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作 者:邱雨美 谢梦蝶 丁小云 张浩 王虎 黄思 蒋芳琴 汤喜兰 QIU Yu-mei;XIE Meng-die;DING Xiao-yun;ZHANG Hao;WANG Hu;HUANG Si;JIANG Fang-qin;TANG Xi-lan(School of Pharmacy,Jiangxi Science&Technology Normal University;Jiangxi Provincial Key Laboratory of Drug Design and Evaluation,Nanchang 330013,China)
机构地区:[1]江西科技师范大学药学院 [2]江西省药物分子设计与评价重点实验室,南昌330013
出 处:《天然产物研究与开发》2025年第3期512-520,共9页Natural Product Research and Development
基 金:国家自然科学基金(81960732,82360787);江西科技师范大学研究生创新专项资金项目(YC2023-X32);江西科技师范大学大学生创新创业训练计划(20221604114)。
摘 要:基于核苷酸结合寡聚化结构域样受体蛋白3(NOD-like receptor protein 3,NLRP3)炎症小体通路研究乳香挥发油(frankincense essential oil,FEO)防治大鼠心脏肥大的作用机制。采用气相色谱-质谱法测定FEO的成分。采用0.225μg/mL FEO预处理心肌细胞1 h,加入10μmol/L异丙肾上腺素(isoproterenol,ISO)作用24 h,观察FEO对ISO诱导的心肌细胞表面积、心脏肥大相关胚胎基因表达、乳酸脱氢酶(lactate dehydrogenase,LDH)释放及NLRP3炎症小体相关基因和蛋白表达的影响。通过冠状动脉结扎(coronary artery ligation,CAL)构建大鼠心脏肥大、心衰模型,给予FEO(50、100 mg/kg)治疗4周,检测大鼠心脏重量、左心室重量、心肌细胞横截面积、心脏肥大相关胚胎基因表达、NLRP3炎症小体相关基因和蛋白表达以及血清LDH含量等。结果表明,FEO能显著抑制ISO诱导的心肌细胞肥大,减少LDH释放,抑制NLRP3炎症小体相关基因和蛋白的表达。CAL诱导大鼠心脏重量、左心室重量、左心室心肌细胞横截面积均增加,心脏肥大相关胚胎基因表达上调,血清LDH含量增加,NLRP3炎症小体相关基因和蛋白表达上调,FEO可抑制CAL诱导的上述变化。因此,FEO可通过抑制NLRP3炎症小体来改善大鼠心脏肥大。This study aims to explore the effect and mechanism of frankincense essential oil(FEO)on cardiac hypertrophy in rats based on NOD-like receptor protein 3(NLRP3)inflammasome pathway.The ingredients of FEO were determined by gas chromatography-mass spectrometry.Cardiomyocytes were pretreated with 0.225μg/mL FEO for 1 h followed by 10μmol/L isoproterenol(ISO)treatment for 24 h.The effects of FEO on ISO-induced cardiomyocyte surface area,hypertrophy-related fetal gene expressions,the release of lactate dehydrogenase(LDH)and NLRP3 inflammasome-related gene and protein expressions were determined.Rats were intragastrically treated with FEO(50 or 100 mg/kg)for four weeks after undergoing coronary artery ligation(CAL)surgery to induce cardiac hypertrophy model.The heart weight,left ventricular weight,cardiomyocyte cross-sectional area,hypertrophy-related fetal gene expressions,NLRP3 inflammasome-related gene and protein expressions,and serum LDH content were measured.The results showed that FEO could significantly inhibit ISO-induced cardiomyocyte hypertrophy,reduce LDH release,and inhibit the expressions of NLRP3 inflammasome-related gene and protein.CAL surgery induced cardiac hypertrophy in rats as shown by increases in heart weight,left ventricular weight,and cardiomyocyte cross-sectional area,as well as upregulation of fetal gene expression.Additionally,CAL surgery also induced NLRP3 inflammasome activation as evidenced by increased serum LDH content and upregulated expressions of NLRP3 inflammasome-related gene and protein.FEO inhibited these above changes induced by CAL.Therefore,FEO can improve cardiac hypertrophy in rats by inhibiting NLRP3 inflammasome.
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