Innovation drives technological progress and industrial development, which in turn fuels economic growth, while fair competition improves resource allocation and sustains market vitality. Intellectual property protection (IPP) acts as a vital instrument for catalyzing creativity and preserving a vibrant commercial ecosystem. However, there is still limited empirical evidence at the micro level regarding how IPP helps enhance economic resilience against external shocks, as well as the mechanisms through which such effects occur. Leveraging the rollout of the National Intellectual Property Model Cities (NIPMC) policy in China, this paper constructs a quasi-experimental framework that examines how IPP bolsters urban economic resilience (UER) and elucidates the mechanisms at work. Evidence from a city-level panel of 282 Chinese cities spanning 2010–2021, analyzed through a difference-in-differences strategy, indicates that the NIPMC policy exerts a positive and significant impact on urban economic resilience.Mechanism-oriented evidence suggests that the identified impact is primarily transmitted via three dimensions: an enlarged labor base, intensified knowledge diffusion, and the clustering of digital industries. In addition, the resilience-enhancing role of the NIPMC policy is stronger in cities characterized by more stringent IPP enforcement, more favorable trade credit environments, and locations in China’s central and western regions. Collectively, these results underscore the importance of IPP in reinforcing urban economic resilience through multiple structural channels.

In recent years, much research has been conducted on the carbon emissions trading scheme policy. However, more studies need to focus on the impact of the carbon emissions trading scheme on corporate strategy. In order to address this research gap, drawing on panel data of Chinese A-share listed companies from 2008 to 2020, a quasi-natural experiment was conducted on the impact of the carbon emissions trading scheme on corporate strategic deviance, using a staggered DID model. The results showed that the carbon emissions trading scheme is positively related to corporate strategic deviance, and this relationship has a significant lag. The mechanism analysis demonstrated that the carbon emissions trading scheme can promote innovation quality and environmental performance, thereby indirectly promoting improvement in corporate strategic deviance. The heterogeneity analysis revealed that the carbon emissions trading scheme has a more significant positive relationship with corporate strategic deviance in non-state-owned enterprises, highly polluting industries, and provinces with weak environmental regulation.

Improving the energy efficiency (EE) of thermal power plants is critical for achieving carbon neutrality in China. This work aims to simulate the long-term and regional energy efficiency and CO2 reduction potential (CRP) of the thermal power sector for 30 provinces/municipalities of China under various socioeconomic conditions by using the Windows DEA method. The results showed that developed regions achieved concentrated EE scores above 0.9, whereas developing and less developed regions exhibited relatively lower scores, ranging from 0.71 to 0.86. This highlights a clear disparity, with developed provinces demonstrating higher energy efficiency compared to less developed ones. Further, the total CRP for 30 provinces/municipalities in 2060 was predicted to be 0.88, 0.85 and 0.75 billion t-CO2 under SSP1, SSP2, and SSP3 scenarios, respectively. These estimates suggest that upgrading low-efficiency plants to the best-performing levels could reduce approximately 24.0%, 23.2%, 20.5% of the total CO2 emissions from China's electricity sector. All these results clearly suggest that China's thermal power sector has tremendous potential to mitigate CO2 through technological advancement for realizing China's carbon neutrality goal by 2060.

Atherosclerotic cardiovascular disease is a leading cause of morbidity and mortality globally. Elevated levels of serum LDL-C (low-density lipoprotein cholesterol) represent a significant risk factor for atherosclerosis. LDLR (low-density lipoprotein receptor) plays a critical role in LDL-C uptake and clearance, with its recycling to the cell surface being essential for maintaining LDLR availability. However, the molecular mechanisms underlying LDLR homeostasis and recycling remain poorly defined. SNX (sorting nexin) proteins and Rab (Ras-associated binding protein) GTPases are key regulators of vesicle transport and endosomal sorting and are implicated in LDLR endocytosis, recycling, and subsequent cholesterol metabolism. This review aims to summarize the data on the roles of SNX17, Rab11, and Rab5 in LDLR recycling and endosomal dynamics, highlighting their potential as therapeutic targets for managing dyslipidemia and associated diseases.

