Effects of Sirt1 on proliferation,migration,and apoptosis of endothelial progenitor cells in peripheral blood of SD rats with chronic obstructive pulmonary disease

Objective:To explore the effect of Sirt1 on the function of endothelial progenitor cells(EPCs)in rats with chronic obstructive pulmonary disease(COPD).Methods:A rat COPD model was established via smoking and endotoxin administration for three months.The peripheral circulating EPCs were isolated by gradient centrifugation,and their functions,cell cycle distribution,apoptosis,and Sirt1 expression were examined.The function changes of EPCs in the presence or absence of Sirt1 agonist and inhibitor were estimated;meanwhile,the expressions of Sirt1,FOXO3a,NF-κB,and p53 were also evaluated.Results:The proliferation,adhesion,and migration of EPCs decreased while the apoptosis rate was increased in the COPD rats.The expression of Sirt1 protein in EPCs of the COPD group was significantly lower than that in the control group(P<0.01).The overexpression of the Sirt1 gene using a gene transfection technique or Sirt1 agonists(SRT1720)improved the proliferation,migration,and adhesion,and decreased the apoptosis of EPC.However,Sirt1 inhibitor(EX527)decreased EPC functions in the COPD group.The effect of Sirt1 expression on EPC function may be related to reduction of FOXO3a and increase of NF-κB and p53 activity.Conclusions:Increased expression of Sirt1 can improve the proliferation and migration of EPCs and reduce their apoptosis in COPD rats.This change may be related to FOXO3a,NF-κB,and p53 signaling pathways.

Role of chronic obstructive pulmonary disease in lung cancer pathogenesis

Chronic obstructive pulmonary disease(COPD) and lung cancer are two important smoking related conditions. However, COPD has been shown to be an independent risk factor for lung cancer regardless of smoking history, suggesting that COPD and lung cancer may share a common pathogenesis. This review summarizes the epidemiology of lung cancer and COPD briefly, as well as discussing the potential for shared genetic risk, and shared genomic mechanisms, such as epigenetic changes or DNA damage induced by smoking. How key areas of COPD pathogenesis, such as inflammation, oxidative stress and protease imbalance may contribute to subsequent development of cancer will also be covered. Finally the possibility that consequences of COPD, such as hypoxia, influence carcinogenesis will be reviewed. By understanding the pathogenesis of COPDand lung cancer in detail it is possible that new treatments may be developed and the risk of lung cancer in COPD may be reduced.

Ubiquitin Reduces Expression of Intercellular Adhesion Molecules and Tumor Necrosis Factor-α in Lung Tissue of Experimental Acute Lung Injury

Background Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are two important cytokines in inflammatory response, which may induce rolling and adhesion of both leukocytes and lymphocytes, while modulating vascular permeability at the same time. These adhesion molecules usually serve as surrogate markers of activation and injury of vascular endothelial cells. Tumor necrosis factor-α (TNF-α) is a key factor to induce the expression and production of the above cell adhesion molecules. However, it remains to be elucidated whether exogenous ubiquitin exerts any effect on the cytokines in sepsis-induced ALI. Methods Sixty mice were devided randomly into five groups with twelve mice in each group, i.e. CLP group, SHAM group, UB1 group (10 mg/kg), UB2 group (5 mg/kg) and UB3 group(1 mg/kg). Mice of SHAM group underwent sham operation, and other four groups underwent CLP. Six hours after surgery, mice of three UB groups received ubiquitin by caudal vein injection while CLP and SHAM group received vehicle. Seven hours after surgery, blood and lungs of all mice were collected. ICAM-1, VCAM-1 and TNF-α level of 9% lung homogenate and serum TNF-α level were measured by ELISA. Results Pulmonary ICAM-1, VCAM-1 and TNF-α level of three UB groups were lower than CLP and SHAM group, and there were several comparisons with a statistically significant difference. Serum TNF-α level of three UB groups were slightly lower than CLP group, but far higher than SHAM group. Pulmonary ICAM-1 level, VCAM-1 level and serum TNF-α level of UB3 group were lower than UB1 and UB2 group, and there was a significant difference in VCAM-1 between UB3 and UB1 group. Pulmonary TNF-α level of UB3 group was slightly higher than UB1 and UB2 group.

