Background Atherosclerosis (AS), a chronic inflammatory disease, remains a leading cause of cardiovascular morbidity. Curcumin, the primary bioactive compound from Curcuma longa, has demonstrated potent anti-atherosclerotic properties in preclinical studies, yet a comprehensive synthesis of its multi-targeted mechanisms is warranted. Purpose This review aims to systematically consolidate the molecular mechanisms by which curcumin inhibits the development and progression of atherosclerosis, providing a foundation for its clinical translation. Methods A structured literature search was conducted in PubMed and Web of Science to identify studies elucidating the anti-atherosclerotic effects of curcumin. Key findings on its molecular targets and pathways were extracted and synthesized. Results Curcumin exerts its anti-atherosclerotic effects through pleiotropic mechanisms. It potently suppresses vascular inflammation by inhibiting key pathways like nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK), and mitigates oxidative stress by activating the Nrf2/HO-1 axis. Curcumin improves lipid metabolism by reducing cholesterol synthesis and promotes reverse cholesterol transport. Furthermore, it inhibits vascular smooth muscle cell (VSMC) proliferation and migration, enhances endothelial function, and stabilizes plaques. Emerging evidence also highlights its role in modulating epigenetic markers (e.g., DNA methylation, histone acetylation) and reshaping gut microbiota homeostasis, which contribute to its protective effects. Conclusion Curcumin is a promising multi-targeted agent against atherosclerosis, impacting a wide spectrum of pathological processes from inflammation and oxidative stress to epigenetics and the gut-vascular axis. While preclinical evidence is compelling, well-designed clinical trials are crucial to definitively establish its efficacy and safety in human patients.

Atherosclerosis (AS) is the main pathological basis of cardiovascular diseases, and its pathogenesis and treatment strategies remain major challenges. Recent advances in single-cell RNA sequencing and lineage tracing have revealed that vascular smooth muscle cells (VSMCs) are not merely passive structural components of atherosclerotic plaques, but highly plastic participants that undergo clonal expansion, phenotypic modulation, and transdifferentiation into functionally diverse cell states. These findings have prompted the emergence of an "athero-oncology" framework, which explores selected tumor-like cellular programs in VSMCs during AS without equating atherosclerosis with cancer. In this review, we summarize the evidence supporting VSMC-derived clonal expansion and phenotypic diversification in atherosclerotic lesions and discuss key mechanisms involved in this process, including proliferative expansion and survival programs, metabolic reprogramming, epigenetic regulation, DNA damage and genomic stress, VSMC senescence, pathological angiogenesis, and remodeling of the inflammatory and immune microenvironment. We further highlight shared signaling pathways between VSMC-driven plaque remodeling and tumor biology, while emphasizing fundamental differences between AS and malignant disease in growth limitation, mutational burden, metastatic potential, and clinical behavior. Finally, we discuss oncology-inspired therapeutic opportunities and boundaries, including pathway-level targeting of proliferative, metabolic, epigenetic, and inflammatory programs, as well as the risks of directly repurposing anticancer therapies for chronic vascular disease. This framework may provide new insights into vascular biology and therapeutic development.

A novel magnetic effervescence-assisted salting-out liquid-liquid extraction (MEASO-LLE) method was developed for the rapid and efficient determination of pyrethroid insecticide residues in fresh samples. Effervescent tablets were prepared by mixing Na2CO3, NaH2PO4, and Fe₃O₄, followed by grinding and compression. The extraction process involves simply adding the effervescent tablet to a fresh sample homogenate containing acetonitrile as the extractant. By integrating effervescence, salting-out, and magnetic nanoparticle aggregation, the method simplifies sample preparation by eliminating labor-intensive vortexing and centrifugation steps, reducing the overall processing time to ∼3 min. Coupled with gas chromatography-electron capture detection, the method demonstrates good linearity (R2 > 0.99), sensitivity (LOD: 0.7-3.5 ng/g), accuracy (relative recoveries: 84.7-115.6 %), and precision (RSD < 9.1 %). Its application to fruits and herbal leaves validated its robustness and versatility. Compared to conventional techniques, MEASO-LLE offers a time-efficient, cost-effective, and user-friendly solution, providing a valuable tool for food safety monitoring.

