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基于钙超载研究滇乌碱诱导大鼠心律失常的毒性机制
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| 篇名： | 基于钙超载研究滇乌碱诱导大鼠心律失常的毒性机制 |
| TITLE： | Study on the Toxicity Mechanism of Yunaconitine-induced Arrhythmia in Rats Based on Calcium Overload |
| 摘要： | 目的：研究滇乌碱诱导大鼠心律失常的毒性机制。方法：将32只大鼠按随机数字表法随机分为正常对照组，滇乌碱低、高剂量组（0.09、0.14mg/kg）和乌头碱组（阳性对照，0.88mg/kg），每组8只。各给药组大鼠每天灌胃相应药物1次，正常对照组大鼠灌胃等体积生理盐水，连续7d。末次灌胃后，观察各组大鼠的心电图变化，测定大鼠心肌组织中腺苷三磷酸（ATP）含量、心肌细胞中Ca2+含量、心肌组织中Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶活性以及雷诺定受体2（RyR2）、Ca2+-ATP酶（SERCA2）蛋白表达水平。结果：与正常对照组比较，滇乌碱低剂量组大鼠QRS波时限、校正后QT期间（QTc间期）均显著延长（P＜0.01），心肌细胞中Ca2+含量显著升高（P＜0.05），心肌组织中ATP含量、Ca2+-Mg2+-ATP酶活性、Na+-K+-ATP酶活性和SERCA2蛋白表达水平均显著降低（P＜0.05或P＜0.01）；滇乌碱高剂量组和乌头碱组大鼠心率均显著增快（P＜0.05或P＜0.01），QRS波时限、QTc间期均显著延长（P＜0.01），心肌细胞中Ca2+含量均显著升高（P＜0.01），心肌组织中ATP含量、Ca2+-Mg2+-ATP酶活性、Na+-K+-ATP酶活性和RyR2、SERCA2蛋白表达水平均显著降低（P＜0.01）。结论：滇乌碱可导致大鼠心律失常；其作用机制可能与降低心肌组织中Ca2+-Mg2+-ATP酶、Na+-K+-ATP酶活性，下调心肌组织中钙转运相关蛋白RyR2、SERCA2的表达，从而导致Ca2+超载有关。 |
| ABSTRACT： | OBJECTIVE：To study the toxicity mechanism of yunacotine-induced arrhythmia in rats. METHODS ：Totally 32 rats were randomly divided by random number table method into normal control group ，yunacotine low-dose and high-dose groups （0.09，0.14 mg/kg），aconitine group （positive control ，0.88 mg/kg），with 8 rats in each group. Administration groups were given the corresponding drugs once a day ，and normal control group was given the constant volume of normal saline ，for consecutive 7 d. After last intragastric administration ，the changes of electrocardiogram （ECG） were observed. The contents of adenosine triphosphate（ATP）in myocardial tissue and Ca 2+ in myocardial cells ，the activities of Na +-K+-ATPase and Ca 2+-Mg2+-ATPase as well as the protein expression of ranolidine receptor 2（RyR2）and Ca 2+-ATPase（SERCA2）in myocardial tissue were determined. RESULTS：Compared with normal control group ，time limit of QRS wave and QTc intervals of rats were prolonged significantly in yunaconitine low-dose group （P＜0.01）. The content of Ca 2 + in myocardial cells ， the ATP contents ， the activities of Ca2+-Mg2+-ATPase and Na +-K+-ATPase as well as the protein expression of SERCA 2 in myocardial tissue were reduced significantly （P＜0.05 or P＜0.01）. The heart rate of rats in yunaconitine high-dose group and aconitine group were increased significantly （P＜ 0.05 or P＜0.01），and time limit of QRS wave and QTc intervals were significantly prolonged （P＜0.01）；the content of Ca 2+ in myocardial cells was increased significantly （P＜0.01）；ATP content ，the activities of Ca 2+-Mg2+-ATPase and Na +-K+-ATPase，and protein expression of RyR 2 and SERCA 2 in myocardial tissue were decreased significantly （P＜0.01）. CONCLUSIONS ： Yunaconitine can induce arrhythmia in rats ，the mechanism of which may be associated with Ca 2+ overload that resulted from reducing the activities of Na +-K+-ATPase and Ca 2+-Mg2+-ATPase and down-regulating the expression of related calcium transporter RyR2 and SERCA 2. |
| 期刊： | 2021年第32卷第23期 |
| 作者： | 张祉思，程婉秋，江涛，沈志滨，陈艳芬，陈聪，司徒莹，唐春萍 |
| AUTHORS： | ZHANG Zhisi， CHENG Wanqiu，JIANG Tao，SHEN Zhibin，CHEN Yanfen，CHEN Cong，SITU Ying，TANG Chunping |
| 关键字： | 滇乌碱；心律失常；钙超载；腺苷三磷酸；雷诺定受体2；Ca2+-ATP酶；毒性机制 |
| KEYWORDS： | Yunaconitine；Arrhythmia；Calcium overload ； |
| 阅读数： | 227 次 |
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