Research progress of red blood cell distribution width in diagnosis and treatment of lung diseases and prognosis

Lung disease is the disease of the lung itself or lung manifestations of other diseases,including COPD,PTE,CAP,etc.In recent years,the incidence rate has been increased year after year.Many of these diseases have hidden onset and complicated causes.Therefore,accurate diagnosis and treatment are very important.Studies have shown that RDW is closely linked to the diagnosis and treatment of lung diseases.This article analyzes the research on RDW and lung diseases at home and abroad,and briefly summarizes the diagnosis,severity and clinical prognosis of lung diseases by RDW,hoping to provide useful clues and reliable basis for clinical workers,to provide assistance for further application research of RDW in lung diseases.

The relationship between platelet endothelial cell adhesion molecule-1 and paraquat-induced lung injury in rabbits

BACKGROUND:Platelet endothelial cell adhesion molecule-1(PECAM-1),also known as CD31,is mainly distributed in vascular endothelial cells.Studies have shown that PECAM-1 is a very significant indicator of angiogenesis,and has been used as an indicator for vascular endothelial cells.The present study aimed to explore the relationship between the expression of PECAM-1 and the degree of acute lung injury(ALI) and fibrosis in paraquat(PQ) induced lung injury in rabbits.METHODS:Thirty-six adult New Zealand rabbits were randomly divided into three groups(12rabbits in each group) according to PQ dosage:8 mg/kg(group A),16 mg/kg(group B),and 32 mg/kg(group C).After PQ infusion,the rabbits were monitored for 7 days and then euthanized.The lungs were removed for histological evaluation.Masson staining was used to determine the degree of lung fibrosis(LF),and semi-quantitative immune-histochemistry analysis to determine the expression of PECAM-1.Pearson's product-moment correlation analysis was performed to evaluate the relationship between the expression of PECAM-1 and the extent of lung injuries expressed by ALI score and degree of LF.RESULTS:Rabbits in the three groups showed apparent poisoning.The rabbits survived longer in group A than in groups B and C(6.47±0.99 days vs.6.09±1.04 days vs.4.77±2.04 days)(P<0.05).ALI score was lower in group A than in groups B and C(8.33±1.03 vs.9.83±1.17 vs.11.50±1.38)(P<0.05),and there was statistically significant difference between group B and group C(P=0.03).LF was slighter in group A than in groups B and C(31.09%±2.05%vs.34.37%±1.62%vs.36.54%±0.44%)(P<0.05),and there was statistically significant difference between group B and group C(P=0.026).The PEACAM-1 expression was higher in group A than in groups B and C(20.31%±0.70%vs.19.34%±0.68%vs.18.37%±0.46%)(P<0.05),and there was statistically significant difference between group B and group C(P=0.017).Pearson's correlation analysis showed that the expression of PECAM-1 was negatively correlated to both ALI score(Coe=-0.732,P=0.001)and degree of LF(Coe=-0.779,P<0.001).CONCLUSIONS:The PECAM-1 expression significantly decreases in New Zealand rabbits after PQ poisoning,and the decrease is dose-dependent.The PECAM-1 expression is negatively correlated with ALI score and LF,showing a significant role in the development of lung injuries induced by PQ.

<i>ARFGEF2</i>Knockdown Enhances TNF-<i>α</i>Induced Endothelial Expression of the Cell Adhesion Molecules <i>VCAM1</i>and <i>ICAM1</i>

Sickle cell anemia (SCA) is an autosomal-recessive hemoglobinopathy with a highly variable phenotype. Multiple clinical complications are characteristic of SCA including inflammatory and oxidant damage to both small and large blood vessels, hemolysis, vasoocclusion, and premature mortality. The overall severity of SCA is affected by multiple genetic modifier loci, including ARFGEF2, a gene known to modify TNF-α receptor release from human endothelial cells. In this report, we examine the effect of siRNA mediated knockdown of ARFGEF2 inhuman pulmonary artery endothelial cells and report that TNF-α induced expression of ICAM1 and VCAM1, both important mediators of endo-thelial-leukocyte adhesion, is significantly enhanced after ARFGEF2 knockdown. Levels of ICAM-1 protein are also increased in TNF-α treated endothelial cells after ARFGEF2 knockdown;the increased ICAM-1 appears to be localized in the cytoplasm. IL-1β stimulation of endothelial cells without ARFGEF2 produced enhanced ICAM1 expression only. Additionally, ARFGEF2 knockdown distinctly altered endothelial cell morphology. Large-vessel pathology in SCA is believed to begin with endothelial activation by inflammatory cytokines and adhesion of sickle erythrocytes and leukocytes, leading to a progressive vasculopathy characterized by smooth muscle cell migration and proliferation. Understanding how variability in the function of ARFGEF2 alters the response of pulmonary vasculature to TNF-α might suggest new targets for SCA treatment.