Atherosclerosis, a leading cause of cardiovascular disease, is driven by a complex interplay of dyslipidemia, inflammation, and arterial plaque formation and progression. Animal models are indispensable to elucidate the pathogenesis and develop novel therapies. Rodent models are widely utilized due to their cost-effectiveness, reproducibility, and rapid disease progression. However, notable species differences exist in lipoprotein composition and lipid metabolism pathways. Mice and rats exhibit an HDL-dominant profile, whereas Syrian golden hamsters express cholesteryl ester transfer protein (CETP) and display a higher LDL fraction, but lower than that of humans, offering a model closer to human metabolically. Divergent CETP activity across species further complicates the translational relevance of the findings from these models for atherosclerosis and related metabolic disorders. This review systematically examines the key factors in rodent model selection and optimization, with consideration on the roles of sex and age. We focus on three commonly used and well-characterized rodent strains prone to atherosclerosis: C57BL/6J mice, Sprague-Dawley (SD) rats, Wistar rats, and golden hamsters. On Apoe-/- or Ldlr-/- backgrounds, male C57BL/6 mice, owing to their pronounced hypercholesterolemia and extended survival with high-fat diet, are preferentially used in late-stage plaque stability studies. In contrast, male SD or Wistar rats develop atherosclerosis slowly with limited lesion progression, while hamsters, despite their human-like lipid metabolism, exhibit substantial individual variability and lesions that typically arrest at early fatty streaks with poor reproducibility. Therefore, rats and hamsters are better suited for studies focusing on early disease mechanisms and human-mimetic lipid metabolism.

Background: Curcumin nicotinate (Curtn), derived from curcumin and niacin, reduces serum LDL-C levels, partly due to its influence on PCSK9. This study investigates IDOL's role in Curtn's lipid -lowering effects. Objective: To elucidate Curtn's regulation of the IDOL/LDLR pathway and potential molecular mechanisms in hepatocytes. Methods: Differential metabolites in Curtn-treated HepG2 cells were identified via LC -MS. Molecular docking assessed Curtn's affinity with IDOL. Cholesterol content and LDLR expression effects were studied in high -fat diet Wistar rats. In vitro evaluations determined Curtn's influence on IDOL overexpression's LDL-C uptake and LDLR expression in hepatocytes. Results: Lipids were the main differential metabolites in Curtn-treated HepG2 cells. Docking showed Curtn's higher affinity to IDOL's FERM domain compared to curcumin, suggesting potential competitive inhibition of IDOL's binding to LDLR. Curtn decreased liver cholesterol in Wistar rats and elevated LDLR expression. During in vitro experiments, Curtn significantly enhanced the effects of IDOL overexpression in HepG2 cells, leading to increased LDL-C uptake and elevated expression of LDL receptors. Conclusion: Curtn modulates the IDOL/LDLR pathway, enhancing LDL cholesterol uptake in hepatocytes. Combined with its PCSK9 influence, Curtn emerges as a potential hyperlipidemia therapy.

Abstract Background Nonalcoholic steatohepatitis (NASH) is a prevalent chronic liver condition. However, the potential therapeutic benefits and underlying mechanism of nicotinate-curcumin (NC) in the treatment of NASH remain uncertain. Methods A rat model of NASH induced by a high-fat and high-fructose diet was treated with nicotinate-curcumin (NC, 20, 40 mg·kg− 1), curcumin (Cur, 40 mg·kg− 1) and metformin (Met, 50 mg·kg− 1) for a duration of 4 weeks. The interaction between NASH, Cur and Aldo-Keto reductase family 1 member B10 (AKR1B10) was filter and analyzed using network pharmacology. The interaction of Cur, NC and AKR1B10 was analyzed using molecular docking techniques, and the binding energy of Cur and NC with AKR1B10 was compared. HepG2 cells were induced by Ox-LDL (25 µg·ml− 1, 24 h) in high glucose medium. NC (20µM, 40µM), Cur (40µM) Met (150µM) and epalrestat (Epa, 75µM) were administered individually. The activities of ALT, AST, ALP and the levels of LDL, HDL, TG, TC and FFA in serum were quantified using a chemiluminescence assay. Based on the changes in the above indicators, score according to NAS standards. The activities of Acetyl-CoA and Malonyl-CoA were measured using an ELISA assay. And the expression and cellular localization of AKR1B10 and Acetyl-CoA carboxylase (ACCα) in HepG2 cells were detected by Western blotting and immunofluorescence. Results The results of the animal experiments demonstrated that NASH rat model induced by a high-fat and high-fructose diet exhibited pronounced dysfunction in liver function and lipid metabolism. Additionally, there was a significant increase in serum levels of FFA and TG, as well as elevated expression of AKR1B10 and ACCα, and heightened activity of Acetyl-CoA and Malonyl-CoA in liver tissue. The administration of NC showed to enhance liver function in rats with NASH, leading to reductions in ALT, AST and ALP levels, and decrease in blood lipid and significant inhibition of FFA and TG synthesis in the liver. Network pharmacological analysis identified AKR1B10 and ACCα as potential targets for NASH treatment. Molecular docking studies revealed that both Cur and NC are capable of binding to AKR1B10, with NC exhibiting a stronger binding energy to AKR1B10. Western blot analysis demonstrated an upregulation in the expression of AKR1B10 and ACCα in the liver tissue of NASH rats, accompanied by elevated Acetyl-CoA and Malonyl-CoA activity, and increased levels of FFA and TG. The results of the HepG2 cell experiments induced by Ox-LDL suggest that NC significantly inhibited the expression and co-localization of AKR1B10 and ACCα, while also reduced levels of TC and LDL-C and increased level of HDL-C. These effects are accompanied by a decrease in the activities of ACCα and Malonyl-CoA, and levels of FFA and TG. Furthermore, the impact of NC appears to be more pronounced compared to Cur. Conclusion NC could effectively treat NASH and improve liver function and lipid metabolism disorder. The mechanism of NC is related to the inhibition of AKR1B10/ACCα pathway and FFA/TG synthesis of liver.