Numerous lipid-lowering medications are commonly used in clinical settings; however, their impact on vascular endothelial function remains unclear. This study employed techniques like flow-mediated dilation (FMD) to demonstrate the relative effects of lipid-lowering medications on vascular function. PubMed, Embase, and World of Science were searched from January 1, 2011 to October 1, 2024, and the language was limited to English. Randomized controlled trials (RCTs) have assessed the impact of lipid-lowering medications versus placebos on FMD in individuals. The outcomes included FMD, pulse wave velocity (PWV), low-density lipoprotein cholesterol (LDL-C), peak O2 consumption (VO2), and intimal media thickness (IMT). We computed standardized mean differences and 95% confidence intervals (CIs). P < 0.05 indicates statistical significance. The quality of the RCTs was assessed according to the methods provided by the Cochrane Handbook, and effective data were extracted. Revman software 5.4 version was used for statistical analysis. Drug type, intervention duration, and underlying diseases were used as covariates in the subgroup analysis. This meta-analysis included 19 RCTs involving 1,004 patients. Compared with placebo, lipid-lowering agents significantly reduced FMD (0.20 [95% CI: 0.05, 0.35], P = 0.007, I2 = 43%, 14 trials, 726 participants), LDL-C (-1.54 [95% CI: -1.78, -1.30], P < 0.00001, I2 = 25%, 7 trials, 350 participants) and PWV (-0.35 [95% CI: -0.57, -0.02], P = 0.04, I2 = 0.0%, 4 trials, 206 participants). Lipid-lowering drugs positively affect endothelial function, while lowering blood lipids and statins are the most effective.

The gut microbiota plays a crucial role in lipid metabolism in both humans and animals. However, the specific contributions of gut microbiota and their associated metabolites to fat deposition, as well as the underlying mechanisms, remain largely unexplored. In this study, we demonstrated that the intestinal microbiota mediated the heterogeneity of mesenteric fat index (MFI), as evidenced by fecal microbiota transplantation (FMT) experiments. Notably, analysis of the 16S rRNA gene amplicon sequencing of 44 samples revealed a significantly higher abundance of Cetobacterium somerae in the Low MFI group, with a positive correlation to reduced MFI. Serum metabolomics analysis confirmed that L-Carnitine emerged as the most differentially abundant metabolite in the Low MFI group and exhibited a strong positive correlation with C. somerae abundance. Metagenomic analysis showed that microbial genes related to L-Carnitine biosynthesis were significantly enriched in the Low MFI group. Further, C. somerae was isolated and cultured, and its subsequent monocolonization in germ-free zebrafish and tilapia demonstrated its lipid-lowering effects by enhancing mitochondrial fatty acid β-oxidation. Whole genome sequencing demonstrated C. somerae could encode the [EC:1.2.1.3] gene, which promotes the production of 4-trimethylammoniobutanoate, a precursor of L-Carnitine, thereby enhancing L-Carnitine biosynthesis by the host and gut microbiota, leading to the reduced fat deposition in Nile tilapia. In conclusion, C. somerae, a core gut microbe with high abundance in aquatic teleost intestines, plays an important role in host lipid metabolism. This study advances our understanding of how core gut microbes shape host phenotypes and provides novel insights into manipulating core gut colonizers to reduce fat deposition.

