【摘要】 目的 :研究原花青素 (proanthocyanidins ,PA)对心肌细胞损伤的保护作用及机理。 方法 :体外培养乳鼠心肌细胞 ,用DOG、ADR、X XO造成损伤模型 ,比色法测定培养液中LDH的活性。用·OH生成系统Fe2 + 抗坏血酸 (Fe2 + VitC)和ADR刺激大鼠心肌组织匀浆 ,用TBA比色法测定MDA生成 ;用自旋捕集ESR法测定PA对·OH的清除作用。结果 :2 5和 5 0mg/LPA均能对抗DOG、ADR、X XO所致心肌细胞损伤 ,使心肌细胞胞浆酶LDH漏出显著减少 (P <0 .0 1) ,且剂量依赖性的抑制自发性及Fe2 + VitC、ADR体系诱导的大鼠心肌组织匀浆MDA的生成 ;ESR法直接抑制·OH的产生 ,5 0mg/LPA的抑制率为 48 41%。 结论 :PA对心肌细胞损伤有一定的保护作用 ,其机理与清除活性氧自由基和抗脂质过氧化作用有关更多还原

【Abstract】 To study the protective effect and mech anism in injured myocardial cells of proanthocyanidins (PA) in vitro. Methods: The LDH activity in cultured myocardial cells injured by deprivation of oxygen and glucose (DOG), system of xanthine (X ) xanthineoxidase (XO) and ADR was assayed colorimetrically. The MDA formation from homogenates of rat heart spontaneously caused or stimulated by hydroxyl rad ical (·OH) generation system (Fe 2+ ascorbic acid) and Adriamycin (ADR) was examined by TBA method. The scavenging action on ·OH was determined by ESR . Results: PA 25mg/L and 50mg/L significantly redu ced the leakage of LDH from myocardial cells injured by DOG, ADR and X XO (P<0. 01), and dose dependently inhibited MDA generation from homogenates of rat hear t spontaneously formed or induced by ·OH generation system (Fe 2+ ascor bic acid) and ADR. It also directly reduced ·OH generation by ESR with inhibiti on rate 48.41% of PA 50mg/L. Conclusion: It is suggested that PA can protect myocardial cells from being injured by DOG, ADR and X XO. Its mechanism maybe h as relation to scavenging active oxygen free radicals and inhibiting lipid perox idation.更多还原