M. Erboğa, Yeliz Bozdemir Donmez, U. Sener, Z. Erboğa, C. Aktas, M. Kanter
{"title":"荨麻通过抑制组织损伤、氧化应激和脂质过氧化作用对抗阿霉素诱导的大鼠心脏毒性","authors":"M. Erboğa, Yeliz Bozdemir Donmez, U. Sener, Z. Erboğa, C. Aktas, M. Kanter","doi":"10.15197/EJGM.1567","DOIUrl":null,"url":null,"abstract":"Objective: Doxorubicin (DOX) is a highly effective anti-cancer drug with limited clinical use due to its serious cardiotoxicity. Urtica dioica L. seeds (UD), have been widely used in folk medicine, particularly in the therapy for advanced cancer patients, possesses a potent anti-oxidant properties. The goal of present study was to investigate the cardioprotective effects of UD on DOX-induced cardiotoxicity. Method: The rats in the UD treated group were given intraperitoneally 2 ml/kg UD. To induce cardiotoxicity, 30 mg/kg DOX was injected intraperitoneally by a single dose and the rats were sacrificed after 48 h. Results: The present study revealed for the first time a protective role of UD against DOXinduced cardiotoxicity. UD therapy significantly protected against DOXinduced myocardial damage which was characterized by conduction abnormalities, vacuolization, inflammatory cell infiltration, hemorrhag es, and myofibrillar disarrangement. As indicators of oxidative stress, DOX caused significantly increase lipid peroxidation and reduction in activities of antioxidant enzymes; superoxide dismutase, glutathione peroxidase, and catalase. UD treatment significantly attenuated DOXinduced oxidative injury. Conclusion: The present study showed that UD might be a suitable cardioprotector against toxic effects of DOX.","PeriodicalId":12017,"journal":{"name":"European journal of general medicine","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2016-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"8","resultStr":"{\"title\":\"Effect of Urtica Dioica against Doxorubicin-InducedCardiotoxicity in Rats through Suppression ofHistological Damage, Oxidative Stress and LipidPeroxidation\",\"authors\":\"M. Erboğa, Yeliz Bozdemir Donmez, U. Sener, Z. Erboğa, C. Aktas, M. Kanter\",\"doi\":\"10.15197/EJGM.1567\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Objective: Doxorubicin (DOX) is a highly effective anti-cancer drug with limited clinical use due to its serious cardiotoxicity. Urtica dioica L. seeds (UD), have been widely used in folk medicine, particularly in the therapy for advanced cancer patients, possesses a potent anti-oxidant properties. The goal of present study was to investigate the cardioprotective effects of UD on DOX-induced cardiotoxicity. Method: The rats in the UD treated group were given intraperitoneally 2 ml/kg UD. To induce cardiotoxicity, 30 mg/kg DOX was injected intraperitoneally by a single dose and the rats were sacrificed after 48 h. Results: The present study revealed for the first time a protective role of UD against DOXinduced cardiotoxicity. UD therapy significantly protected against DOXinduced myocardial damage which was characterized by conduction abnormalities, vacuolization, inflammatory cell infiltration, hemorrhag es, and myofibrillar disarrangement. As indicators of oxidative stress, DOX caused significantly increase lipid peroxidation and reduction in activities of antioxidant enzymes; superoxide dismutase, glutathione peroxidase, and catalase. UD treatment significantly attenuated DOXinduced oxidative injury. Conclusion: The present study showed that UD might be a suitable cardioprotector against toxic effects of DOX.\",\"PeriodicalId\":12017,\"journal\":{\"name\":\"European journal of general medicine\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2016-04-06\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"8\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"European journal of general medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.15197/EJGM.1567\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"European journal of general medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15197/EJGM.1567","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Effect of Urtica Dioica against Doxorubicin-InducedCardiotoxicity in Rats through Suppression ofHistological Damage, Oxidative Stress and LipidPeroxidation
Objective: Doxorubicin (DOX) is a highly effective anti-cancer drug with limited clinical use due to its serious cardiotoxicity. Urtica dioica L. seeds (UD), have been widely used in folk medicine, particularly in the therapy for advanced cancer patients, possesses a potent anti-oxidant properties. The goal of present study was to investigate the cardioprotective effects of UD on DOX-induced cardiotoxicity. Method: The rats in the UD treated group were given intraperitoneally 2 ml/kg UD. To induce cardiotoxicity, 30 mg/kg DOX was injected intraperitoneally by a single dose and the rats were sacrificed after 48 h. Results: The present study revealed for the first time a protective role of UD against DOXinduced cardiotoxicity. UD therapy significantly protected against DOXinduced myocardial damage which was characterized by conduction abnormalities, vacuolization, inflammatory cell infiltration, hemorrhag es, and myofibrillar disarrangement. As indicators of oxidative stress, DOX caused significantly increase lipid peroxidation and reduction in activities of antioxidant enzymes; superoxide dismutase, glutathione peroxidase, and catalase. UD treatment significantly attenuated DOXinduced oxidative injury. Conclusion: The present study showed that UD might be a suitable cardioprotector against toxic effects of DOX.