)C組的病理評(píng)分顯著低于B組(P0.05),但仍然高于A組(P0.05)。(7)與A組比較,B、C組的心肌組織超微結(jié)構(gòu)均發(fā)生嚴(yán)重改變,但C組的改變較輕。 結(jié)論:(1)ADM化療乳腺癌裸鼠模型可引起心肌損傷,SMI的干預(yù)治療可減輕心肌的再次受損;(2)SMI的干預(yù)治療降低了裸鼠機(jī)體的脂質(zhì)過(guò)氧化反應(yīng)、增強(qiáng)了抗氧化能力,減少心肌線粒體的損傷;(3)SMI降低了ADM對(duì)核基因NRF-1表達(dá)的抑制作用、增加腺苷酸池中高能磷酸化合物含量,保護(hù)了心肌能量代謝途徑。
[Abstract]:Aim: to study the protective effect and possible mechanism of Shenmai injection on myocardial protection in nude mice model of breast cancer treated with ADM chemotherapy during perioperative period. Methods: breast cancer cell line MCF-7 was implanted into breast pad of nude mice to establish nude mouse model of breast cancer. 27 nude mice were randomly divided into 3 groups: group A (normal saline group). Group B was treated with normal saline group and group C was treated with SMI. Blood samples were collected at 20 min after anesthesia to detect the activity of cTnI and the content of MDA in serum. The expression of NRF-1 was detected in myocardium after anesthesia. The content and light of adenylate cell were observed under electron microscope. Results the cTnI of T1T 2 group was significantly higher than that of A group (P 0.01). The cTnI of group C was significantly lower than that of group B (P 0.01). The cTnI of group A was lower than that of group C (P < 0.01). The cTnI of group B at T _ 2 and T _ 3 was significantly higher than that of group A at T _ 1 and T _ 1. There was no statistical difference in SOD activity among the three groups (P > 0.05). The SOD of group C was significantly lower than that of group A (P < 0.01) and group B was lower than that of group C (P < 0.05). The activity of SOD in group T 3 was significantly higher than that in group B (P 0.01). The SOD of group A was significantly lower than that of group C at T _ 2 and T _ 3. The content of MDA in group C was significantly higher than that in group A (P 0.05). The expression of MDA in group C was significantly higher than that in group C at T1 and T3, respectively. The expression of NRF-1mRNA in group C was significantly higher than that in group B (P0.05A). The ATP content of group C was significantly higher than that of group B (P 0.05). The content of AMP in group B was significantly higher than that in group A (P 0.05). The total amount of adenylate metabolism pool in group A was significantly lower than that in group B (P 0.05), but still higher than that in group A (P 0.05). The ultrastructure of myocardial tissue in group C was significantly changed, but the change in group C was mild. Conclusion the nude mice model of chemotherapy with ADM can induce myocardial injury and the intervention of SMI can reduce the myocardial redamage. The intervention of SMI decreased lipid peroxidation, enhanced antioxidant capacity and reduced myocardial mitochondria damage in nude mice. SMI decreased the inhibitory effect of ADM on the expression of nuclear gene NRF-1, increased the content of high-energy phosphates in adenylic acid pool, and protected myocardial energy metabolism pathway.
【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】:2013
【分類(lèi)號(hào)】:R737.9;R-332
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