Temperature extremes are established triggers of cardiovascular events in the general population, while cancer patients face elevated atrial fibrillation (AF) risk due to disease- and treatment-related factors. However, whether cancer confers additional vulnerability to temperature-related AF events remains unclear. This study aimed to examine the association between extreme temperatures and AF hospitalizations in cancer patients compared with non-cancer controls. Data were derived from the real-world study of the Chinese AF registry (2014–2023), comprising 1,665,014 AF hospitalizations. This study is an exploratory, cancer-focused secondary analysis of the RWS-CAF registry. Overall associations between ambient temperature and AF hospitalization in the full registry have been reported separately. We used a time-stratified case-crossover design with distributed lag nonlinear models to assess temperature-AF associations. Cancer patients (n = 243482) were compared with demographically matched non-cancer controls, and unmatched analyses were performed in the full cohort. Subgroup analyses examined effect modification by age, sex, and geographic region. Extreme cold (1st percentile, − 5.6 °C) was associated with higher AF hospitalization risk in cancer patients (RR 1.80, 95

Background: We aimed to evaluate the impact of a nationwide Atrial Fibrillation Center (AFC) program on oral anticoagulation (OAC) initiation patterns, institutional homogeneity, and long-term clinical outcomes. Methods: In this nationwide, longitudinal, multicentre registry study, we included inpatients with non-valvular AF across China between 2017 and 2024. We assessed temporal trends in OAC initiation, regimen composition, and inter-hospital heterogeneity (measured by the intraclass correlation coefficient [ICC]). Interrupted time-series analysis was used to evaluate the temporal impact of AFC certification. Furthermore, a prospective follow-up sub-cohort with valid indications for anticoagulation was established, utilizing inverse probability of treatment weighting (IPTW) to ensure its representativeness of the overall cohort. We compared clinical outcomes between OAC and non-OAC groups using multivariable Cox proportional hazards models, supplemented by as-treated and 30-day landmark analyses. Findings: A total of 1,499,629 inpatients were included, comprising 55·1% males, with a mean age of 71·3 years (SD 11·6) and a mean CHA₂DS₂-VASc score of 3·1 (SD 1·8). Hospital-level OAC rate increased from 28·9% in 2017-Q1 to 81·8% in 2024-Q4 (Ptrend < 0·001). The proportion of non-vitamin K antagonist oral anticoagulants use rose from 13·9% to 68·5%, while vitamin K antagonist use declined from 22·2% to 4·3% (Ptrend < 0·001). Institutional heterogeneity decreased significantly (ICC 0·317 to 0·111, Ptrend < 0·001). AFC accreditation was associated with an increased likelihood of OAC prescription (odds ratio 1·112, 95% CI 1·107–1·118, P<0·001). In the follow-up cohort (n=145,268), intention-to-treat analysis showed that OAC therapy was associated with lower risks of all-cause mortality (adjusted hazard ratio [aHR] 0·42, 95% CI 0·38–0·46, P<0·001) and stroke/systemic embolism (aHR 0·63, 0·56–0·70, P<0·001). These associations remained consistent in the as-treated and landmark analyses. Omission of OAC at discharge was independently associated with adverse events. Interpretation: The nationwide AFC program substantially improved OAC prescription rates and clinical homogeneity across Chinese hospitals. These system-level improvements translated into significant survival and stroke-prevention benefits, demonstrating the effectiveness of structured, large-scale quality improvement initiatives in managing chronic cardiovascular diseases within emerging healthcare systems.

