Objectives: Reducing endoplasmic reticulum stress (ERS)-induced cardiomyocyte apoptosis is a key strategy for preventing hypertensive heart disease. In our previous study, Icariside II can improve left ventricular remodelling in spontaneously hypertensive rats (SHRs). This study aims to determine whether Icariside II can exert its effect by inhibiting ERS-induced cardiomyocyte apoptosis via the PERK/ATF-4/CHOP signalling pathway.
Methods: Spontaneously hypertensive rats were randomly divided into model group and Icariside II groups. The rats in the Icariside II groups were intragastrically administrated with Icariside II 4, 8 and 16 mg/kg from 14 to 26 week-age, respectively. The left ventricular function was measured at the 18, 22 and 26 week-age by small animal ultrasound. At the end of the 26th week, cardiomyocyte apoptosis was analysed and the levels of GRP78, PERK, ATF-4 and CHOP gene and protein were detected.
Key Findings: The function of left ventricular became declined with age in SHRs, but improved in Icariside II groups. Myocardial apoptosis was aggravated in SHRs, but alleviated in Icariside II groups. Icariside II could reduce the levels of GRP78, PERK, ATF-4, CHOP gene and protein that increased in SHRs.
Conclusions: Icariside II prevents hypertensive heart disease by alleviating ERS-induced cardiomyocyte apoptosis, and its mechanism is related to the impediment of the PERK/ATF-4/CHOP signalling pathway.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/jphp.13041 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Bufalin Ameliorates Myocardial Ischemia/Reperfusion Injury by Suppressing Macrophage Pyroptosis via P62 Pathway.
J Cardiovasc Transl Res
December 2024
Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
Bufalin, which is isolated from toad venom, exerts positive effects on hearts under pathological circumstance. We aimed to investigate the effects and mechanisms of bufalin on myocardial I/R injury. In vivo, bufalin ameliorated myocardial I/R injury, which characteristics with better ejection function, decreased infarct size and less apoptosis.
View Article and Find Full Text PDFBisphenol S exposure interrupted human embryonic stem cell derived cardiomyocytes differentiation through ER-NF-κB/ERK signaling pathway.
Ecotoxicol Environ Saf
December 2024
Department of Nutrition and Food Safety, West China School of Public Health/West China Fourth Hospital, Sichuan University, Chengdu, China; Food Safety Monitoring and Risk Assessment Key Laboratory of Sichuan Province, Chengdu, China. Electronic address:
Bisphenol S (BPS) has been put into production as a wide range of Bisphenol A (BPA) alternatives, while little is known regarding its cardiac developmental toxicity. To explore the effect of BPS on cardiomyocyte differentiation and its mechanism, our study established the human embryonic stem cell-cardiomyocyte differentiation model (hESC-CM), which was divided into early period of differentiation (DP1:1-8d), anaphase period of differentiation (DP2:9-16d) and whole stage of differentiation (DP3:1-16d) exposed to human-related levels of BPS. We found that the survival rate of cardiomyocytes was more sensitive to BPS at the early stage of differentiation than at the anaphase stage of differentiation, and exposure to higher than 30 µg/mL BPS throughout the differentiation period decreased the expression of cTnT.
View Article and Find Full Text PDFSUZ12-Increased NRF2 Alleviates Cardiac Ischemia/Reperfusion Injury by Regulating Apoptosis, Inflammation, and Ferroptosis.
Cardiovasc Toxicol
December 2024
Department of Cardiovascular Center, Beijing Tongren Hospital, Capital Medical University, No. 3 Chongwenmennei Street, Dongcheng District, Beijing, 100730, China.
Nuclear factor erythroid 2-related factor 2 (NRF2) is a redox-sensitive transcriptional factor that enables cells to resist oxidant responses, ferroptosis and inflammation. Here, we set out to probe the effects of NRF2 on cardiomyocyte injury under acute myocardial infarction (AMI) condition and its potential mechanism. Human cardiomyocytes were exposed to hypoxia/reoxygenation (H/R) to induce cell injury.
View Article and Find Full Text PDFPotential of natural drug modulation of endoplasmic reticulum stress in the treatment of myocardial injury.
J Pharm Anal
November 2024
Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.
Myocardial injury (MI) is a common occurrence in clinical practice caused by various factors such as ischemia, hypoxia, infection, metabolic abnormalities, and inflammation. Such damages are characterized by a reduction in myocardial function and cardiomyocyte death that can result in dangerous outcomes such as cardiac failure and arrhythmias. An endoplasmic reticulum stress (ERS)-induced unfolded protein response (UPR) is triggered by several stressors, and its intricate signaling networks are instrumental in both cell survival and death.
View Article and Find Full Text PDFTRPC5 Promotes Intermittent Hypoxia-Induced Cardiomyocyte Injury Through Oxidative Stress.
Nat Sci Sleep
December 2024
Department of Cardiovasology, the Traditional Chinese Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, People's Republic of China.
Purpose: Intermittent hypoxia (IH), a defining feature of obstructive sleep apnea (OSA), is associated with heart damage and linked to transient receptor potential canonical channel 5 (TRPC5). Nonetheless, the function of TRPC5 in OSA-induced cardiac injury remains uncertain. For this research, we aimed to explore the role and potential mechanism of TRPC5 in cardiomyocyte injury induced by intermittent hypoxia.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!