Adhesion molecule and proinflammatory cytokine gene expression in hepatic sinusoidal endothelial cells following cecal ligation and puncture

INTRODUCTIONMultiple organ dysfunction syndrome (MODS) isthought to be a frequent consequence of sepsis[1-3].Despite substantial advances in our knowledge and understanding of the basic pathophysiologic mechanisms[4-7], in critically ill patients infections and sepsis are still associated with a high mortality[8,9].

Circulating Adhesion Molecules in Patients with Keshan Disease and Their Relationship with Coxsackie B Virus Infection

This study determined the levels of serum soluble intercellular adhesion molecule-1 （sI-CAM-l） and soluble vascular cell adhesion molecular-1 （sVCAM-1） in patients with different types of Keshan disease （KD）, examined the relationship between Coxsackie B virus-specific IgM antibody （CBV-IgM） and slCAM-1 or sVCAM-1 in KD patients, and investigated the role of these adhesion molecules in the pathogenesis of KD and their clinical implications. The levels of serum slCAM-1, sVCAM-1 and CBV-IgM were measured by using enzyme-linked immunosorbent assay in 22 patients with chronic Keshan disease （CKD）, 27 with latent Keshan disease （LKD） and 28 healthy controis. The subjects in different groups were adjusted for sex and age. Echocardiography was adopted to determine left ventricular ejection fraction （LVEF） in 22 patients with CKD. The results showed that CKD patients had significantly higher levels of slCAM-1 and sVCAM-1 than LKD patients and healthy controls （P〈0.01 for all）. And there was significant difference in the levels of the 2 adhesion molecules between LKD patients and healthy controls （P〈0.05）. A negative correlation was found between LVEF and slCAM-1 or sVCAM-1 in CKD patients. The percentage of CBV-specific IgM positive individuals in KD patients was significantly higher than that of healthy controls. In CVB-specific IgM positive patients, the levels of serum slCAM-1 and sVCAM-1 were significantly greater than those in CBV-specific IgM negative counterpart. It was concluded that the increase in the levels of slCAM-1 and sVCAM-1 suggests the progression of inflammation in KD. slCAM-1 and sVCAM-1 can promote the development of myocardial pathology and lead to poor myocardial function. The increased serum slCAM-1 and sVCAM-1 in KD patients may be related to CBV infection.

Heart Valve Lesions Due to the Formation of a Beta-Hemolytic Streptococ Role of Adhesion Molecules

Objectives: A rise in the levels of adhesion molecules such as VCAM-1, ICAM-1and E-selectin in valve disease patients has been reported lately. In our study, by detecting the presence of adhesion molecule expression in the valve endothelium we will try to show the level of adhesion molecules in peripheral blood leucocytes. Materials and Methods: Valve samples were obtained from patients having undergone aortic and mitral valve replacement due to symptomatic aortic stenosis/aortic insufficiency and/or mitral stenosis/mitral insufficiency. The clinical preoperative diagnosis was made using two-dimensional echocardiography and Doppler echocardiography. Rheumatic valves were in group B (n = 20). Group A (n = 8) constituted the control group. Immunohistochemical staining was performed using CD4, CD8, CD54/ICAM-1, and CD106/VCAM-1. Flow cytometric analysis was performed. The Kolmogorov-Smirnov test and Fisher’s exact test were used for the comparison of categorical variables. Results: Group A (non-rheumatic) patients were found to be older than group B (rheumatic) patients (59.8 ± 11.4 years vs. 45.3 ± 11.8 years, p = 0.008). In group B VCAM-1 level was higher than that of group A (296.6 ± 21.2 vs. 258.5 ± 42.1, p = 0.004). CD11b monocyte in group B was higher than in group A (98.8 ± 0.5 vs. 92.9 ± 9.7, p = 0.003). CD11b granulocyte was higher in group B than in group A (99.96 ± 0.05 vs. 93.79 ± 13.26, p = 0.33). Significant differences were not determined in the other parameters. Conclusion: The fact that increases in serum VCAM-1 and CD-11b only occurred in patients with rheumatic valvular disease in our study suggests that inflammation in patients with the same hemodynamic disorder is higher in rheumatic valvular disease than in the ones with non-rheumatic valvular disease.