BACKGROUND:Previous studies have evaluated extreme temperatures' impact on cardiovascular health, but few have specifically focused on atrial fibrillation (AF)-related hospitalizations across a wide temperature range. OBJECTIVES:This study aimed to quantify and investigate the association between ambient nonoptimal temperatures and AF hospitalizations. METHODS:A two-stage time-stratified case-crossover study was conducted using a nationwide registry of 1,665,014 AF patients from 251 cities between 2014 and 2023. Conditional quasi-Poisson and distributed lag nonlinear models analyzed associations between nonoptimal temperature and AF hospitalizations. Subgroup and attributable burden analyses identified potentially susceptible subpopulations. RESULTS:The minimum hospitalization temperature for AF was 24.3 °C (74th percentile). Compared to the minimum hospitalization temperature over a lag of 0 to 14 days, cumulative relative risks for extreme cold and heat (1st and 99th percentiles) were 1.32 (95% CI: 1.24-1.42) and 1.03 (95% CI: 0.99-1.07), respectively. Hospitalization risks related to extreme temperatures were similar across subgroups of age, sex, and baseline diseases. Overall, 14.3% (95% empirical CI [eCI]: 12.2%-14.8%) of AF hospital admissions were attributable to nonoptimal temperatures, with higher burden in northern China (18.4%; 95% eCI: 15.7%-19.4%) than southern China (12.4%; 95% eCI: 9.6%-13.6%). CONCLUSIONS:In this nationwide sample, extreme cold temperatures were associated with a greater risk of AF hospitalization. Excess risk was observed in northern China, where low temperatures prevail. This evidence highlights the importance of effective health care management and early resource allocation in high-risk regions.

Doxorubicin (Dox)-induced cardiotoxicity in patients with cancer, mediated primarily through cardiomyocyte ferroptosis and mitochondrial dysfunction, presents both life-threatening risks and significant limitations to Dox chemotherapeutic efficacy. The study investigated the therapeutic potential and mechanistic role of Maresin1-a novel proinflammatory regression mediator (SPM) -in Dox-induced cardiomyocyte ferroptosis. We employed both in vitro and in vivo models: H9C2 cells and human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) for in vitro ferroptosis modeling and C57BL/6 mice for in vivo validation. Our key findings showed that Maresin1 in Dox-treated cardiomyocytes attenuated lipid peroxidation, upregulated the anti-ferroptosis-related protein expression via the NRF2/GPX4 axis and mitigated mitochondrial structural and functional impairment. However, inhibition of NRF2 signaling abolished the cardioprotective effects of Maresin1 against Dox-induced ferroptosis. In conclusion, Maresin1 preserved cardiac function by preventing Dox-associated cardiomyocyte ferroptosis and mitochondrial impairment through the NRF2/GPX4 axis activation.

BACKGROUND:Data concerning young patients with atrial fibrillation (AF) are currently limited. HYPOTHESIS:This study aimed to assess the clinical characteristics and risk factors for AF recurrence in young patients following catheter ablation (CA). METHODS:All AF patients aged ≤ 45 years who underwent CA were identified from the China Atrial Fibrillation Center database between September 2018 and September 2023. Baseline clinical characteristics, procedural details, and follow-up outcomes were compared between the paroxysmal and non-paroxysmal cohorts. RESULTS:A total of 6,531 young patients with AF were included in the final analysis, with an average age of 37.7 ± 5.5 years, 77.1% were male, and 65.2% with paroxysmal AF. The primary comorbidities were hypertension (16.2%), heart failure (8.4%), valvular heart disease (3.5%), diabetes mellitus (3.2%), peripheral arterial disease (2.8%), stroke/transient ischemic attack (2.5%), and cardiomyopathy (2.2%). Following CA, the recurrence rate of AF post-CA was 14.4% across the entire cohort, with a lower recurrence rate in the paroxysmal AF group compared to the non-paroxysmal AF group (10.6% vs. 19.7%, p < 0.001). Non-paroxysmal AF (HR 2.34, 95% CI 1.62 to 3.36, p < 0.001) and hypertension (HR 1.69, 95% CI 1.09 to 2.63, p = 0.019) were identified as independent predictors for AF recurrence. CONCLUSION:Young AF patients who undergo CA exhibit a low recurrence rate and a notable improvement in symptoms post-CA. Non-paroxysmal AF and hypertension emerge as primary contributors to AF recurrence following CA in this population.

