We investigated the potential cardioprotective effects of misoprostol (MP) on doxorubicin (DOX) induced cardiac damage using histologic and biochemical assessment of rat heart. We used 21 male rats divided randomly into three groups: group 1, control; group 2, DOX; group 3, DOX + MP. The control group was given 0.5 ml 0.9% NaCl intraperitoneally (i.p.) and 1 ml 0.9% NaCl orally for 6 days. DOX was administered as a single dose of 20 mg/kg i.p. on day 3. MP was administered orally for 6 days. We found that treatment with MP decreased significantly serum cardiac troponin-I, brain natriuretic peptide levels, and lactate dehydrogenase, aspartate aminotransferase, alanine transaminase and creatine kinase isoenzyme-MB activities. DOX increased the malondialdehyde level and decreased the catalase, superoxide dismutase activities and glutathione levels; MP prevented these alterations. MP also decreased NADPH oxidase-4 and caspase-3 levels. In the DOX + MP group, oxidative stress was decreased, antioxidant activity was increased and histopathological changes were decreased compared to the DOX group. Cardiac damage caused by DOX was attenuated by MP treatment owing to the antioxidative and anti-apoptotic effects of MP. MP may be useful for reducing the severity of DOX induced damage.

我们使用大鼠心脏的组织学和生化评估研究了米索前列醇（MP）对阿霉素（DOX）引起的心脏损害的潜在心脏保护作用。我们使用21只雄性大鼠随机分为三组：第1组，对照组；第2组。第2组，DOX；第3组，DOX + MP。对照组腹膜内（ip）给予0.5 ml 0.9％NaCl，口服1 ml 0.9％NaCl，持续6天。在第3天以20 mg / kg ip的单次剂量口服DOX。MP口服6天。我们发现用MP进行治疗可显着降低血清心肌肌钙蛋白I，脑利钠肽水平以及乳酸脱氢酶，天冬氨酸转氨酶，丙氨酸转氨酶和肌酸激酶同工酶MB的活性。DOX增加丙二醛水平，降低过氧化氢酶，超氧化物歧化酶活性和谷胱甘肽水平；MP阻止了这些更改。MP还降低了NADPH氧化酶4和caspase-3的水平。与DOX组相比，DOX + MP组的氧化应激降低，抗氧化活性增加，组织病理学变化降低。由于MP的抗氧化和抗凋亡作用，MP处理可减轻DOX引起的心脏损害。MP可能有助于降低DOX诱导的损害的严重性。