Correlation between endothelia cells activation and imbalance of cytokines in pulmonary hypertension of congenital heart disease

Objective To explore the correlation between endothelia cells activation and cytokines (ET-1, NO) levels in patients with pulmonary hypertension (PH), and to discuss their roles in the development of PH. Methods Twenty patients with simple ventricular septal defect (VSD) were chosen as controls, and 30 patients with PH were studied. Plasma levels of ET-1 and NO were measured by radioimmunoassay or colorimetric method. Before cardiopulmonary bypass was established, the specimens from right lung were fixed with formaldehyde solution, embedded with paraffin and stained by SP immunohistochemistry. Intercellular adhesion molecule-1 (ICAM-1) expression was measured through the determination of the light density with computer imaging technology. Results Compared with that of the patients with simple VSD, the light density of ICAM-1 and plasma level of ET-1 increased in patients with PH; but plasma level of NO decreased (P<0.05). Positive correlation was observed between ICAM-1 and ET-1/NO (P<0.05). Conclusion Endothelia cells activation and imbalance of ET-1/NO might play an important role in the development of PH.

Promising new treatment targets in patients with fibrosing lung disorders

The processes of lung fibrogenesis and fibrotic healing are common to a number of conditions with different etiologies. The lungs are the only affected organ in some cases, whereas in others, several organ systems are involved. Therapeutic options can be discussed from various perspectives. In this review, we address the localization of therapeutic targets with regard to cell compartments, including secreted ligands, cell surface, plasma membrane-cytosol interplay, cytosol and nucleus. Complex approach using stem cell therapy is also discussed. As the prognosis of patients with these disorders remains grim, treatment combinations targeting different molecules within the cell should sometimes be considered. It is reasonable to assume that blocking specific pathways will more likely lead to disease stabilization, while stem cell-based treatments could potentially restore lung architecture. Gene therapy could be a candidate for preventive care in families with proven specific gene polymorphisms and documented familial lung fibrosis. Chronobiology, that takes into account effect of circadian rhythm on cell biology, has demonstrated that timed drug administration can improve treatment outcomes. However, the specificrecommendations for optimal approaches are still under debate. A multifaceted approach to interstitial lung disorders, including cooperation between those doing basic research and clinical doctors as well as tailoring research and treatment strategies toward(until now) unmet medical needs, could improve our understanding of the diseases and, above all, provide benefits for our patients.

Expressions of ICAM-1 and its mRNA in sera and tissues of patients with hepatocellular carcinoma

INTRODUCTIONThe increased expression of ICAM-1 on a widerange of cells and in the sera of patients withmalignancies, chronic liver diseases andinflammation diseases has been described since thelate 1980s[1-22]. Recently rapid progress in studieson expression of ICAM-1 in patients withhepatocellular carcinoma ( HCC ) have beenachieved, including clinical and experimentalresearches[23-31].

冠心病患者血清VCAM-1、miR-145、Gal-3、SFRP5水平变化

目的探讨冠心病患者血清血管细胞黏附分子-1(VCAM-1)、miR-145、半乳糖凝集素-3(Gal-3)、分泌型卷曲蛋白5(SFRP5)水平变化及意义。方法选取冠心病患者80例为冠心病组,另收集健康志愿者40名为健康对照组。采集清晨空腹肘静脉血,酶联免疫吸附法测定血清VCAM-1、Gal-3、SFRP5浓度;RT-PCR检测血清miR-145表达水平。根据冠脉造影检查诊断的病变支数分为单支病变、双支病变、多支病变。收集两组受试者人口学特征及冠心病患者实验室指标;进行1 a随访,记录不良预后发生情况(病情加重再入院、死亡)。结果冠心病组患者血清VCAM-1、Gal-3水平明显高于健康对照组,miR-145、SFRP5水平明显低于健康对照组(均P<0.01)。急性心肌梗死组患者血清VCAM-1、Gal-3水平明显高于不稳定型心绞痛组、稳定型心绞痛组患者,血清miR-145、SFRP5水平明显低于不稳定型心绞痛组、稳定型心绞痛组患者(均P<0.05)。多支病变患者血清VCAM-1、Gal-3水平明显高于双支病变和单支病变患者,血清miR-145、SFRP5水平明显低于双支病变和单支病变患者(均P<0.05)。预后不良组患者血清VCAM-1、Gal-3水平明显高于预后良好组患者,miR-145、SFRP5水平明显低于预后良好组患者(均P<0.01)。VCAM-1、miR-145、Gal-3、SFRP5水平是冠心病患者预后的独立影响因素;ROC曲线分析显示,血清VCAM-1、miR-145、Gal-3、SFRP5水平联合检测对冠心病患者预后具有较高的预测价值(AUC=0.928)。结论冠心病患者血清VCAM-1、Gal-3水平高表达,miR-145、SFRP5水平低表达,且与冠心病分类、冠脉病变支数密切相关,联合检测对预后具有较高的预测价值。