BACKGROUND Previous studies have evaluated extreme temperatures'impact on cardiovascular health, but few have specifically focused on atrial fibrillation (AF)-related hospitalizations across a wide temperature range. OBJECTIVES This study aimed to quantify and investigate the association between ambient nonoptimal temperatures and AF hospitalizations. METHODS A two-stage time-stratified case-crossover study was conducted using a nationwide registry of 1,665,014 AF patients from 251 cities between 2014 and 2023. Conditional quasi-Poisson and distributed lag nonlinear models analyzed associations between nonoptimal temperature and AF hospitalizations. Subgroup and attributable burden analyses identified potentially susceptible subpopulations. RESULTS The minimum hospitalization temperature for AF was 24.3 degrees C (74th percentile). Compared to the minimum hospitalization temperature over a lag of 0 to 14 days, cumulative relative risks for extreme cold and heat (1st and 99th percentiles) were 1.32 (95% CI: 1.24-1.42) and 1.03 (95% CI: 0.99-1.07), respectively. Hospitalization risks related to extreme temperatures were similar across subgroups of age, sex, and baseline diseases. Overall, 14.3% (95% empirical CI [eCI]: 12.2%-14.8%) of AF hospital admissions were attributable to nonoptimal temperatures, with higher burden in northern China (18.4%; 95% eCI: 15.7%-19.4%) than southern China (12.4%; 95% eCI: 9.6%-13.6%). CONCLUSIONS In this nationwide sample, extreme cold temperatures were associated with a greater risk of AF hospitalization. Excess risk was observed in northern China, where low temperatures prevail. This evidence highlights the importance of effective health care management and early resource allocation in high-risk regions. (JACC Adv. 2025;4:102143) (c) 2025 Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

This study aimed to assess the status of oral anticoagulant (OAC) therapy among Chinese patients with atrial fibrillation (AF) across various hospital departments, influenced by recent changes in medical insurance policies. It retrospectively analyzed data from 70,187 AF patients treated between January 2018 and December 2023 across 20 hospitals. The average patient age was 72.3 years, with 54.4% male. The study found a significant increase in OAC use over time, particularly in cardiology, where the usage rose from 29.8% pre-2018 to 68.8% in 2021-2023. However, OAC usage in non-cardiology departments remained below 50% during the same period. Tertiary hospitals had higher OAC prescription rates compared to non-tertiary hospitals. Despite 77.4% of the cohort being at high risk for stroke, their OAC usage rates were not higher than the non-high-risk group. Factors such as advanced age, history of bleeding, hemoglobin levels, and concurrent antiplatelet therapy hindered OAC use, while upstream treatments facilitated its acceptance. The study concludes that while progress has been made in OAC prescription in China, significant gaps remain, especially in internal medicine and surgery departments, necessitating targeted interventions and better interdisciplinary collaboration for improved patient outcomes.

