Minocycline alleviates lipopolysaccharide-induced cardiotoxicity by suppressing the NLRP3/Caspase-1 signaling pathway DOI Creative Commons
Huijuan Li, Xiaozhong Li, Xu Guohai

et al.

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: Sept. 11, 2024

Language: Английский

Tanshinone IIA inhibits cardiomyocyte pyroptosis through TLR4/NF-κB p65 pathway after acute myocardial infarction DOI Creative Commons

Ruoning Chai,

Zelin Ye,

Wenjing Xue

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2023, Volume and Issue: 11

Published: Sept. 12, 2023

Background: Tanshinone IIA, derived from Radix Salviae Miltiorrhizae (Salvia miltiorrhiza Bunge), constitutes a significant component of this traditional Chinese medicine. Numerous studies have reported positive outcomes regarding its influence on cardiac function. However, comprehensive comprehension the intricate mechanisms responsible for cardioprotective effects is still lacking. Methods: A rat model heart failure (HF) induced by acute myocardial infarction (AMI) was established via ligation left anterior descending coronary artery. Rats received oral administration tanshinone IIA (1.5 mg/kg) and captopril (10 8 weeks. Cardiac function assessed through various evaluations. Histological changes in tissue were observed using staining techniques, including Hematoxylin Eosin (HE), Masson, transmission electron microscopy. Tunel used to detect cell apoptosis. Serum levels NT-pro-BNP, IL-1β, IL-18 quantified enzyme-linked immunosorbent assay (ELISA). Expression TLR4, NF-κB p65, pyroptosis-related proteins determined western blotting (WB). H9C2 cardiomyocytes underwent hypoxia-reoxygenation (H/R) simulate ischemia-reperfusion (I/R) injury, viability apoptosis post treatment with different concentrations (0.05 μg/ml, 0.1 μg/ml). ELISA measured IL-18, LDH expression supernatant, while WB analysis evaluated protein levels. p65 nuclear translocation laser confocal Results: exhibited enhanced function, mitigated histological damage, lowered serum suppressed Moreover, downregulated pro-IL-1β, NLRP3, Caspase-1, GSDMD-N tissue. Additionally, it bolstered H/R cardiomyocyte viability, curbed apoptosis, reduced cells. Furthermore, hindered translocation. Conclusion: These findings indicate that enhances alleviates injury HF rats following AMI. demonstrates potential suppression pyroptosis. likely arise inhibition TLR4/NF-κB signaling pathway, presenting promising therapeutic target.

Language: Английский

Citations

31

Application of lipopolysaccharide in establishing inflammatory models DOI
Xiao Zhang, Xiao Tian, Yan Wang

et al.

International Journal of Biological Macromolecules, Journal Year: 2024, Volume and Issue: 279, P. 135371 - 135371

Published: Sept. 6, 2024

Language: Английский

Citations

11

NLRP3 Inflammasome Targeting Offers a Novel Therapeutic Paradigm for Sepsis-Induced Myocardial Injury DOI Creative Commons

Yuzi Jin,

Joshua S. Fleishman,

Yudong Ma

et al.

Drug Design Development and Therapy, Journal Year: 2025, Volume and Issue: Volume 19, P. 1025 - 1041

Published: Feb. 1, 2025

Cardiac or myocardial dysfunction induced by sepsis, known as sepsis-induced cardiomyopathy injury (SIMI), is a common complication of sepsis and associated with poor outcomes. However, the pathogenesis molecular mechanisms underlying SIMI remain poorly understood, requiring further investigations. Emerging evidence has shown that NOD-, LRR-, pyrin domain-containing protein 3 (NLRP3) inflammasomes contribute to SIMI. Compounds inhibit NLRP3-associated pyroptosis may exert therapeutic effects against In this review, we first outlined principal elements NLRP3 signaling cascade summarized recent studies highlighting how activation contributes We selective small-molecule modulators function inhibitors delineated their action attenuate Finally, discuss major limitations current paradigm propose possible strategies overcome them. This review highlights pharmacological inhibition promising strategy.