血清IL-8、ESM-1、VAP-1在慢性阻塞性肺疾病临床诊断及病情评估中的应用

目的探讨慢性阻塞性肺疾病(COPD)患者血清白细胞介素-8(IL-8)、内皮特异性分子-1(ESM-1)、血管黏附蛋白-1(VAP-1)表达水平,分析其与病情程度相关性及其对COPD的诊断价值。方法选取2021年11月至2022年8月郑州大学第一附属医院收治的153例COPD患者为研究对象,其中COPD稳定期42例(设为SCOPD组)、COPD急性加重期111例(设为AECOPD组),同时选取同期于医院体检的健康志愿者51例为对照组。比较两组临床资料及血清IL-8、ESM-1、VAP-1水平。对比不同病情程度患者血清IL-8、ESM-1、VAP-1水平。分析血清各指标与肺功能、生化指标、病情程度相关性。评价血清各指标对SCOPD、AECOPD的诊断价值。结果AECOPD组、SCOPD组血清IL-8、ESM-1、VAP-1水平高于对照组,且AECOPD组高于SCOPD组(P<0.05);IL-8、ESM-1、VAP-1与生化指标、COPD评估测试表(CAT)、病情程度呈正相关,与肺功能呈负相关(P<0.05);血清各指标联合诊断SCOPD与AECOPD的曲线下面积(AUC)大于单独指标诊断(P<0.05)。结论血清IL-8、ESM-1、VAP-1与COPD病情严重程度相关,联合检测其水平对COPD具有一定诊断价值,可能作为疾病诊断、病情评估的重要指标。

2型糖尿病下肢血管病变患者介入治疗后血清NLRP3及sVCAM-1水平对再狭窄的意义

目的探讨2型糖尿病下肢血管病变患者介入治疗后血清NOD样受体蛋白3(NLRP3)及可溶性血管细胞黏附分子-1(sVCAM-1)水平对再狭窄的意义。方法回顾性分析2022年1月~2023年1月于河北省邯郸市中心医院血管介入科104例成功行血管介入治疗的2型糖尿病下肢血管病变患者的临床资料。根据介入后再狭窄发生情况分为再狭窄组(n=20)和无再狭窄组(n=84),比较两组患者一般资料及介入后24 h血清NLRP3、sVCAM-1水平,采用多因素Logistic回归模型分析再狭窄发生的影响因素;创建受试者工作特征(ROC)曲线,分析血清NLRP3、sVCAM-1检测对再狭窄的预测价值。结果与无再狭窄组相比,再狭窄组患者2型糖尿病病程、下肢动脉病变长度更长,Fontaine分期Ⅳ期占比、下肢动脉完全闭塞占比及血清糖化血红蛋白(HbA1c)、超敏C反应蛋白(hs-CRP)、NLRP3、sVCAM-1水平更高(P<0.05);多因素Logistic回归分析显示,下肢动脉完全闭塞、下肢动脉病变长度、HbA1c、NLRP3及sVCAM-1是2型糖尿病下肢血管病变患者介入后再狭窄发生的影响因素(P<0.05);ROC曲线显示,血清NLRP3、sVCAM-1联合检测对2型糖尿病下肢血管病变患者介入后再狭窄发生的预测价值较高,敏感度为95.00%,特异度为71.43%,ROC曲线下面积为0.929。结论血清NLRP3、sVCAM-1水平高表达均是2型糖尿病下肢血管病变患者介入治疗后再狭窄发生的危险因素,二者联合检测能提高2型糖尿病下肢血管病变患者介入治疗后再狭窄预测的准确性。