BackgroundAtherosclerosis is a widely studied pathophysiological foundation of cardiovascular diseases. Inflammation and dyslipidemia are risk factors that promote the formation of atherosclerotic plaques. The gut microbiota and their metabolites are considered independent risk factors for atherosclerosis. Polydatin combined with hawthorn flavonoids, as the extracts of Polygonum cuspidatum Sieb. et Zucc. and Crataegus pinnatifida Bunge, have shown excellent cardiovascular protective effects. However, the underlying mechanism requires further investigation. Our study aimed to explore the anti-atherosclerotic mechanism through gut microbiota and their metabolites.MethodsApoE−/− mice were fed either a normal-chow diet or a high-fat diet. The polydatin combined with hawthorn flavonoids group received varied doses of polydatin and hawthorn flavonoids: a high dose (polydatin 200 mg/kg daily; hawthorn flavonoids 100 mg/kg daily), a medium dose (polydatin 100 mg/kg daily; hawthorn flavonoids 50 mg/kg daily), and a low dose (polydatin 50 mg/kg daily; hawthorn flavonoids 25 mg/kg daily). The control and model groups were administered distilled water (0.2 mL daily). The experiment lasted for 24 weeks.ResultsPolydatin combined with hawthorn flavonoids administration significantly reduced lipid and inflammatory cytokine levels, meanwhile, the atherosclerotic lesions in a high-fat diet-induced ApoE−/− mice were significantly decreased. Additionally, polydatin combined with hawthorn flavonoids also inhibited the enhancement of trimethylamine N-oxide (TMAO), trimethylamine (TMA) levels of HFD-induced ApoE−/− mice by regulating the expression of hepatic flavin-containing enzyme monooxygenase 3 (FMO3). 16S rRNA sequencing results demonstrated that high-dose polydatin combined with hawthorn flavonoids treatment increased the abundance of Actinobacteriota, Atopobiaceae and Coriobacteriaea_UCG-002, and decreased the abundance of Desulfobacterota. Norank_f_Muribaculaceae was enriched in the medium-dose polydatin combined with hawthorn flavonoids and simvastatin groups, and Lactobacillus was mainly increased in the simvastatin and the low-dose polydatin combined with hawthorn flavonoids groups. According to the metagenetic results, functional annotations also suggested that the biological processes of each group mainly focused on metabolism-related processes. Specifically, polydatin combined with hawthorn flavonoids may regulate the abundance of TMA-producing bacteria (Coriobacteriaceae, Desulfovibrio, Muribaculum, and Clostridium) and related enzymes in glycolipid metabolic pathways to exert an important effect on the prevention of atherosclerosis.ConclusionOur results suggested that polydatin combined with hawthorn flavonoids could regulate the glucolipid metabolism-related pathway, attenuate inflammatory cytokine levels, and reduce atherosclerotic plaques by remodeling gut microbiota.

Hematological parameters are among the most accessible and routinely performed clinical tests. Recent studies have gradually revealed their potential for risk prediction. This study aimed to assess the association between hematological parameters and major adverse cardiovascular events (MACEs) in patients with coronary artery disease. This prospective study included 2,970 Chinese participants who underwent coronary angiography, with hematological and biochemical indicators measured at baseline. MACEs, comprising myocardial infarction, stroke, revascularization, and all-cause mortality, were recorded during follow-up. Univariate and multivariate analyses were conducted to evaluate the relationship between the hematological parameters and MACEs. Over a median follow-up period of 79 months, 474 MACEs were documented. Kaplan-Meier analysis indicated that the participants with lower levels of RBC, PLT, PCT, LYMPH% and BASO%, as well as higher RDW-CV, RDW-SD, MONO% and NEUT%, exhibited reduced survival probability. Multivariate Cox regression analysis identified elevated RDW-CV as a significant risk factor for MACE (T3 HR, 1.292; 95% CI, 1.013-1.647; P=0.039), while lower BASO% demonstrated a protective effect (T3 HR, 0.750, 95 % CI: 0.591-0.953; P=0.018). LYMPH% also showed a significant association with MACEs. Additionally, nonlinear correlations were observed between PLT and PCT and MACEs. In conclusion, RDW-CV, BASO%, PLT, PCT and LYMPH% were closely associated with MACEs and may serve as potential predictors for cardiovascular risk in patients with coronary artery disease.