Aim: To explore the association of hyperhomocysteinaemia (HHcy) and diabetes synergies with cardiovascular events in the adult population of northern China. Methods: Data were collected from the Asymptomatic Polyvascular Abnomalities Community study for 2010 to 2019. Serum homocysteine (Hcy) levels were determined by enzyme-linked immunosorbent assay. The participants were categorized into four groups based on their Hcy levels and diabetes status: non-diabetes/non-HHcy, non-diabetes/HHcy, diabetes/non-HHcy and diabetes/HHcy. The composite endpoint consisted of the occurrence of first-ever stroke, myocardial infraction (MI) or all-cause mortality. Cox regression analyses were performed to evaluate the associations of diabetes and HHcy with cardiovascular disease (CVD) events. Results: In total, 5278 participants were eligible (average age 55.1 years, 60% male). Over a follow-up of 9.1 years, 618 events were identified, 202 stroke, 52 MI and 406 all-cause deaths. Compared with the non-diabetes/non-HHcy group, hazard ratios with 95% confidence intervals in the diabetes/HHcy group for stroke, MI, major adverse cardiovascular event (MACE), all-cause death and composite endpoint were 1.85 (1.12-3.04), 1.33 (0.42-4.23), 1.78 (1.13-2.80), 2.24 (1.56-3.23) and 1.97 (1.47-2.65), respectively. Significant interactions between HHcy and diabetes status were found for stroke, MI and MACE (P for interaction = .002, .027 and .044, respectively). In addition, the association of diabetes/HHcy with stroke was modified by age (< 60 and >= 60 years; P for interaction = .016). Conclusions: The findings highlight the synergistic impact of diabetes and HHcy on CVD. Joint assessments of diabetes and Hcy levels should be emphasized for risk stratification and primary prevention of CVD.

Sustainable development has become society's focal point. In this context, China's paper industry needs to be more concerned about a low-carbon strategy. Therefore, a carbon performance evaluation system must be built to guide the low-carbon enterprise transformation. Based on the carbon value flow analysis, this study takes JX Paper (a paper-making enterprise) as an example to construct a carbon performance evaluation system consisting of carbon input, transfer, and output indicators. The quantitative and qualitative index weights were determined through a principal component analysis and an analytical hierarchy process. The overall carbon performance increased from 2012 to 2021, but room remains for improvement. These results show that the performance evaluation system provides a helpful reference for enterprises to identify the key factors affecting carbon emissions and evaluate their carbon performance. Moreover, objective criteria should be developed to improve sustainable enterprise carbon performance and low-carbon competitiveness.

