|
|
|
| Effect of total flavonoids of fructus choerospondiatis on arsenic trioxide-induced cardiomyocyte injury |
| YANG Xiuhua1 ZHI Hui1 AI Dan1 XIAO Yunfeng2▲ |
1.Department of Mongolian Medicine, Hulun Buir Vocational Technical College, Inner Mongolia Autonomous Region, Hulun Buir 021000, China;
2.Department of Pharmacy, Inner Mongolia Medical University, Inner Mongolia Autonomous Region, Hohhot 010110, China |
|
|
|
Abstract Objective To study the effect of total flavnoids of fructus choerospondiatis (TFFC) on arsenic trioxide (ATO)-induced cardiomyocyte injury, and to explore its mechanism of action. Methods Cardiomyocytes were isolated and cultivated by neonatal rats and the morphology of cardiomyocytes at different time periods was observed under an inverted microscope. Cardiomyocyte injure models were use established by 6 μg/ml ATO, the experiment set up blank group, model group, and TFFC low, medium, and high concentration groups. The CCK-8 method was used to detect the survival rate of each group of cells, the activity of glutamic oxaloacetic transaminase (GOT)，creatine kinase (CK) and lactate dehydrogenase (LDH) in cell culture medium were determined by automatic bio-chemical instrument; the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) in the cells were detected by kit method. The degree of apoptosis was observed by Hoechst 33342 fluorescence staining. Cell apoptosis rates were measured by flow cytomety. Results The cells cultured for 48 hours were basically all attached to the wall. Most of the cells stuck out the pseudopodia and were accompanied by spontaneous beating, which can meet the experimental requirements. The cell survival rate was reduced by 6 μg/ml ATO. Compared with the model group, the cell survival rate of each TFFC concentration group significantly increased, the vitality of LDH, CK, and GOT in the cell culture fluid was significantly reduced, the vitality of SOD, GSH-Px, and CAT in the cell were significantly increased, and the apoptosis rate was significantly reduced, and the differences were statistically significant (P ＜ 0.05). Conclusion TFFC can improve the state of ATO-induced myocardial injury, thereby protecting the myocardium damaged by ATO.
|
|
|
|
|
|
[1] 钟赣生.中药学[M].北京：中国中医药出版社，2018，457.
[2] 陈亚娟，卿晨.三氧化二砷抗肿瘤作用研究进展[J].昆明医学院学报，2012，33（1B）：251-254.
[3] Craig WF，Chelsea EP，Yun M，et al. Herpes zoster during arsenic trioxide therapy for acute promyelocytic leukemia [J]. Leuk Lymphoma，2021，62（3）：696-702.
[4] 赵丽凤，李晓强，任汝静，等.三氧化二砷联合双氢青蒿素对THP-1细胞增殖及凋亡的影响[J].中国实验方剂学杂志，2020，26（17）：42-48.
[5] 沈秀芸，吕保江，武敏，等.三氧化二砷联合用药治疗乳腺癌的研究进展[J].中国现代应用药学，2020，37（11）：1392-1396.
[6] 季秋兰，丁景弦.三氧化二砷对人三阴性乳腺癌细胞株MDA-MB-231教化单核细胞的影响[J].医疗装备，2021， 34（5）：15-16.
[7] 孙佳富，孙潇，罗云，等.丹酚酸B对三氧化二砷诱导HepaRG人肝细胞损伤的保护作用[J].中国实验方剂学杂志，2020，26（4）：68-74.
[8] 胡训豪，邓小，张宏文.三氧化二砷治疗肝癌的进展[J]蛇志，2018，30（4）：735-738.
[9] Song P，Hai Y，Ma W，et al. Arsenic trioxide combined with transarterial chemoembolization for unresectable primary hepatic carcinoma：Asystematic review and meta-analysis [J]. Medicine，2018，97（18）：e0613.
