人参总次苷对心肌细胞肥大性改变的改善作用及机制
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篇名: 人参总次苷对心肌细胞肥大性改变的改善作用及机制
TITLE: Improvement effects and mechanism of total secondary ginsenosides on hypertrophic changes in cardiomyocytes
摘要: 目的 探讨人参总次苷(TSG)对血管紧张素Ⅱ(AngⅡ)诱导原代心肌细胞肥大性改变的改善作用及潜在机制。方法从新生SD乳鼠心脏中分离原代心肌细胞,将其分为对照组、AngⅡ组(2µmol/L)、TSG组(7.5µg/mL)、PFK-015组[6-磷酸果糖-2-激酶/果糖-2,6-二磷酸酶3(PFKFB3)抑制剂10nmol/L]和TSG+PFK-015组(TSG7.5µg/mL+PFK-01510nmol/L),检测各组细胞表面积、蛋白合成情况、能量代谢相关指标[游离脂肪酸(FFA)、辅酶A(CoA)、乙酰辅酶A(acetyl-CoA)]含量、糖酵解相关因子[缺氧诱导因子1α(HIF-1α)、葡萄糖转运蛋白4(GLUT-4)、乳酸脱氢酶A(LDHA)、丙酮酸脱氢酶激酶1(PDK1)、PFKFB3]的表达情况。结果与对照组相比,AngⅡ组细胞表面积显著增大,蛋白合成显著增多,FFA含量和HIF-1α、LDHA、PDK1、PFKFB3蛋白及mRNA的表达均显著升高或上调,CoA、acetyl-CoA含量和GLUT-4蛋白及mRNA的表达均显著降低或下调(P<0.05)。与AngⅡ组相比,TSG组和PFK-015组细胞上述指标均显著改善,且TSG+PFK-015组细胞的改善程度普遍优于TSG组和PFK-015组(P<0.05)。结论TSG可缩小AngⅡ诱导原代心肌细胞的表面积,减少蛋白合成,抑制其肥大性改变;上述作用可能与改善细胞能量代谢、抑制糖酵解活动有关。
ABSTRACT: OBJECTIVE To investigate the ameliorative effects and potential mechanism of total secondary ginsenosides (TSG) on hypertrophic changes of primary cardiomyocytes stimulated by angiotensin Ⅱ (Ang Ⅱ). METHODS Primary cardiomyocytes were isolated from the hearts of neonatal SD rats and divided into the following groups: control group, AngⅡ group (2 µmol/L), TSG group (7.5 µg/mL), PFK-015 group [6-phosphofructo-2-kinase/fructose-2, 6-bisphosphatase 3 (PFKFB3) inhibitor, 10 nmol/L], and TSG+PFK-015 group (TSG 7.5 µg/mL+PFK-015 10 nmol/L). The surface area, protein synthesis, energy metabolism-related indicators [free fatty acid (FFA), coenzyme A (CoA), acetyl coenzyme A (acetyl-CoA)], and the expressions of glycolysis-related factors [hypoxia-inducible factor 1α (HIF-1α), glucose transporter protein 4 (GLUT-4), lactate dehydrogenase A (LDHA), pyruvate dehydrogenase kinase 1 (PDK1) and PFKFB3] in primary cardiomyocytes of each group were measured. RESULTS Compared with the control group, the surface area of primary cardiomyocytes and protein synthesis were significantly increased, the content of FFA, protein and mRNA expressions of HIF-1α, LDHA, PDK1 and PFKFB3 were significantly increased or up-regulated in the AngⅡ group, while the contents of CoA and acetyl-CoA, the protein and mRNA expressions of GLUT-4 were significantly decreased or down-regulated (P<0.05). Compared with the AngⅡ group, both TSG group and PFK-015 group showed significant improvements in these indexes, with the TSG+PFK-015 group generally demonstrating superior effects compared to either treatment alone (P<0.05). CONCLUSIONS TSG can reduce the surface area of AngⅡ-induced primary cardiomyocytes, decrease protein synthesis, and inhibit their hypertrophic changes. These effects may be related to improving energy metabolism and the inhibition of glycolysis activity.
期刊: 2025年第36卷第12期
作者: 李彬;李佳;袁中杰;朱明军;谢世阳;高原;于瑞;王新陆
AUTHORS: LI Bin,LI Jia,YUAN Zhongjie,ZHU Mingjun,XIE Shiyang,GAO Yuan,YU Rui,WANG Xinlu
关键字: 人参总次苷;心力衰竭;心肌细胞;肥大性改变;能量代谢;糖酵解
KEYWORDS: total secondary ginsenosides; heart failure; cardiomyocyte; hypertrophic change; energy metabolism; glycolysis
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