循环经济以资源的高效利用和循环利用为核心,是实现"双碳"目标的有效手段.微观企业作为实现"双碳"目标的主力军,实施低碳循环发展策略是企业可持续发展的关键.基于此背景,文章借鉴资源价值流会计分析方法,构建了循环经济"物质流—碳素流—价值流"三维分析框架并将其运用于重庆钢铁.根据重庆钢铁碳素流与价值流分析结果识别出炼铁、焦化两个高排放、低资源利用率、高环境损害环节;对比循环发展前后环境效益与经济效益发现:循环发展策略实施后碳排放减少了1 078 497.31 吨,经济效益增加了9 837.07 万元."物质流—碳素流—价值流"三维分析框架的应用为重庆钢铁进一步降低碳排放、优化循环经济发展策略指明了方向,也验证了上述理论与分析框架对实现资源节约、经济增值、环境保护具有重要意义,能够促进企业循环经济发展.

低碳经济赋予企业价值新的内涵,开发碳资产是提升企业低碳价值最有效的途径之一.本文以利益相关者、可持续发展及价值链等理论为基础,以丰田汽车公司的低碳实践为研究对象,采用单案例研究法,探索并构建碳资产价值创造机制.研究表明:碳资产与企业价值创造之间存在积极的互动关系;企业的低碳价值创造首先要均衡利益相关者的利益,碳资产可以满足利益相关者的低碳要求,从而为企业的低碳价值创造提供必要条件;碳资产利用低碳价值链得以充分和有效开发,并在低碳基础价值活动和辅助价值活动中得到价值增值和价值实现,为企业创造长期、协同的经济价值和环境价值,促进企业的可持续发展.

Early identification of high-risk patients with Major depressive disorder (MDD) having suicide attempts (SAs) is essential for timely targeted and tailored psychological interventions and medications. This study aimed to develop and validate a web-based dynamic nomogram as a personalized predictor of SA in MDD patients. A dynamic nomogram was developed using data collected from 1718 patients in China. The dynamic model was established based on a machine learning-based regression technique in the training cohort. We validated the nomogram internally using 1000 bootstrap replications. The nomogram performance was assessed using estimates of discrimination (via the concordance index) and calibration (calibration plots). The nomogram incorporated five predictors, including Hamilton anxiety rating scale (odds ratio [OR]: 1.255), marital status (OR: 0.618), clinical global impressions (OR: 2.242), anti-thyroid peroxidase antibodies (OR: 1.002), and systolic pressure levels (OR: 1.037). The model demonstrated good overall discrimination (Harrell’s C -index = 0.823). Using decision curve analysis, this model also demonstrated good clinical applicability. An online web server was constructed ( https://odywong.shinyapps.io/PRSM/ ) to facilitate the use of the nomogram. Based on these results, our study developed a nomogram to predict SA in MDD patients. The application of this nomogram may help for patients and clinicians to make decisions.

BackgroundNicotinamide adenine dinucleotide (NAD+) is a coenzyme and plays a crucial role in several metabolic processes. This study explored the association of nicotinamide adenine dinucleotide (NAD+) levels with metabolic disease (MD) in adults.MethodsIn this cross-sectional study, all data were collected from the Jidong community. MD was defined as the presence of one or more of the following disease components: hypertension, dyslipidemia, diabetes, hyperuricemia, obesity, and non-alcoholic fatty liver disease (NAFLD). The MD components were categorized into three groups: those with one component, those with two components, and those with three to six components. The whole blood NAD+ level was measured using a cycling assay and LC-MS/MS analysis. The participants were divided into four groups based on their NAD+ level quartiles. Multivariable logistic regression was used to evaluate the association of the whole blood NAD+ levels with MD.ResultsOf the 1,394 eligible participants, the average age was 43.2 years, and 74.3% had MD. In the top quartile of NAD+, the prevalence of MD and each of its components (hypertension, hyperlipidemia, diabetes, hyperuricemia, obesity, and NAFLD) were 87.9% 35.2%, 62.3%, 8.7%, 36.9%, 21.0%, and 60.5%, respectively. As compared with the lowest NAD+ quartile (≤29.4 μmol/L), the adjusted odds ratios and 95% confidence interval of the highest quartile were 3.01 (1.87-4.87) for MD, 2.48 (1.44-4.29) for 1 MD component, 2.74 (1.45-5.17) for 2 MD components, and 4.30 (2.32-7.98) for 3-6 MD components. The risk of MD began to increase at NAD+ levels of 31.0 μmol/L, as revealed by the gradient associations of NAD+ levels with MD. There was no significant interaction between age, sex, drinking, smoking, and NAD+ for MD (p for interaction ≥0.10).ConclusionsIncreased NAD+ was significantly associated with MD, as well as its individual components. Our findings provide new evidence for the relationship between blood NAD+ levels and MD.