[10] 邓运宗，黄兴，王红玲，等.三氧化二砷治疗胃癌的作用机制[J]中医学报，2018，33（6）：961-966.
[11] 杭海芳，王莹莹，唐勇，等.三氧化二砷联合环腺苷酸拟似物诱导骨髓瘤细胞凋亡的实验研究[J].中国癌症杂志，2019，29（3）：166-170.
[12] 蒋碧佳，曾锦荣，王绩英，等.三氧化二砷联合维生素C抑制耐药性肺腺癌裸鼠移植瘤生长机制的研究[J].中国实验方剂学杂志，2011，17（4）：196-200.
[13] Kim PG，Bridgham K，Chen EC，et al. Incident adverse events following therapy for acute promyelocytic leuke-mia [J]. Leuk Res Rep，2018，9（1）：79-83.
[14] Alamolhodaei NS，Shirani K，Karimi G. Arsenic Cardiotoxicity：An Overview [J]. Environ Toxicol Pharmacol，2015，40（3）：1005-1014.
[15] Zhou J，Meng R，Wang W，et al. Study on cardiac toxicity in acute promyelocyte leukemia treatment of arsenic trioxide intravenous infusion in general dose [J]. Zhonghua Nei Ke Za Zhi，2003，42（11）：785-788.
[16] 张静宜，孙桂波，王敏，等.三氧化二砷心脏毒性研究进展[J].中国药理学通报，2016，32（9）：1194-1198.
[17] Unnikrishnan D，Dutcher JP，Varshneya N，et al. Torsadesdepointes in 3 patients with leukemia treated with arsenic trioxide [J]. Blood，2001，97（5）：1514-1516.
[18] 赵冬冬，王瑞芳，何静波，等.广枣叶和广枣中黄酮类成分的提取、含量测定的对比实验[J].包头医学院学报，2019，35（3）：70-72.
[19] 张浩楠，杨玉梅，邬国栋，等.蒙药广枣抗心律失常作用有效成分的分离[J].包头医学院学报，2013，29（3）：1-4.
[20] 刘冠男，陈国权，赵明.广枣总黄酮对豚鼠心室肌细胞动作电位的作用研究[J].当代医学，2009，15（4）：38-39.
[21] 满达，王小龙，王华新，等.广枣总黄酮干预早期激素性股骨头坏死的作用及其机制[J].中华实验外科杂志，2020，37（6）：1022-1025.
[22] 汤喜兰，刘建勋，李磊，等.广枣模拟总有机酸对心肌缺血再灌注损伤的保护作用[J].中国实验方剂学杂志，2013， 19（4）：168-172.
[23] 宁小伟，苏和，张瑞芬.蒙药治疗心肌缺血再灌注损伤的研究进展[J].中医药学报，2019，47（4）：109-111.
[24] 郭英，贝玉祥，王雪梅，等.广枣提取物体外清除活性氧自由基及抗氧化作用研究[J].微量元素与健康研究，2008， 25（5）：22-24.
[25] 杨云舒，姜子涛，李荣.广枣黄酮清除自由基能力及抗氧化性能的细胞模型法评价[J].食品科学，2016，37（9）：92-97.
[26] 刘博，刘小雷，潘桂兰，等.乳鼠心肌细胞的原代培养方法改良[J].中南药学，2017，15（1）：18-21.
[27] Liu YB. Clinical significance of four myocardial markers in the diagnosis of acute myocardial infarction [J]. Clin Lab，2014，8（15）：80-81.
[28] 秦伟，王清，李丽.联合检测超氧化物歧化酶和同型半胱氨酸及高敏C反应蛋白在冠状动脉粥样硬化性心脏病诊断中的价值[J].中国医药，2019，14（1）：37-40.
[29] 张国建，韦丽虹，肖云峰，等.Micro PET/CT分子显像观察广枣-7味丸抗缺血/再灌注损伤作用机制[J].中国医学影像技术，2020，36（7）：967-970. |
|
|
|