Background and Aims Despite advances in technology and techniques, the recurrence rate of persistent atrial fibrillation (AF) following catheter ablation remains high. The Shensong Yangxin (SSYX) capsule, a renowned traditional Chinese medicine formula, is used in the treatment of cardiac arrhythmias. This trial aimed to investigate whether the SSYX can improve clinical outcomes in patients who have undergone catheter ablation for persistent AF.Methods A multi-centre, randomized, double-blind, placebo-controlled clinical trial was conducted at 66 centres in China among 920 patients with persistent AF undergoing first ablation. Participants were randomized to oral SSYX, 1.6 g (.4 g/granule) thrice daily (n = 460), or matched placebo (n = 460) for 12 months. The primary endpoint was recurrent atrial tachyarrhythmias lasting for >= 30 s following a blanking period of 3 months. Secondary endpoints included time to first documented atrial tachyarrhythmias, AF burden, cardioversion, stroke/systemic embolism, changes in echocardiographic parameters, and quality-of-life (QoL) score. Analyses were performed according to the intention-to-treat principle.Results A total of 920 patients underwent randomization (460 assigned to SSYX group and 460 assigned to placebo group). During the follow-up of 12 months, patients assigned to SSYX had a higher event-free rate from recurrent atrial tachyarrhythmias when compared with the placebo group (12-month Kaplan-Meier event-free rate estimates, 85.5% and 77.7%, respectively; hazard ratio, .6; 95% confidence interval .4-.8; P = .001). Patients assigned to receive SSYX had a better QoL score at 12 months compared to those randomized to placebo. There was no significant difference in the incidence of serious adverse events between the two groups.Conclusions Treatment with SSYX following radiofrequency catheter ablation for persistent AF reduced the incidence of recurrent atrial tachyarrhythmias and led to clinically significant improvements in QoL during a 12-month follow-up in a Chinese population. Structured Graphical Abstract A total of 920 Chinese patients with persistent AF undergoing first ablation were randomized to oral SSYX or matched placebo for 12 months. The recurrence of atrial arrhythmia (left), Kaplan-Meier curves depicting the time to the first recurrence of atrial arrhythmia after the 3-month blanking period (middle), and quality of life at 12-month follow-up (right) were evaluated. SSYX, Shensong Yangxin; CI, confidence interval; AF, atrial fibrillation; RD, rate difference; HR, hazard ratio.

Phenylacetylglutamine (PAGln), a gut metabolite is substantially elevated in heart failure (HF). The increase of PAGln in plasma is associated with atrial fibrillation (AF), and contributes to AF pathogenesis. However, the role of PAGln in AF with HF remains uncertain. Therefore, this study aimed to determine the effect of PAGln on AF after HF. Thoracic aortic coarctation (TAC) created overpressure-induced HF mice for 4 weeks. Histopathology, biochemical, echocardiographic for assessment of cardiac function, and electrophysiological examination of several electrophysiological indexes (ERP, SNRT, and the occurrence rate of AF) were performed at the end of the HF mice model. We found that plasma PAGln levels were significantly elevated in PAGln-treated HF mice and that PAGln aggravated maladaptive structural remodeling and electrical remodeling, which aggravated the vulnerability of AF, shortened the ERP duration, prolonged the SNRT, increased the occurrence rate of AF in HF mice. Mechanistically, PAGln exacerbated ROS accumulation and increased the levels of phosphorylated PLB and CAMK II. Overall, PAGln played a vital role in promoting the occurrence of AF in HF mice by activating the CAMK II signaling pathway.

Inherited cardiac arrhythmias are a group of genetic diseases predisposing to sudden cardiac arrest, mainly resulting from variants in genes encoding cardiac ion channels or proteins involved in their regulation. Currently available therapeutic options (pharmacotherapy, ablative therapy and device-based therapy) can not preclude the occurrence of arrhythmia events and/or provide complete protection. With growing understanding of the genetic background and molecular mechanisms of inherited cardiac arrhythmias, advancing insight of stem cell technology, and development of vectors and delivery strategies, gene therapy and stem cell therapy may be promising approaches for treatment of inherited cardiac arrhythmias. Recent years have witnessed impressive progress in the basic science aspects and there is a clear and urgent need to be translated into the clinical management of arrhythmic events. In this review, we present a succinct overview of gene and cell therapy strategies, and summarize the current status of gene and cell therapy. Finally, we discuss future directions for implementation of gene and cell therapy in the therapy of inherited cardiac arrhythmias.

