Previous studies have shown that stromal interaction molecule1 (STIM1)-mediated store-operated Ca entry (SOCE) contributes to intracellular Ca accumulation in H9C2 cells subjected to hypoxia/reoxygenation(H/R) injury. The aim of the present study was to investigate the effect of resveratrol on STIM1-mediated intracellular Ca accumulation and subsequent cell death in the context of myocardial ischemia/reperfusion (I/R) injury. C57 BL/6 mice were fed with either saline or resveratrol (50 mg/kg daily for 2 weeks) and then subjected to myocardial I/R injury. TTC/Evans Blue staining and TUNEL assay were performed to quantify the infarct size and apoptosis index. The cardiac function was evaluated by echocardiography. Neonatal rat ventricular cardiomyocytes (NRVCs) underwent hypoxia/reoxygenation (H/R) to establish the in vitro model. To achieve over-expression, NRVCs were transfected with STIM1-adenovirus vector. Apoptosis was analyzed by TUNEL assay. Cell viability was measured using MTS assay and cell necrosis was determined by LDH release assay. Intracellular Ca concentration was detected by laser scanning confocal microscopy using a Fluo-3AM probe. Resveratrol significantly reduced apoptosis, decreased infarct size, and improved cardiac function in mice subjected to myocardial I/R injury. In NRVCs, resveratrol also downregulated STIM1 expression accompanied by decreased intracellular Ca accumulation elicited by H/R injury. In addition, resveratrol reduced cell apoptosis, upregulated the Bcl-2, decreased Bax, and cleaved caspase-3 expression. Furthermore, the effects of resveratrol on STIM1-mediated intracellular Ca accumulation, apoptotic proteins, and H/R-induced cell injury were exacerbated by STIM1 over-expression and were partly abolished by SOCE inhibitor SKF96365 in NRVCs in vitro. Our findings demonstrate that resveratrol exerts anti-apoptotic activity and improves cardiac functional recovery following myocardial I/R by inhibiting STIM1-induced intracellular Ca accumulation.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s13105-019-00704-5 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
SmCSN5 is a synergist in the transcription factor SmMYB36-mediated biosynthesis of tanshinones and phenolic acids in .
Hortic Res
April 2025
College of Life Sciences, Northwest A&F University, No.22 Xinong Road, Yangling 712100, China.
The ubiquitin-26S proteasome system (UPS) is associated with protein stability and activity, regulation of hormone signaling, and the production of secondary metabolites in plants. Though the mechanism of action of SmMYB36 on the tanshinone and phenolic acid biosynthesis is well understood, its regulation through post-translational modifications is unclear. A constitutive photomorphogenesis 9 (COP9) signalosome subunit 5 (SmCSN5), which interacted with SmMYB36 and inhibited its ubiquitination-based degradation, was identified in .
View Article and Find Full Text PDFAffects the Synthesis of Polysaccharides by Regulating the Reactive Oxygen Species in .
Foods
February 2025
Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education, College of Biotechnology, State Key Laboratory of Food Nutrition and Safety, Tianjin University of Science & Technology, Tianjin 300457, China.
Alternative oxidase (AOX) is a terminal oxidase in the mitochondrial electron transport chain that does not contribute to the generation of ATP. It plays a critical role in maintaining the balance between reactive oxygen species (ROS) production and intracellular redox homeostasis within the mitochondria. In the study, overexpression and knockdown approaches were employed to investigate the function of .
View Article and Find Full Text PDFSodium Iodate-Induced Ferroptosis in Photoreceptor-Derived 661W Cells Through the Depletion of GSH.
Int J Mol Sci
March 2025
Institute of Genomics, School of Medicine, Huaqiao University, 668 Jimei Road, Xiamen 361021, China.
Oxidative stress-induced photoreceptor cell death is closely associated with the etiology of age-related macular degeneration (AMD), and sodium iodate (SI) has been widely used as an oxidant stimulus in AMD models to induce retinal pigment epithelium (RPE) and photoreceptor cell death. However, the mechanism underlying SI-induced photoreceptor cell death remains controversial and unclear. In this study, we elucidate that ferroptosis is a critical form of cell death induced by SI in photoreceptor-derived 661W cells.
View Article and Find Full Text PDFKinsenoside Suppresses DGAT1-Mediated Lipid Droplet Formation to Trigger Ferroptosis in Triple-Negative Breast Cancer.
Int J Mol Sci
March 2025
School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 311402, China.
Triple-negative breast cancer (TNBC) presents limited therapeutic options and is characterized by a poor prognosis. Although Kinsenoside (KIN) possesses a wide range of pharmacological activities, its effect and mechanism in TNBC remain unclear. The objective of this research was to explore the therapeutic effectiveness and the molecular mechanisms of KIN on TNBC.
View Article and Find Full Text PDF-Derived Exosome-like Nanovesicles Alleviate Metabolic Dysfunction-Associated Fatty Liver Disease by Promoting Mitophagy and Inhibiting NLRP3 Inflammasome Activation.
Int J Mol Sci
March 2025
College of Pharmaceutical Science, Yunnan University of Chinese Medicine, 1076 Yuhua Road, Kunming 650500, China.
Metabolic dysfunction-associated fatty liver disease (MAFLD) affects approximately one-quarter of the world's adult population, and no effective therapeutic drugs are available. is a fungus used as a herb and food nutrient for centuries as well as for MAFLD treatment. Exosome-like nanovesicles have many pharmacological activities; however, studies on the effects of -derived exosome-like nanovesicles (PCELNs) on MAFLD are lacking.
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!