BackgroundObservational studies suggest an association between telomere length (TL) and blood lipid (BL) levels. Nevertheless, the causal connections between these two traits remain unclear. We aimed to elucidate whether genetically predicted TL is associated with BL levels via Mendelian randomization (MR) and vice versa.MethodsWe obtained genetic instruments associated with TL, triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein A-1 (ApoA-1) and apolipoprotein B (ApoB) from large-scale genome-wide association studies (GWASs). The causal relationships between TL and BL were investigated via bidirectional MR, multivariable MR and mediation analysis methods. The inverse variance weighted (IVW) method was employed as the principal methodology, complemented by several other estimators to enhance the robustness of the analysis.ResultsIn the forward MR analyses, we identified significant positive correlation between genetically predicted TL and the levels of TG (β=0.04, 95% confidence interval [CI]: 0.01 to 0.06, p = 0.003). In the reverse MR analysis, TG (β=0.02, 95% CI: 0.01 to 0.03, p = 0.004), LDL-C (β=0.03, 95% CI: 0.01 to 0.04, p = 0.001) and ApoB (β=0.03, 95% CI: 0.01 to 0.04, p = 9.71×10–5) were significantly positively associated with TL, although this relationship was not observed in the multivariate MR analysis. The mediation analysis via two-step MR showed no significant mediation effects acting through obesity-related phenotypes in analysis of TL with TG, while the effect of LDL-C on TL was partially mediated by body mass index (BMI) in the reverse direction, with mediated proportion of 12.83% (95% CI: 0.62% to 25.04%).ConclusionsOur study indicated that longer TL were associated with higher TG levels, while conversely, higher TG, LDL-C, and ApoB levels predicted longer TL, with BMI partially mediating these effects. Our findings present valuable insights into the development of preventive strategies and interventions that specifically target TL-related aging and age-related diseases.

Purpose The purpose of this study was to investigate the relationship between serum immunoglobulin M (IgM) and the severity of coronary artery disease in Chinese patients who underwent coronary angiography. Methods A total of 2,045 patients who underwent coronary angiography (CAG) from March 2017 to March 2020 at Beijing Hospital were included in this study. Serum IgM concentration and biochemical indicators were measured before coronary angiography (CAG). The triquartile IgM levels at baseline in the population were analysed. Spearman rank correlation was used to analyse the association between IgM and traditional risk factors for coronary artery disease (CAD). CAD patients were divided into subgroups by affected area, number of affected vessels, and Gensini score to analyse the relationship between IgM and CAD severity. Multivariable logistic regression analysis was used to evaluate the association between IgM and CAD severity. Results Serum IgM levels were significantly lower in the CAD group (63.5 mg/dL) than in the non-coronary artery disease (NCAD) group (72.3 mg/dL) (P < 0.001). Serum IgM levels were significantly associated with sex. Serum IgM levels were positively correlated with traditional CAD risk factors such as TG, TC and LDL-C (P < 0.05), and negatively associated with the number of obstructed vessels, the number of affected areas, and Gensini scores. After adjusting for age, sex, smoking status, hypertension, dyslipidaemia, diabetes, stroke, and statin use history, a high IgM level was independently negatively associated with the severity of CAD expressed by the Gensini score. Conclusion We determined that serum IgM was independently negatively associated with the severity of CAD diagnosed by angiography in Chinese adults.

