Yunzhi Chen, Jiaxu Chen, Jie Gao, Yihui Chai, Wen Li, Zhong Qin
School of Preclinical Medicine, Beijing University of Chinese Medicine, No. 11, Beisanhuan Donglu, Chaoyang, Beijing, China 100029.
School of Preclinical Medicine, Guiyang University of Chinese Medicine, No.50, Shidonglu, Guiyang, Guizhou, China 55000.
Afr J Tradit Complement Altern Med. 2017 Jun 5;14(4):278-288. doi: 10.21010/ajtcam.v14i4.31. eCollection 2017.
, which is one of the main components of , has been widely used in the treatment of congestive heart failure in China, and it can protect cardiomyocytes. Its mechanism of action remains unclear. Therefore, the present study was carried out to investigate the influence of on rat cardiomyocytes stimulated with endothelin-1 (ET-1), and explored the underlying mechanism.
ET-1 was used to stimulate primary rat cardiomyocytes and establish a cardiomyocyte hypertrophy model. Different doses were administered in combination with ET-1. Cardiomyocyte hypertrophy and apoptosis were examined using transmission electron microscopy (TEM) and flow cytometry, respectively. The molecular mechanism was explored by analyzing the mRNA of the vitamin D receptor (VDR), cytochrome P450 family 27 subfamily B member 1(CYP27B), cytochrome P450 family 24 subfamily A member 1(CYP24A) and renin mRNA levels by quantificational real-time polymerase chain reaction(qRT-PCR).
Rat cardiomyocyte hypertrophy model was established successfully. administration significantly affected cell apoptosis and significantly inhibited ET-1-induced cardiomyocyte hypertrophy in a dose-dependent manner. treatment affected the expression of signaling molecules in the vitamin D axis.
inhibits ET-1-induced cardiomyocyte hypertrophy. This effect can be reversed by regulating the levels of the relevant factors in the vitamin D axis.
[具体物质名称]是[相关物质名称]的主要成分之一，在中国已广泛用于治疗充血性心力衰竭，且能保护心肌细胞。其作用机制尚不清楚。因此，本研究旨在探讨[具体物质名称]对内皮素-1（ET-1）刺激的大鼠心肌细胞的影响，并探索其潜在机制。
用ET-1刺激原代大鼠心肌细胞，建立心肌细胞肥大模型。将不同剂量的[具体物质名称]与ET-1联合给药。分别使用透射电子显微镜（TEM）和流式细胞术检测心肌细胞肥大和凋亡情况。通过定量实时聚合酶链反应（qRT-PCR）分析维生素D受体（VDR）、细胞色素P450家族27亚家族B成员1（CYP27B）、细胞色素P450家族24亚家族A成员1（CYP24A）和肾素mRNA水平，探索分子机制。
成功建立大鼠心肌细胞肥大模型。[具体物质名称]给药显著影响细胞凋亡，并以剂量依赖方式显著抑制ET-1诱导的心肌细胞肥大。[具体物质名称]处理影响维生素D轴中信号分子的表达。
[具体物质名称]抑制ET-1诱导的心肌细胞肥大。这种作用可通过调节维生素D轴中相关因子的水平来逆转。