城乡发展过程中面临的资源耗竭和环境污染等生态问题,成为城市可持续发展与乡村振兴的重要制约因素,如何实现城乡经济社会与生态协调发展成为焦点.论文以粤港澳大湾区为例,利用夜间灯光遥感数据(VIIRS)、植被净初级生产力遥感数据(NPP)搭建评价模型量化2020年粤港澳大湾区市级与区县级的城乡经济社会发展和生态水平,并通过空间相关性模型(Moran's I)、耦合协调度模型分析粤港澳城乡经济社会系统与城乡生态系统之间的空间分布特征和交互耦合关系.研究发现,粤港澳城乡经济社会协调度较高的区域与城乡生态协调度较高的区域空间分布差异显著,城乡经济发展与生态水平之间存在权衡关系.耦合协调度方面,粤港澳大湾区城乡经济社会协调度与城乡生态协调度的耦合协调度普遍良好,珠海以0.871的耦合协调度得分位列第一,但肇庆和深圳以0.315、0.314的耦合协调度得分排在末位,依然存在轻度失调现象.最后,针对研究结果给出相应的政策建议.

面对日益严格的碳排放管制,高排放企业迫切需要科学合理的制度和方法加强碳减排管理.在众多的管理制度和方法中,由预算衍生出的碳预算具有规划碳管理活动、量化碳减排损益等功能和优势.然而,目前并没有通用的碳预算体系指导企业碳排放、碳减排和碳交易活动的开展.基于此背景,本文首先尝试构建由碳排放子预算、碳减排量及成本子预算、碳排放权交易子预算、碳减排净损益子预算组成的企业碳预算体系,进而借鉴交互控制思想,综合考虑碳价、能源价格、政策准则等因素的变动对碳减排损益的影响,构建交互控制视角下的碳预算管理体系,并将其应用于AC航空公司中进行检验.研究结果表明,交互控制下的碳预算体系能根据能源价格等因素的变化动态调整碳管理行为,选择最优的碳减排方案,从而使碳预算成为行之有效的碳减排工具和制度安排.

Curcumin nicotinate (Curtn) is a synthesized ester derivative of curcumin and niacin. Our previous study has shown that Curtn lowers serum low-density lipoprotein cholesterol (LDL-C) levels in apoE-/- mice and promotes LDL-C uptake into HepG2 cells in vitro. The present study was to test the hypothesis that Curtn decreases serum LDL-C levels through decreased expression of pro-protein convertase subtilisin/kexin type 9 (PCSK9) and subsequent increase in LDL receptor expression. Male Wistar rats on high-fat diet (HFD) were treated with Curtn or rosuvastatin. Curtn or rosuvastatin treatment significantly decreased serum levels of total cholesterol (TC) and LDL-C in rats on HFD with increased liver LDL receptor expression. LDL-C-lowering effect of Curtn was not observed in LDL receptor deficient (LDLR-/-) mice on HFD, while rosuvastatin still decreased serum lipid levels in LDLR-/- mice, indicating that the reduction of serum LDL-C levels by Curtn treatment was LDL receptor-dependent. Curtn treatment also significantly decreased the protein expression of PCSK9 in Wistar rats and LDLR-/- mice. In HepG2 cells with overexpression of human PCSK9, Curtn treatment significantly increased LDL-C uptakes into hepatocytes, and increased LDL receptor distribution on cell surface in association with decreased PCSK9 protein expression. RNAi-LDLR significantly attenuated the effect of Curtn on LDLR distribution on cell surface. These data indicates that Curtn would decrease serum LDL-C level at least partially through inhibition of PCSK9 expression, and subsequent increase in LDL receptor expression and distribution in hepatocytes, serving as a potential novel compound to treat hyperlipidemia.