Copper is an essential micronutrient that plays a pivotal role in numerous physiological processes in virtually all cell types. Nevertheless, the dysregulation of copper homeostasis, whether towards excess or deficiency, can lead to pathological alterations, such as atherosclerosis. With the advent of the concept of copper-induced cell death, termed cuproptosis, researchers have increasingly focused on the potential role of copper dyshomeostasis in atherosclerosis. In this review, we provide a broad overview of cellular and systemic copper metabolism. We then summarize the evidence linking copper dyshomeostasis to atherosclerosis and elucidate the potential mechanisms underlying atherosclerosis development in terms of both copper excess and copper deficiency. Furthermore, we discuss the evidence for and mechanisms of cuproptosis, discuss its interactions with other modes of cell death, and highlight the role of cuproptosis-related mitochondrial dysfunction in atherosclerosis. Finally, we explore the therapeutic strategy of targeting this novel form of cell death, aiming to provide some insights for the management of atherosclerosis.

Fritillaria cirrhosa is a remarkably representative endangered species on the plateau, and its phenotype has undergone dramatic alterations due to global climate change and habitat destruction. However, the mechanism behind the phenotypic change associated with color variation has not been characterized, and subsequent physiological responses are still unknown. We investigated different phenotypes of cultivated F. cirrhosa and conducted a comprehensive transcriptomic analysis. Their agronomic traits, photosynthetic parameters, and the content of pharmaceutical ingredients were also compared. In the transcriptomic profiling, the purple phenotype had 754 up-regulated and 980 down-regulated genes compared with the green F. cirrhosa, in which a total of 37 significant differential expression genes (DEGs) regulated the anthocyanin biosynthesis by coding 6 vital enzymes (C4H, F3′H, ANS, DFR, DFT, and BA1). These DEGs were key genes responsible for the form of the purple phenotype of F. cirrhosa. Moreover, 10 DEGs were observed to be related to biotic and abiotic stress responses, such as regulation of defense response to bacterium and UV regulation in the actual unshaded field environment. The results of agronomic traits indicated that the purple phenotype exhibited a multitude of merits in plant height and stem diameter (p < 0.05), and produced more high-quality fruit and seeds, which demonstrated that the purple phenotype has high regeneration ability and potential resistance to cultivation conditions. Importantly, the content of total alkaloids as bioactive ingredients in medicinal bulbs of purple F. cirrhosa was significantly higher than that in the green phenotype by 57.14

This study aimed to evaluate the relationship between aromatic amino acids (AAAs), - phenylalanine (Phe), tyrosine (Tyr) and tryptophan (Trp) - and coronary artery disease (CAD) in a prospective study involving 2970 participants undergoing coronary angiography at Beijing Hospital. Serum levels of Phe, Tyr and Trp were analysed. The cross-sectional data revealed that serum Tyr and Trp levels were significantly and inversely associated with CAD. During a median follow-up period of 44 months, 343 major adverse cardiovascular events (MACEs) and 138 all-cause deaths were recorded. MACE included myocardial infarction, stroke, revascularisation and all-cause mortality. Low serum Trp levels predicted an increased risk of MACE and death. High serum Phe levels were linked to an increased risk of MACE, while low Tyr levels were associated with a higher risk of death. Collectively, our findings underscore a close correlation between AAAs and CAD, as well as their potential predictive value for adverse cardiovascular outcomes.

Purpose:Individuals with chronic kidney disease (CKD) face an elevated residual risk of cardiovascular events, but the relationship between this residual risk and 1,5-anhydroglucitol (1,5-AG) is uncertain. Our study aimed to examine the effect of 1,5-AG on major adverse cardiovascular events (MACEs) and all-cause mortality in acute coronary syndrome (ACS) individuals. Methods:1253 ACS participants hospitalized were enrolled at Beijing Hospital between March 2017 and March 2020. All participants were classified into 2 groups based on their eGFR (60 ml/min/1.73 m2). The link between 1,5-AG and adverse outcome was investigated in non-CKD and CKD participants. Results:CKD patients had reduced concentrations of 1,5-AG than those without CKD. Throughout a median follow-up duration of 43 months, 1,5-AG was an autonomous hazard factor for MACEs and all-cause mortality. 1,5-AG<14 μg/ml participants had greater MACEs and all-cause mortality risk than those with 1,5-AG≥14 μg/ml, regardless of renal function. Furthermore, concomitant reduced concentrations of 1,5-AG and CKD portended a dismal prognosis in ACS patients. Conclusions:1,5-AG was autonomously linked to MACEs and all-cause mortality in ACS participants with both non-CKD and CKD. Co-presence of reduced concentrations of 1,5-AG and CKD may portend adverse clinical outcomes.

