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作 者:李紫洪 张晨晨 王靖 李鹏[1] 高乐 李雪玲 李婧[1] LI Zihong;ZHANG Chenchen;WANG Jing;LI Peng;GAO Le;LI Xueling;LI Jing(Department of Cardiology,Affiliated Hospital of Inner Mongolia Medical University,Hohhot 010059,China;State Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock,Inner Mongolia University,Hohhot 010020,China)
机构地区:[1]内蒙古医科大学附属医院心内科,呼和浩特010059 [2]内蒙古大学省部共建草原家畜生殖调控与繁育国家重点实验室,呼和浩特010020
出 处:《内蒙古大学学报(自然科学版)》2023年第2期158-168,共11页Journal of Inner Mongolia University:Natural Science Edition
基 金:国家自然科学基金项目(82260075;32160172);内蒙古自然科学基金面上项目(2018LH08043);内蒙古教育厅高等学校科学研究项目(NJZY18106);内蒙古医科大学附属医院博士启动项目(NYFY BS 2018);内蒙古医科大学致远人才项目(ZY0202013)。
摘 要:使用中药改善病理性心肌肥厚,对防治心力衰竭具有重要意义,目前中药牛蒡子苷(arctiin,ARC)对心血管疾病预防和治疗的相关研究备受关注。深入研究ARC干预心肌肥厚过程中蛋白质网络的变化,不仅有助于识别疾病检测的生物标志物和治疗靶点,也为心血管疾病药物研发提供依据。本研究首先利用100 nmol/L异丙肾上腺素(isoprenaline ISO)建立H9c2大鼠心肌细胞肥大模型,接着利用ARC进行处理,然后利用液相色谱质谱串联技术检测ARC处理前后肥大心肌细胞蛋白质组的变化,最后通过对蛋白组进行深入分析获得ARC对肥大心肌细胞影响的信号通路,明确ARC治疗引起的蛋白质组的变化、网络重组和可能的调控机制。为深入研究ARC对肥大心肌细胞治疗机制奠定基础。Study the effects traditional Chinese medicine on myocardial hypertrophy before heart failure remains a challenge.Arctiin(ARC)is an extractive substrate of mature fruits of Arctium lappa L,and its functions on cardiovascular treatment attracts a lot of attention.Analysis of the protein networks changes during myocardial hypertrophy after ARC treatment will helpful for the identification of biomarkers of myocardial hypertrophy as well as for therapeutic targets.In this study,rat H9c2 cardiomyocyte was treated by 100 nmol/L isoprenaline(ISO)to derive the cardiomyocyte hypertrophy model,then the cells was subjected to ARC treatment.The proteome of hypertrophic cardiomyocytes before and after ARC treatment was detected using liquid chromatography mass spectrometry tandem technology.The obtained proteome was analyzed in depth to obtain the signal pathway of ARC to hypertrophic cardiomyocytes,and to clarify the proteomic changes caused by ARC treatment and the possible regulatory mechanisms of the signal pathway.This study will lay a foundation for further study of the therapeutic mechanism of ARC on hypertrophic cardiomyocytes.
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