BACKGROUND:The latest information regarding the awareness of atrial fibrillation (AF) remains limited in China. OBJECTIVES:The present study aimed to understand the variation and disparity in awareness of AF in China. METHODS:The cross-sectional study used data from the 2020 nationwide epidemiology survey on AF among adults aged 18 years or older in mainland China to assess the prevalence of AF awareness. The awareness of AF diagnostic methods and outcomes was also assessed using an interviewer-administered questionnaire. RESULTS:Of the 114,039 adults responding to the survey, 1463 (age-standardized prevalence, 55.3% (95% confidence interval [CI], 47.7-62.9%) and 10,202 (8.2%, 95%CI 5.4-10.9%) were aware of AF in participants with and without AF, respectively. Of these, 36.4% (95%CI 30.0-42.9%) and 6.3% (95%CI 3.6-9.1%) considered electrocardiogram as a method of diagnosing AF, and 30.0% (95% CI 3.2-8.2%) and 5.2% (95%CI 2.7-7.6%) considered stroke as an outcome of AF. The proportion of participants who being aware of AF varied significantly across sociodemographic and cardiovascular disease subgroups, and was almost consistently lower in rural areas than those in urban areas. Overall, lack of AF awareness was associated with rural areas, geographical region, lower education levels, and without history and had no risk factors of cardiovascular disease. CONCLUSIONS:Nearly half of adults with AF, and >90% non-AF population are unaware of AF in China, with significant variation and disparity. Focused public health initiatives are needed to improve awareness and knowledge of AF among high-risk populations.

BACKGROUND:Heart failure is usually accompanied by activation of the sympathetic nerve, and excessive activation of the sympathetic nerve promotes cardiac remodeling and cardiac dysfunction. In the isoproterenol (ISO)-induced animal model, it is often accompanied by myocardial hypertrophy, fibrosis, and inflammation. Leukocyte immunoglobulin-like receptor B4a (Lilrb4a), an immunosuppressive regulatory receptor, plays a vital role in cardiovascular disease. However, the effect of Lilrb4a on ventricular arrhythmia in an ISO-induced mouse model remains unclear. OBJECTIVE:The purpose of this study was to explore the role and molecular mechanism of Lilrb4a in ISO-induced arrhythmogenic remodeling. METHODS:Lilrb4a knockout mice and Lilrb4a overexpression mice were infused with ISO (15 mg/kg per 24 hours, 4 weeks). Echocardiography and histology evaluations of myocardial hypertrophy and cardiac structural remodeling were conducted. Surface electrocardiography and electrophysiologic examination were used to evaluate cardiac electrical remodeling and susceptibility to ventricular arrhythmias. Quantitative reverse transcriptase-polymerase chain reaction analysis and Western blotting were used to detect the expression levels of ion channel proteins and signal pathway proteins. RESULTS:The results discovered that ISO induced cardiac hypertrophy, fibrosis, and inflammation and led to electrical remodeling and the occurrence of ventricular arrhythmias. Lilrb4a alleviated cardiac structural and electrical remodeling and protected against the occurrence of ventricular arrhythmias in ISO-induced mice by gain-of-function or loss-of-function approaches. The mechanism is that Lilrb4a inhibited NF-κB signaling and MAPK signaling activation mediated by transforming growth factor kinase 1. CONCLUSION:Lilrb4a alleviates cardiac dysfunction and ISO-induced arrhythmogenic remodeling associated with cardiac fibrosis and inflammation through the regulation of NF-κB signaling and MAPK signaling activation.