BackgroundGut microbiota has significant impact on the cardio-metabolism and inflammation, and is implicated in the pathogenesis and progression of atherosclerosis. However, the long-term prospective association between trimethylamine N-oxide (TMAO) level and major adverse clinical events (MACEs) in patients with coronary artery disease (CAD) with or without diabetes mellitus (DM) habitus remains to be investigated.MethodsThis prospective, single-center cohort study enrolled 2090 hospitalized CAD patients confirmed by angiography at Beijing Hospital from 2017-2020. TMAO levels were performed using liquid chromatography-tandem mass spectrometry. The composite outcome of MACEs was identified by clinic visits or interviews annually. Multivariate Cox regression analysis, Kaplan-Meier analysis, and restricted cubic splines were mainly used to explore the relationship between TMAO levels and MACEs based on diabetes mellitus (DM) habitus.ResultsDuring the median follow-up period of 54 (41, 68) months, 266 (12.7%) developed MACEs. Higher TMAO levels, using the tertile cut-off value of 318.28 ng/mL, were significantly found to be positive dose-independent for developing MACEs, especially in patients with DM (HR 1.744, 95%CI 1.084-2.808, p = 0.022).ConclusionsHigher levels of TMAO are significantly associated with long-term MACEs among CAD patients with DM. The combination of TMAO in patients with CAD and DM is beneficial for risk stratification and prognosis.

The morbidity and mortality of cardiovascular diseases (CVDs) are increasing in recent years, and atherosclerosis (AS), a major CVD, becomes a disorder that afflicts human beings severely, especially the elders. AS is recognized as the primary cause and pathological basis of some other CVDs. The active constituents of Chinese herbal medicines have garnered increasing interest in recent researches owing to their influence on AS and other CVDs. Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is a naturally occurring anthraquinone derivative found in some Chinese herbal medicines such as Rhei radix et rhizome, Polygoni cuspidati rhizoma et radix and Polygoni multiflori root. In this paper, we first review the latest researches about emodin's pharmacology, metabolism and toxicity. Meanwhile, it has been shown to be effective in treating CVDs caused by AS in dozens of previous studies. Therefore, we systematically reviewed the mechanisms by which emodin treats AS. In summary, these mechanisms include anti-inflammatory activity, lipid metabolism regulation, anti-oxidative stress, anti-apoptosis and vascular protection. The mechanisms of emodin in other CVDs are also discussed, such as vasodilation, inhibition of myocardial fibrosis, inhibition of cardiac valve calcification and antiviral properties. We have further summarized the potential clinical applications of emodin. Through this review, we hope to provide guidance for clinical and preclinical drug development.

