Liu Chi-Feng, Lin Chia-Hsien, Chen Chin-Fa, Huang Tian-Chyuan, Lin Song-Chow
National Taipei College of Nursing, Taipei 112, Taiwan.
Am J Chin Med. 2005;33(6):981-8. doi: 10.1142/S0192415X05003570.
Acute p.o. administration of 99.5% ethanol (0.1 ml) to fasted mice produced heart toxicity. Pretreatment with p.o. administration of tetramethylpyrazine (TMP) could prevent such toxicity effectively and dose-dependently. The maximal antioxidative effect against 99.5% ethanol-induced heart toxicity could be observed at 1 hour after TMP administration. In order to further investigate the heart protective mechanism of TMP, both lipid peroxidation level in vivo and superoxide scavenging activity were conducted. TMP exhibited a dose-dependently anti-lipid peroxidation effect in mice heart homogenate, and results indicated that 99.5% ethanol-induced intoxicated mice hearts have higher malonic dialdehyde (MDA) levels compared with those in TMP administrated mice hearts. These results suggest that the potentially heart protective mechanism of TMP could be contributed, at least in part, to its prominent anti-lipid peroxidation and anti-free radical formation effects, hence it could protect the heart from lipid peroxidation-induced heart toxicity.
给禁食小鼠经口急性给予99.5%乙醇(0.1毫升)会产生心脏毒性。经口给予川芎嗪(TMP)进行预处理可有效且剂量依赖性地预防此类毒性。在给予TMP后1小时可观察到对99.5%乙醇诱导的心脏毒性的最大抗氧化作用。为了进一步研究TMP的心脏保护机制,对体内脂质过氧化水平和超氧阴离子清除活性进行了检测。TMP在小鼠心脏匀浆中呈现出剂量依赖性的抗脂质过氧化作用,结果表明,与给予TMP的小鼠心脏相比,99.5%乙醇诱导中毒的小鼠心脏丙二醛(MDA)水平更高。这些结果表明,TMP潜在的心脏保护机制可能至少部分归因于其显著的抗脂质过氧化和抗自由基形成作用,因此它可以保护心脏免受脂质过氧化诱导的心脏毒性。