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作 者:侯佳华 韦秋 黄露 胡增美 王小莹 Hou Jiahua;Wei Qiu;Huang Lu;Hu Zengmei;Wang Xiaoying(Key Laboratory of Chinese Pharmacology of the Ministry of Education,Research Institute of Traditional Chinese Medicine,Tianjin University of Traditional Chinese Medicine,Tianjin 301617,China)
机构地区:[1]天津中医药大学中医药研究院方剂学教育部重点实验室,天津301617
出 处:《南开大学学报(自然科学版)》2022年第6期7-14,共8页Acta Scientiarum Naturalium Universitatis Nankaiensis
基 金:国家自然科学基金(81873104,82141213);天津市教委科研计划重点项目(2019ZD13)。
摘 要:在甘草次酸预给药7 d后腹腔注射阿霉素建立小鼠心脏毒性模型,造模期间继续给药,观察甘草次酸对阿霉素心脏毒性的影响.结果发现累积剂量20 mg/kg阿霉素可明显引起小鼠心脏损伤,与阿霉素组相比,甘草次酸可显著回调小鼠的射血分数(EF)和短轴缩短率(FS),降低血清中肌酸激酶(CK)、肌酸激酶同工酶(CKMB)、乳酸脱氢酶(LDH)、心肌肌钙蛋白T(cTnT)、丙酮酸激酶(PK)、丙二醛(MDA)、谷草转氨酶(AST)和谷丙转氨酶(ALT)水平,减轻心肌损伤和骨髓抑制,促进心脏中p-STAT3和Bcl-2蛋白表达.提示甘草次酸可通过抑制细胞凋亡拮抗阿霉素心脏毒性.In this study, a mouse cardiotoxicity model was established by intraperitoneal injection of doxorubicin 7 days after pre-administration of glycyrrhetinic acid, and the administration was continued during the modeling period to observe the effect of glycyrrhetinic acid on the cardiotoxicity of doxorubicin.The results showed that cumulative dose of 20 mg/kg doxorubicin could significantly induce cardiac injury in mice, compared with the doxorubicin group, glycyrrhetinic acid significantly regressed the ejection fraction(EF) and shortening fraction(FS) of mice, and decrease the serum creatine kinase(CK), creatine kinase isoenzyme(CK-MB), lactate dehydrogenase(LDH), cardiac troponin T(cTnT), pyruvate kinase(PK), and malondialdehyde(MDA), glutathione aminotransferase(AST) and glutamic acid aminotransferase(ALT) levels, attenuate myocardial injury and myelosuppression, and promote p-STAT3 and Bcl-2 protein expression in the heart. It is suggested that glycyrrhetinic acid may antagonize doxorubicin cardiotoxicity by inhibiting apoptosis.
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