Objective: To investigate the predictive value of glycosylated hemoglobin A1c/apolipoprotein A-1 (HbA1c/ApoA-1) ratio for major adverse cardiovascular events (MACEs) in patients with acute coronary syndrome (ACS). Methods: The present study is a retrospective cohort study. ACS patients who were hospitalized and underwent coronary angiography at Beijing Hospital from March 2017 to March 2019 were enrolled. Baseline information such as sex, age, previous history, Gensini score, HbA1c and ApoA-1 were analyzed. Patients were divided into two groups according to presence or absence of MACEs and the difference on HbA1c/ApoA-1 ratio was compared between the two groups. According to the tertiles of HbA1c/ApoA-1 levels, patients were divided into high (5.87-16.12), medium (4.50-5.83) and low (2.11-4.48) HbA1c/ApoA-1 groups. Cox proportional risk model was used to evaluate the differences in MACEs and all-cause mortality among the three groups. Kaplan-Meier survival analysis was used to compare the differences of MACEs between the various HbA1c/ApoA-1 groups. Results: A total of 366 ACS patients were included in this study. The mean age of the patients was (65.9±10.3) years. There were 59 MACEs and 10 all-cause deaths during the mean of (22.3±4.4) months follow-up. After adjusting for age, systolic blood pressure, history of diabetes and Gensini score, the incidence of MACEs was 2.45 times higher in the high HbA1c/ApoA-1 group than in the low HbA1c/ApoA-1 group (95%CI 1.16-5.18, P=0.019). There was no significant difference in all-cause mortality between the high and low HbA1c/ApoA-1 groups (P=1.000). Kaplan-Meier survival analysis showed that patients in the high HbA1c/ApoA-1 group had the highest risk of MACEs, while patients in the low HbA1c/ApoA-1 group had the lowest risk of MACEs (P<0.01). Spearman rank correlation analysis showed that HbA1/ApoA-1 ratio was positively correlated with Gensini score in ACS patients (r=0.274, P<0.01). Conclusion: High HbA1c/ApoA-1 ratio was an independent risk factor for MACEs in ACS patients. Patients with high HbA1c/ApoA-1 ratio had more severe coronary artery disease lesions. HbA1c/ApoA-1 ratio may be used as a potential risk stratification biomarker for ACS patients, it might be useful for the early identification of high-risk population and for predicting the incidence of MACEs among ACS patients.

Abstract Background Atherosclerosis is a widely studied pathophysiological foundation of cardiovascular diseases. The gut microbiota and their metabolites are considered independent risk factors for atherosclerosis. Polydatin combined with hawthorn flavonoids (PH), as the extracts of Polygonum cuspidatum Sieb. et Zucc. (P. cuspidatum) and Crataegus pinnatifida Bunge (C. pinnatifida), have shown excellent cardiovascular protective effects. However, the underlying mechanism requires further investigation. Our study aimed to explore the anti-atherosclerotic mechanism of PH through gut microbiota and their metabolites. Methods ApoE−/− mice were fed either a normal-chow diet or a high-fat diet. The PH group received varied doses of polydatin and hawthorn flavonoids: a high dose (polydatin 200 mg/kg daily; hawthorn flavonoids 100 mg/kg daily), a medium dose (polydatin 100 mg/kg daily; hawthorn flavonoids 50 mg/kg daily), and a low dose (polydatin 50 mg/kg daily; hawthorn flavonoids 25 mg/kg daily). The control and model groups were administered distilled water (0.2 mL daily). The experiment lasted for 24 weeks. Results PH administration significantly reduced lipid and inflammatory cytokine levels, meanwhile, the atherosclerotic lesions in a high-fat diet-induced ApoE−/− mice were significantly decreased. Additionally, PH also inhibited the enhancement of trimethylamine N-oxide (TMAO), trimethylamine (TMA) levels of HFD-induced ApoE−/− mice by regulating the expression of hepatic flavin-containing enzyme monooxygenase 3 (FMO3). 16S rRNA sequencing results demonstrated that high-dose PH treatment reduced Firmicutes/Bacteroidetes ratio, increased the abundance of Actinobacteriota, Atopobiaceae and Coriobacteriaea_UCG-002, and decreased the abundance of Desulfobacterota. Norank_f_Muribaculaceae was enriched in the medium-dose PH and simvastatin groups, and Lactobacillus was mainly increased in the simvastatin and the low-dose PH groups. According to the metagenetic results, functional annotations also suggested that the biological processes of each group mainly focused on metabolism-related processes. Specifically, PH may regulate the abundance of TMA-producing bacteria (Coriobacteriaceae, Desulfovibrio, Muribaculum, and Clostridium) and related enzymes in glycolipid metabolic pathways to exert an important effect on the prevention of atherosclerosis. Conclusions Our results suggested that PH could regulate the glucolipid metabolism-related pathway, attenuate inflammatory cytokine levels, and reduce atherosclerotic plaques by remodeling gut microbiota. Trial registration: Not applicable.