Doxorubicin (DOX) is a widely used chemotherapeutic drug known to cause dose-dependent myocardial toxicity, which limits its clinical potential. DL-3-n-butylphthalide (NBP), a substance extracted from celery seed species, has a number of pharmacological properties, such as antioxidant, anti-inflammatory, and anti-apoptotic actions. However, whether NBP can protect against DOX-induced acute myocardial toxicity is still unclear. Therefore, this study was designed to investigate the potential protective effects of NBP against DOX-induced acute myocardial injury and its underlying mechanism. By injecting 15 mg/kg of DOX intraperitoneally, eight-week-old male C57BL6 mice suffered an acute myocardial injury. The treatment group of mice received 80 mg/kg NBP by gavage once daily for 14 days. To mimic the cardiotoxicity of DOX, 1uM DOX was administered to H9C2 cells in vitro. In comparison to the DOX group, the results showed that NBP improved cardiac function and decreased serum levels of cTnI, LDH, and CK-MB. Additionally, HE staining demonstrated that NBP attenuated cardiac fibrillar lysis and breakage in DOX-treated mouse hearts. Western blotting assay and immunofluorescence staining suggested that NBP attenuated DOX-induced oxidative stress, apoptosis, and inflammation both in vivo and in vitro. Mechanistically, NBP significantly upregulated the Nrf2/HO-1 signaling pathway, while the Nrf2 inhibitor ML385 prevented NBP from protecting the myocardium from DOX-induced myocardial toxicity in vitro. In conclusion, Our results indicate that NBP alleviates DOX-induced myocardial toxicity by activating the Nrf2/HO-1 signaling pathway.

Background: Intermediate-conductance calcium-activated potassium channels (KCa3.1) are important for automaticity of sinus nodes. Previous studies have identified that cardiomyocytes with pacemaker activities are existent in pulmonary vein (PV), superior vena cava (SVC). The aim of the present study was to explore the electrophysiological characteristics and differential densities of KCa3.1 in rabbit atrium. Methods: Immune-staining techniques and western blots were used to determine the KCa3.1 expression in PV, SVC, right atrium (RA), and left atrium (LA). Transmembrane action potentials (APs) of PVs, SVC, RA, and LA were recorded. Isoproterenol (1uM) and high calcium (5.4mM) were used to induce delayed afterdepolarization (DAD) and DAD-induced trigger activity. Results: The expression of KCa3.1 was significantly higher in the PVs and SVC than in the RA and LA. After super-fusion with isoproterenol (1μM) and high calcium (5.4mM), the delayed afterdepolarization (DAD) and DAD-induced triggered activity was induced in the PVs and SVC, but not in the RA and LA with isoproterenol and high calcium administration. TRAM-34 (5uM), a KCa3.1 inhibitor, inhibited DAD and DAD-induced triggered activity. Conclusions: Compared with atrium, thoracic veins are the most common sites genesis AF due to different distribution of KCa3.1. Blockade of KCa3.1 could eliminate DAD and DAD-induced trigger activity, KCa3.1 might be a promising target for foci AF.

Our study was conducted to investigate whether cadherin-5 (CDH5), a vascular endothelial cell adhesion glycoprotein, could facilitate the differentiation of human induced pluripotent stem cells (hiPSCs) into sinoatrial node-like pacemaker cells (SANLPCs), following previous findings of silk-fibroin hydrogel-induced direct conversion of quiescent cardiomyocytes into pacemaker cells in rats through the activation of CDH5. In this study, the differentiating hiPSCs were treated with CDH5 (40 ng/mL) between Day 5 and 7 during cardiomyocytes differentiation. The findings in the present study demonstrated that CDH5 stimulated the expression of pacemaker-specific markers while suppressing markers associated with working cardiomyocytes, resulting in an increased proportion of SANLPCs among hiPSCs-derived cardiomyocytes (hiPSC-CMs) population. Moreover, CDH5 induced typical electrophysiological characteristics resembling cardiac pacemaker cells in hiPSC-CMs. Further mechanistic investigations revealed that the enriched differentiation of hiPSCs into SANLPCs induced by CDH5 was partially reversed by iCRT14, an inhibitor of beta-catenin. Therefore, based on the aforementioned findings, it could be inferred that the regulation of beta-catenin by CDH5 played a crucial role in promoting the enriched differentiation of hiPSCs into SANLPCs, which presents a novel avenue for the construction of biological pacemakers in forthcoming research.