Respiratory infectious diseases have seriously harmed people's daily lives. The analysis of urban functional spatial structure from the perspective of prevention and control of respiratory infectious diseases has practical significance for optimizing the urban functional spatial structure and slowing down the spread of infectious diseases. In this study, kernel density, random forest, geographic weighted spatial analysis, and other methods were used to investigate the spatial relationship between the urban functional spatial structure constructed from multi-source data and confirmed tuberculosis cases. A summary of the main driving factors and the heterogeneous influence of patient gender was provided. Results showed that: (1) the infection risk of confirmed cases in the urban central area was highest and relatively concentrated; (2) the main functional area characteristics that led to the cluster of patients were commercial services (0.4217, 0.2693, 0.3647), and shopping services were the first driving factor of infection risk; (3) In the stratified analysis, the spatial distribution of male patients was greater than that of female patients. Compared to the overall analysis of patients, the spatial correlation between male patients and park green space was the most significant over three years.There is an increasing spatial correlation between public management and the influence location of each functional area. Because of the similarities in spatial transmission and pathology between tuberculosis and COVID-19, this study provides a scientific basis and methodological reference for the scientific prevention and control and precise policy implementation of COVID-19.

文章以石油化工行业2013—2020年沪深A股上市的企业为研究样本,实证研究了石油化工行业上市企业董事会异质性、低碳技术创新与企业绩效之间的关系,进一步验证企业低碳技术创新的中介作用.主要发现和结论是:(1)董事会学术异质性对企业绩效有显著正向影响,对企业低碳技术创新有显著负向影响;(2)董事会社会异质性对企业绩效和企业低碳技术创新有正相关关系,但无显著影响;(3)低碳技术创新对董事会学术异质性与企业绩效的关系起部分中介作用.据此提出了相应的政策建议.

Hyperlipidemia has been demonstrated to evoke Alzheimer disease (AD) pathologies such as Amyloid-β (Aβ) deposition and synaptogenesis dysfunction in the hippocampus. Curcumin gives protection against anti-amyloid properties and synaptogenesis dysfunction. Curcumin-Nicotinate (CurTn), a new type of curcumin derivative, ameliorates cognitive impairment by rescuing autophagic flux in the CA1 hippocampus of diabetic rats. However, whether Curtn possesses an antagonistic effect on AD-related pathologies in the hippocampus induced by hyperlipidemia remains ill-defined. The present study aims to investigate whether CurTn alleviates synaptogenesis dysfunction by promoting the activation of brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrkB)/cAMP-response element binding protein (CREB) signaling and whether the underlying fundamental mechanism involves the elimination of Aβ deposition due to Idol/low-density lipoprotein receptor (LDLR) signaling in the hippocampus of high-fat diet (HFD)-induced hyperlipidemia rats. The results demonstrated that CurTn not only improved synaptogenesis dysfunction in the hippocampus of HFD rats, as evidenced by the increases in the expressions of synapse-related proteins postsynaptic density protein 95 (PSD-95), synapsin-1, and Glutamate receptor 1 (GluR1), but also activated BDNF/TrkB/CREB signaling, as evidenced by the elevation of the expressions of BDNF, pTrkB, and CREB. Moreover, CurTn modulated the Idol/LDLR pathway in the hippocampus of HFD rats, as evidenced by the decreased expression of Idol and the increased expression of LDLR. Furthermore, CurTn eliminated the deposition of Aβ, as evidenced by the reduction in the content of Aβ40 and Aβ42. These results reveal that CurTn may attenuate synaptogenesis dysfunction by activating BDNF/TrkB/CREB signaling, as the possible result of the modulation of Idol/LDLR signaling to eliminate Aβ deposition in the hippocampus of HFD rats.

Endothelial cell (EC) dysfunction is one of the initiating factors of atherosclerosis. EC dysfunction is primarily caused by oxidative damage and inflammation. As a classic non-specific antioxidant and anti-inflammatory drug, curcumin has been widely used in studies of lipid metabolism disorders. However, whether curcumin is able to alleviate H2O2-induced EC damage and its related mechanisms has remained to be elucidated. The present study confirmed the protective effects of curcumin on human umbilical vein endothelial cells (HUVECs). A HUVEC injury model was established using H2O2 and the optimal concentrations and time of curcumin to achieve therapeutic effects were explored. Curcumin was observed to inhibit H2O2-induced pyroptosis by inhibiting the activation of NOD-, LRR- and pyrin domain-containing protein 3. In addition, curcumin improved HUVEC function by restoring αvβ3 and reducing endothelin-1 expression. In conclusion, the results of the present study revealed the mechanism through which curcumin inhibits pyroptosis and indicated that curcumin may have a potential utility in treating diseases of EC dysfunction.