Astragaloside IV Reduces OxLDL-Induced BNP Overexpression by Regulating HDAC

Journal of Healthcare Engineering

Xin Wang¹  Jun Shao²  Wenting Zhang²  Lu Xu³  Xiaolu Ren⁴  Huiying Liu⁵  Jing Li⁶  Mingyuan Xu⁷ 

[1] Department of Cardiovascular Medicine, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China, qmu.edu.cn;Department of Clinical Pharmacy, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China, qmu.edu.cn;Department of Pharmacy, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China, qmu.edu.cn;Department of Ultrasound, The Second Hospital of Qiqihar, Qiqihar 161000, China;Ethics Committee of Clinical Trial, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China, qmu.edu.cn;Office of the Agency for Clinical Trials of Drugs, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China, qmu.edu.cn;The First Affiliated Hospital, Heilongjiang University of Chinese Medicine, Harbin 150040, China, hljucm.edu.cn;

DOI  :  10.1155/2021/3433615

来源: Hindawi Publishing Corporation

【 摘 要 】

Effective drug intervention is the most important method to improve the prognosis, improve the quality of life, and prolong the life of patients with heart failure. This study aimed to explore the protective effect of astragaloside IV on myocardial cell injury induced by oxidized low-density lipoprotein (OxLDL) and its regulatory mechanism on the increase of brain natriuretic peptide (BNP) caused by myocardial cell injury. The model of myocardial cell injury, protection, and histone deacetylase (HDAC) inhibition in HL-1 mice was established by OxLDL treatment, astragaloside IV intervention, and UF010 coincubation. The effects of OxLDL and astragaloside IV on apoptosis were detected by flow cytometry. The expression level of BNP mRNA and protein in cells was investigated by real-time fluorescence quantification, western blot, and enzyme-linked immunosorbent assay. HDAC activity in nucleus was calibrated by fluorescence absorption intensity. Enzyme-linked immunosorbent assay (ELISA) was applied to test eNOS level in myocardial cells. OxLDL significantly promoted apoptosis, upregulated BNP mRNA, increased BNP protein level inside and outside cells, and decreased eNOS level. Compared with OxLDL treatment group, apoptosis decreased, BNP mRNA expression level decreased, BNP protein concentration decreased, and eNOS level increased significantly combined with low and high concentration astragaloside IV treatment group. HDAC activity significantly increased in OxLDL treatment group and significantly decreased after combined incubation with low and high concentrations of astragaloside IV. Inhibition of HDAC significantly increased eNOS level and decreased BNP protein level. In conclusion, astragaloside IV can reverse the low level of eNOS caused by OxLDL by regulating HDAC activity to protect myocardial cells from oxide damage, which is manifested by the decrease of BNP concentration.

【 授权许可】

Unknown