Objective To explore the effect of zingerone（ZGR） on the myocardium of rats after acute myocardial infarction.Methods The experiment was conducted at the Institute of Cardiovascular Disease, People’s Hospital, Wuhan University from July to September 2022. Thirty male SPF grade SD rats were randomly divided into Sham group, MI group, and MI+ZGR group using a number table method, with 10 rats in each group. The MI+ZGR group and MI group were treated with ZGR(6 mg·kg -1 ·d -1 ) and an equal amount of physiological saline by gavage for 21 days, respectively. On the 14th day of drug treatment, the left anterior descending branch of the coronary artery was ligated. Cardiac ultrasound examination was performed 7 days after surgery. Open the chest and take the heart for HE staining to observe the pathological changes of the heart. Enzyme linked immunosorbent assay（ELISA） for detecting serum interleukin-6（IL-6） and tumor necrosis factor-α（TNF-α）, and the levels of superoxide dismutase（SOD） and malondialdehyde（MDA） in myocardium. Protein immunoblotting technology was used for detecting nuclear transcription factor erythroid 2 related factor（Nrf2）, heme oxygenase-1（HO-1）, and nuclear factor κ B（NF-κ B） expression level in cardiac tissue.Results Cardiac ultrasound examination showed that compared with the MI group, the LVEDd and LVEDs of the MI+ZGR group rats significantly decreased（F/P=45.21/＜0.001,95.45/＜0.001）, while LVEF and LVFS increased（F/P=61.13/＜0.001,83.90/＜0.001）. ELISA detection showed that compared with the MI group, the serum IL-6 and TNF-α levels in the MI+ZGR group of rats were significantly higher Significantly reduced（F/P=237.40/＜0.001,532.70/＜0.001）, myocardial tissue SOD significantly increased（F/P=516.50/＜0.001）, and MDA significantly decreased（F/P=105.90/＜0.001）. HE slices showed that ZGR treatment can significantly reduce the infiltration of inflammatory cells and improve the degree of cell swelling in MI rats. Protein immunoblotting technology showed that compared with the MI group, the MI+ZGR group significantly increased the expression levels of Nrf2 and HO-1 proteins in the myocardial tissue of rats（P＜0.01）, and NF-κB protein level significantly decreased（P＜0.01）.Conclusion ZGR treatment can protect cardiac function by improving inflammation and oxidative stress levels after MI.

Ginsenoside Rh2 (GRh2) is a monomer isolated from red ginseng that has extensive pharmacological effects. However, whether GRh2 has a protective effect on ischaemia/reperfusion (I/R) in the myocardium has yet to be elucidated. The present study aimed to identify the anti-inflammatory and antioxidant effects of GRh2 on I/R in the myocardium and its underlying mechanism. A rat model of myocardial I/R injury was constructed by ligating the left anterior descending coronary artery, which was subsequently treated with GRh2. A total of 40 male Sprague-Dawley rats were divided into the following four groups: The sham group, the I/R group, the I/R+GRh2 (10 mg/kg) group and the I/R+GRh2 (20 mg/kg) group. Neonatal rat cardiomyocytes were also used to evaluate the protective effect of GRh2 on hypoxia/reoxygenation (H/R)-induced myocardial injury in vitro. The GRh2 pre-treatment reduced the I/R- or H/R-induced release of myocardial enzymes and the production of IL-1β, IL-18 and TNF-α. GRh2 reduced the area of myocardial infarction and the histological changes in the myocardium and improved cardiac functions. In addition, GRh2 reduced the expression levels of NOD-like receptor family pyrin domain-containing 3 (NLRP3), apoptosis-associated speck-like protein, caspase-1, malondialdehyde and reactive oxygen species and increased the expression levels of nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), glutathione peroxidase and superoxide dismutase. In conclusion, the present study confirmed that GRh2 could reduce oxidative stress and inflammation in cardiomyocytes after reperfusion, and its mechanism of action may be related to its regulation of the Nrf2/HO-1/NLRP3 signalling pathway.

