论文部分内容阅读
目的：探讨茶多酚（ｔｅａｐｏｌｙｐｈｅｎｏｌｓ，ＴＰ）减轻阿霉素心脏毒性的作用及其机制。方法：以病理记分法记录心肌损害程度；用ＴＢＡ法测定大鼠心肌组织的脂质过氧化水平；用邻苯三酚自氧化法测定心肌组织、红细胞的ＳＯＤ活力；用ＤＴＮＢ法测定心肌ＧＳＨＰｘ活力。结果：阿霉素两周累积用量１６ｍｇ·ｋｇ－１（第２天，第４天１ｍｇ·ｋｇ－１；第６天，第８天２ｍｇ·ｋｇ－１；第１０天，第１２天３ｍｇ·ｋｇ－１；第１４天４ｍｇ·ｋｇ－１；ｉｐ）可致大鼠心肌损害，心肌ＭＤＡ水平升高，ＧＳＨＰｘ活性下降，心肌和红细胞ＳＯＤ活性降低，ＴＰ２８，５６和８４ｍｇ·ｋｇ－１具有减轻阿霉素所致的大鼠心肌毒性作用。结论：茶多酚减轻阿霉素心肌毒性机制可能与其清除自由基作用、保护心肌ＳＯＤ及ＧＳＨＰｘ活性有关，从而有效地对抗阿霉素引起的大鼠心肌脂质过氧化有关
Objective: To investigate the effect of tea polyphenols (TP) on cardiotoxicity of adriamycin and its mechanism. Methods: The degree of myocardial damage was recorded by pathological scoring method; the myocardial lipid peroxidation level was measured by TBA method; the SOD activity of myocardial tissue and erythrocyte was measured by pyrogallol auto-oxidation method; the myocardial GSH was measured by DTNB method. Px vitality. RESULTS: The cumulative dose of adriamycin for two weeks was 16 mg·kg -1 (day 2 and day 4; 1 mg·kg-1; day 6, day 8 2 mg·kg-1; day 10, day 12 3 mg· Kg-1; Day 14 4mg·kg-1; ip) can cause myocardial damage in rats, increased myocardial MDA levels, decreased GSHPx activity, myocardial and red blood cell SOD activity decreased, TP28, 56 and 84 mg·kg-1 Has to reduce doxorubicin-induced myocardial toxicity in rats. Conclusion: The mechanism of tea polyphenols in reducing myocardial toxicity of doxorubicin may be related to its scavenging free radicals, protection of myocardial SOD and GSHPx activity, and thus effectively related to the myocardial lipid peroxidation induced by doxorubicin in rats.