Objective:To develop and synthesize a novel derivative of ethyl pyruvate,named TZC02,and investigate its radioprotective effects against ionizing radiation(IR)-induced intestinal injury in mice. Methods:Male C57BL/6J mice weighing(20±2)g in the survival experiment were randomly divided into five groups(n=10 in each):control group,IR group,IR+TZC02(50 mg/kg)group,IR+TZC02(100 mg/kg)group,and IR+TZC02(200 mg/kg)group.Mice's survival rates were monitored for 7 d.In other experiments,the male mice were randomly divided into three groups(n=5 per group):control group,IR group,and IR+TZC02(100 mg/kg)group.TZC02 was intragastrically administered 1 h before 12 Gy abdominal γ-ray irradiation(ABI)and 24 h,48 h after irradiation,respectively.Three days after IR exposure,small intestinal tissues were collected and the number of small intestinal crypts was determined using hematoxylin & eosin(H&E)staining.Immunohis-tochemical analysis was used to assess the regenerative capacity of the small intestine(SI)and radiation-induced damage,stemness markers or DNA repair surrogates,including Ki67,lysozyme,and villus.The expressions of histone H2AX phosphorylation(γH2AX)and caspase-3 were evaluated through immunofluorescence analyses.Additionally,in vitro cultured small intestinal organoids were employed to investigate the effects of TZC02 on SI regeneration after irradiation. Results:The administration of TZC02 significantly improved the 7 d-survival rate of mice exposed to 12 Gy ABI(P＜0.05).Compared to the IR group,TZC02 treatment attenuated the decrease of SI Ki67-positive cells[(59.60± 6.33)vs.(37.70±7.82),t=11.89,P＜0.0001)and Paneth cells[(9.90±1.37)vs.(5.50±1.71),t=6.02,P＜0.001)in five crypts,and reduced structural damage to the SI[villus height,(349.49±60.17)pm vs.(294.72± 40.09)pm;t=3.39;P＜0.05].TZC02 also significantly decreased the crypt apoptosis detected by caspase-3[(10.75±1.26)vs.(29.83±2.56),t=13.39,P＜0.0001)and DNA damage detected by gH2AX[(10.40± 1.14)vs.(29.60±2.70),t=10.13,P＜0.0001)].The organoid survival 7 d post-irradiation further confirmed the protective effects of TZC02(area of organoids,(0.119±0.081)mm2 vs.(0.080±0.037)mm2;t=2.30;P＜0.05). Conclusions:This study demonstrate that TZC02 can offer effective protection against IR-induced intestinal injury,suggesting its potential as a promising protective compound for patients treated with radiotherapy.

Factors affecting the angiographic outcomes of coronary de novo lesions treated with drug-coated balloons (DCBs) have not been well illustrated. The aim of the study is to establish a nomogram for predicting the risk of suboptimal diameter stenosis (DS) at angiographic follow-up. A retrospective analysis was performed on a cohort of patients who underwent DCB intervention for coronary de novo lesions with angiographic follow-up data. Multivariable logistic regression analysis was applied to determine the independent predictors of DS ≥ 30

The risk of cardiovascular disease (CVD) is associated with unusual changes in the human gut microbiota, most commonly coronary atherosclerotic heart disease, hypertension, and heart failure. Immune mechanisms maintain a dynamic balance between the gut microbiota and the host immune system. When one side changes and the balance is disrupted, different degrees of damage are inflicted on the host and a diseased state gradually develops over time. This review summarizes the immune mechanism of the gut microbiota and its metabolites in the occurrence of common CVDs, discusses the relationship between gut-heart axis dysfunction and the progression of CVD, and lists the currently effective methods of regulating the gut microbiota for the treatment of CVDs.