Aims: To investigate the effects of M-CSF on myocardial injury in mice after MI by regulating different types of cardiac macrophages through the P2X7R/NLRP3/IL-1β signal pathway. Methods: A total of 60 C57BL/6J WT mice were used, with the Sham Group subjected to ligation without ligation through the LAD, the MI model was prepared by ligation of the LAD in the MC Group and MM Group, with the M-CSF reagent (500 μg/kg/d) being given an intraperitoneal injection for the first 5 days after surgery in the MM Group. All mice were fed in a barrier environment for 1 week. After the study, myocardial tissues were collected and IL-4, IL-6, IL-10, TNF-α, MCP-1, IFN-α, ANP, BNP, β-MHC, Collage I, Collage III, P2X7R, NLRP3, IL-1β, Bax, Caspase 3, C-Casp 3, Bcl-2, M1/2 macrophage, the apoptosis of cardiomyocytes, and the collagen deposition were detected. Results: The inflammatory response was significantly lower in the MM Group, the cardiomyocyte apoptosis, fibrosis, and hypertrophy were inhibited compared to the MC Group, and the levels of P2X7R, NLRP3, and IL-1β were also statistically lower in the MM Group. Additionally, the expression of M2 macrophages increased in the MM Group while the M1 macrophages statistically decreased compared to the MC Group. Conclusion: M-CSF can significantly increase the expression of M2 macrophage and reduce the level of M1 macrophage by inhibiting the levels of NLRP3/IL-1β-related proteins, thereby inhibiting inflammation, ameliorating reducing myocardial hypertrophy, apoptosis, and fibrosis, improve myocardial injury in mice after MI.

Cardiotoxicity linked to doxorubicin (DOX) is primarily caused by inflammation, oxidative stress, and apoptosis. The role of tubeimoside I (TBM) in DOX-induced cardiotoxicity remains ambiguous, despite growing evidence that it could reduce inflammation, oxidative stress, and apoptosis in various diseases. This study was designed to investigate the role of TBM in DOX-induced cardiotoxicity and uncover the underlying mechanisms. H9c2 cell line and C57BL/6 mice were used to construct an in vitro and in vivo model of DOX-induced myocardial injury, respectively. We observed that DOX treatment provoked inflammation, oxidative stress, and cardiomyocyte apoptosis, which were significantly alleviated by TBM administration. Mechanistically, TBM attenuated DOX-induced downregulation of sirtuin 3 (SIRT3), and SIRT3 inhibition abrogated the beneficial effects of TBM both in vitro and in vivo. In conclusion, TBM eased inflammation, oxidative stress, and apoptosis in DOX-induced cardiotoxicity by increasing the expression of SIRT3, suggesting that it holds great promise for treating DOX-induced cardiac injury.

目的 探讨达格列净(dapagliflozin,DAPA)对肺动脉高压(pulmonary arterial hypertension,PAH)致右心衰竭(right heart failure,RHF)大鼠房性心律失常(atrial tachyarrhythmia,AT)的影响.方法 60只♂SD大鼠随机分为4组:对照组(CTL组)、模型组(MCT组)、MCT+低剂量DAPA干预组(MCT+LD组)和MCT+高剂量DAPA干预组(MCT+HD组),持续干预35 d后,完成模型及心功能评价,心房结构重构评估,炎症因子检测,在体心脏电生理实验.结果 DAPA可降低模型大鼠的平均肺动脉压(PAP)及平均右心室压(mRVP)(P<0.05),减轻炎症反应(P<0.05),减轻右心房纤维化(P<0.05),降低AT诱发率(P<0.05)及平均AT持续时间(mean atrial tachyarrhythmia duration,MATD)(P<0.05),其程度在高剂量DAPA干预组中更明显.结论 DAPA能够降低PAH致RHF大鼠的AT易感性,其机制主要可能与DAPA抑制系统炎症和抗心房纤维化有关.