Language: Английский

Citations

1

The stems of Syringa oblata Lindl. exert cardioprotective effects against acute myocardial ischemia by inhibiting the TLR4/MyD88/NF-κB and NLRP3 inflammasome signaling pathways in mice DOI
Jixuan Xu,

Lulu Kang,

Badalahu Tai

et al.

Journal of Ethnopharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 119563 - 119563

Published: Feb. 1, 2025

Language: Английский

Citations

1

Protective effects of carvacrol on lipid profiles, oxidative stress, hypertension, and cardiac dysfunction – A comprehensive review DOI Creative Commons
Mohammad Reza Khazdair, Mozhgan Moshtagh, Akbar Anaeigoudari

et al.

Food Science & Nutrition, Journal Year: 2024, Volume and Issue: 12(5), P. 3137 - 3149

Published: Feb. 5, 2024

Abstract Cardiovascular diseases (CVDs) are a class of illnesses that affect the heart or blood vessels, leading to most common causes death worldwide. In 2017, CVD caused approximately 17.8 million deaths were increased 20.5 in 2021, globally. Also, nearly 80% worldwide occur some countries. Some herbs and their constituents due several pharmacological activities have been used for medicinal purposes. Carvacrol is phenolic mono‐terpenoid found oils aromatic with biological properties. The possible therapeutic effects carvacrol on lipid profiles, oxidative stress, hypertension, cardiac dysfunction summarized current study. data from this review article obtained by searching terms including; “Carvacrol”, “Hypertension”, Hypotensive, “Cardiac dysfunction”, “Ischemia”, “Lipid profile”, Oxidative stress web databases such as Web Sciences, PubMed Central, Google Scholar, until November 2023. results reviewed studies revealed inhibits acetylcholinesterase (AchE) activity alters reducing rate well systolic diastolic pressure (BP). also decreased proinflammatory cytokine (IL‐1β), while increasing secretion anti‐inflammatory (IL‐10). Moreover, improved mitigated number apoptotic cells. might be through its antioxidative, anti‐inflammatory, antiapoptotic effects. mentioned profile, indicate remedy effect treatment CVD.

Language: Английский

Citations

7

Epigenetic regulation of diverse regulated cell death modalities in cardiovascular disease: Insights into necroptosis, pyroptosis, ferroptosis, and cuproptosis DOI Creative Commons
Cong Chen, Jie Wang,

Shan Zhang

et al.

Redox Biology, Journal Year: 2024, Volume and Issue: 76, P. 103321 - 103321

Published: Aug. 19, 2024

Cell death constitutes a critical component of the pathophysiology cardiovascular diseases. A growing array non-apoptotic forms regulated cell (RCD)-such as necroptosis, ferroptosis, pyroptosis, and cuproptosis-has been identified is intimately linked to various conditions. These RCD are governed by genetically programmed mechanisms within cell, with epigenetic modifications being common crucial regulatory method. Such include DNA methylation, RNA histone acetylation, non-coding RNAs. This review recaps roles modifications, RNAs in diseases, well which regulate key proteins involved death. Furthermore, we systematically catalog existing pharmacological agents targeting novel their action article aims underscore pivotal role precisely regulating specific pathways thus offering potential new therapeutic avenues that may prove more effective safer than traditional treatments.

Language: Английский

Citations

7

Mechanisms of the septic heart: From inflammatory response to myocardial edema DOI Creative Commons

Dihan Fan,

Rongxue Wu

Journal of Molecular and Cellular Cardiology, Journal Year: 2024, Volume and Issue: 195, P. 73 - 82

Published: Aug. 13, 2024

Language: Английский

Citations

6

Exosomes Derived from Apelin-Pretreated Mesenchymal Stem Cells Ameliorate Sepsis-Induced Myocardial Dysfunction by Alleviating Cardiomyocyte Pyroptosis via Delivery of miR-34a-5p DOI Creative Commons

Ting Li,

Yuechu Zhao,

Zhi Cao

et al.

