1,6-二磷酸果糖对阿霉素导致大鼠心肌细胞凋亡的影响

目的　研究 1,6 二磷酸果糖 (FDP)对阿霉素 (ADM )导致大鼠心肌细胞凋亡的影响。方法　给大鼠腹腔注射ADM ( 2 5 0mg·kg-1,隔日 1次 ,共 6次 )处理大鼠 ;给ADM处理的大鼠腹腔注射不同剂量的FDP(隔日 1次 ,共 2 1次 )进行干预。分别用TBA法、硝酸还原酶法、DTNB法、邻苯三酚自氧化法测定心肌的脂质过氧化物 (LPO)含量、一氧化氮 (NO)含量、谷胱甘肽过氧化物酶 (GPx)活性、超氧化物歧化酶 (SOD)活性 ;用透射电镜技术和TUNEL法检测心肌细胞凋亡 ;用原位杂交法检测心肌的诱导型一氧化氮合酶 (iN OS)mRNA表达。结果　FDP( 3 0 0 ,60 0 ,12 0 0mg·kg-1)干预ADM处理的大鼠后 ,均可降低心肌的LPO及NO含量、减少心肌细胞的凋亡数量、降低心肌iNOSmRNA的表达水平、增加心肌的SOD及GPx活性。结论　FDP抑制ADM导致心肌细胞凋亡 ,减轻ADM对心肌的毒性损伤 ,其机制2 0 0 1 0 4 12收稿 ,2 0 0 1 0 5 30修回 广西自然科学基金 (No 982 40 0 1)和广西教育厅科学基金 (No 1999 34 9)资助1 广西肿瘤研究所生化室 ,南宁　 5 30 0 2 1作者简介 :阳冠明 ,男 ,39岁 ,医学硕士 ,副研究员 ,硕士生导师。Tel:0 771 5 35 8130 (O) ,5 35 130 5 (H) ;林善修 ,男 ,67岁 ,教授 ,博士生导师可能与其保护心肌的SOD及GPx活性、抗脂质?

Effect of fructose-1, 6-diphosphate on adriamycin induced cardiomyocyte apoptosis in rats

AIM To study the effect of fructose 1, 6 diphosphate (FDP) on adriamycin(ADM) induced cardiomyocyte apoptosis in rats. METHODS Rats were treated ADM by intraperitoneal injection (2 50 mg·kg -1 body weight at six times every other day), and then the rats of ADM treated were intervened by FDP on different dosage by intraperitoneal injection (at twenty one times every other day). TBA method, nitrate reductase method, DTNB method and pyrogallol autoxidation method were used to determine the content of lipid peroxide (LPO) and nitric oxide (NO), the activity of glutathione peroxidase (GPx) and superoxide dismutase (SOD) in myocardium, respectively. The cardiomyocyte apoptosis was detected by transmission electron microscope and TUNEL method. The expression of inducible nitric oxide synthase(iNOS) mRNA of myocardium was detected by in situ hybridization. RESULTS FDP (300, 600, 1200 mg·kg -1 ) could significantly reduced the content of LPO and NO in myocardium, significantly reduced the amount of cardiomyocyte apoptosis and expression level of iNOS mRNA in myocardium, and significantly increased the activity of SOD and GPx in myocardium, when rats were ADM treated. CONCLUSION FDP can inhibit cardiomyocyte apoptosis induced by ADM, and reduce injury of cardiotoxicity induced by ADM. The mechanism FDP may be relate to protecting the activity of SOD and GPx in myocardium, to preventing lipid peroxidation, and reducing generation of NO.