International Journal of Nanomedicine, Journal Year: 2025, Volume and Issue: Volume 20, P. 687 - 703

Published: Jan. 1, 2025

Background: Exosomes sourced from mesenchymal stem cells (MSC-EXOs) have become a promising therapeutic tool for sepsisinduced myocardial dysfunction (SMD).Our previous study demonstrated that Apelin pretreatment enhanced the benefit of MSCs in infarction by improving their paracrine effects.This aimed to determine whether EXOs Apelin-pretreated (Apelin-MSC-EXOs) would potent cardioprotective effects against SMD and elucidate underlying mechanisms.Methods: MSC-EXOs Apelin-MSC-EXOs were isolated identified.Mice neonatal cardiomyocytes (NCMs) treated with or under lipopolysaccharide (LPS) condition vitro.Cardiomyocyte pyroptosis was determined TUNEL staining.RNA sequencing used identify differentially expressed functional miRNAs between Apelin-MSC-EXOs.MSC-EXOs transplanted into mouse model induced cecal ligation puncture (CLP) via tail vein.Heart function evaluated echocardiography.Results: Compared MSC-EXOs, Apelin-MSC-EXO transplantation greatly cardiac mice.Both suppressed cardiomyocyte vivo vitro, latter exhibiting superior protective effects.miR-34a-5p effectively mediated exert high mobility group box-1 (HMGB1) as potential target.Mechanistically, delivered miR-34a-5p injured cardiomyocytes, thereby ameliorating regulation HMGB1/AMPK axis.These partially abrogated downregulation Apelin-MSC-EXOs.Conclusion: Our revealed key component protected mediation signaling pathway.

Language: Английский

Citations

0

Active ingredients of traditional Chinese medicine inhibit NOD-like receptor protein 3 inflammasome: a novel strategy for preventing and treating heart failure DOI Creative Commons

Ruifang Lin,

Yunfeng Yu,

Lixin Du

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: Jan. 24, 2025

Heart failure (HF) has emerged as a significant global public health challenge owing to its high rates of morbidity and mortality. Activation the NOD-like receptor protein 3 (NLRP3) inflammasome is regarded pivotal factor in onset progression HF. Therefore, inhibiting activation NLRP3 may represent promising therapeutic approach for preventing treating The active ingredients serve foundation effects traditional Chinese medicine (TCM). Recent research revealed advantages TCM enhancing cardiac structure function study aimed explore impact on HF, review current advancements utilizing inhibit This provides novel perspective future development precise intervention strategies targeting prevent treat

Language: Английский

Citations

0

Carvacrol Regulates the Expression of SLC25A6 by Inhibiting VDAC1 to Improve Mitochondrial Function and Reduce LPS-Induced Inflammatory Injury in HMEC-1 Cells DOI Creative Commons
Cheng-Wei Lü, Bin Yang, Ying Liu

et al.

ACS Omega, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 19, 2025

Carvacrol has been demonstrated to possess anti-inflammatory and antioxidant properties. This study aims further explore the mechanisms by which carvacrol mitigates LPS-induced human microvascular endothelial cells injury improving mitochondrial function. An inflammatory model of was established using LPS. The expression levels cytokines (IL-1β, IL-6, IL-18, TNF-α) were measured. Assessment apoptosis, necrosis, proliferation conducted YO-PRO-1/PI apoptosis necrosis detection kit EdU assay. evaluation oxidative stress facilitated use ROS, MDA, SOD assay kits. Angiogenic capacity cytoskeletal changes also examined. function energy metabolism achieved measuring membrane potential (MMP), permeability transition pore (mPTP) opening, ROS levels, ATP production. Western blot analysis performed detect VDAC1 SLC25A6. results show that significantly reduced IL-1β, TNF-α alleviated effects LPS on cell HMEC-1. It decreased inhibited excessive tube formation capacity, promoted remodeling. Furthermore, shown reduce protein expression, improve regulating MMP, mPTP production, increase SLC25A6 expression. Importantly, knockdown exhibited similar effects. In mechanism injury, may act as a downstream effector VDAC1. this demonstrate exerts protective effect alleviating through inhibition

Language: Английский

Citations

0