规范管理在非小细胞肺癌合并慢性阻塞性肺疾病患者中的应用效果分析

目的:分析规范管理在非小细胞肺癌(NSCLC)合并慢性阻塞性肺疾病(COPD)患者中的应用效果。方法:选取2021年1月—2022年6月佛山市第一人民医院收治的NSCLC合并COPD患者60例为研究对象,按照随机数字表法分为对照组与观察组,各30例。对照组实施常规护理,观察组在对照组基础上开展规范管理。比较两组住院情况、肺功能、负性情绪、生活质量。结果:观察组机械通气时间、住院时间短于对照组,差异有统计学意义(P<0.001);护理后,两组第1秒用力呼气容积、用力肺活量水平升高,观察组高于对照组,差异有统计学意义(P<0.05);护理后,两组焦虑自评量表、抑郁自评量表评分降低,观察组低于对照组,差异有统计学意义(P<0.05);护理后,两组欧洲癌症研究及治疗组织生活质量核心量表评分降低,观察组低于对照组,差异有统计学意义(P<0.05)。结论:规范管理可缩短NSCLC合并COPD患者恢复时间,改善其肺功能,缓解其负性情绪,提高其生活质量。

冠心病患者外周血miR-126水平与PCI术后支架内再狭窄、血清hs-CRP及sVCAM-1水平的关系

目的分析冠状动脉粥样硬化性心脏病(冠心病)患者外周血miR-126水平与经皮冠状动脉介入治疗(PCI)术后支架内再狭窄(ISR)、血清超敏C反应蛋白(hs-CRP)及可溶性血管细胞黏附分子-1(sVCAM-1)水平的关系。方法选取2021年2月至2022年2月于北京航天总医院收治的冠心病患者103例(病例组),所有患者均接受PCI。病例组中急性心肌梗死32例(AMI组),不稳定型心绞痛42例(UAP组),稳定型心绞痛29例(SAP组),另选取同期50例非冠心病的健康体检者作为对照组。分别检测外周血miR-126、hs-CRP、sVCAM-1水平及PCI术后ISR的发生情况,分析miR-126水平与PCI术后支架内再狭窄、hs-CRP及sVCAM-1水平的相关性。结果病例组的miR-126表达水平明显低于对照组,hs-CRP、sVCAM-1表达水平明显高于对照组(P<0.05);三组不同类型冠心病患者的miR-126、hs-CRP、sVCAM-1水平比较,差异有统计学意义(P<0.05)。AMI组的miR-126表达水平明显低于UAP组和SAP组(P<0.05),UAP组的miR-126表达水平明显低于SAP组(P<0.05),AMI组的hs-CRP、sVCAM-1表达水平明显高于UAP组和SAP组(P<0.05)。UAP组的hs-CRP、sVCAM-1表达水平明显高于SAP组(P<0.05);ISR组的miR-126表达水平明显低于未ISR组,hs-CRP、sVCAM-1表达水平明显高于未ISR组(P<0.05)。冠心病患者miR-126水平与hs-CRP、sVCAM-1水平均呈明显负相关(P<0.05),hs-CRP水平与sVCAM-1水平呈明显正相关(P<0.05)。结论miR-126水平与冠心病患者PCI术后ISR密切相关,可能通过患者的炎症反应、动脉粥样硬化促进PCI术后ISR的发生。

血清ESM-1、sICAM-1水平对帕金森病患者发生认知障碍的预测价值

目的:分析血清内皮细胞特异性分子-1(ESM-1)、可溶性细胞间黏附分子-1(sICAM-1)水平对帕金森病(PD)患者发生认知障碍的预测价值。方法:选取2020年8月至2022年12月该院收治的93例PD患者进行前瞻性研究,根据蒙特利尔认知评估量表(MoCA)评分将其分为认知正常组(n=50)和认知障碍组(n=43),另选取同期50名健康体检者,设为对照组。比较三组ESM-1、sICAM-1水平及MoCA评分,采用Pearson相关性分析血清ESM-1、sICAM-1水平与认知障碍的相关性,并绘制受试者工作特征(ROC)曲线分析血清ESM-1、sICAM-1单项及联合检测预测PD患者发生认知障碍的价值。结果:认知障碍组、认知正常组血清ESM-1水平、MoCA评分均低于对照组,且认知障碍组低于认知正常组,差异有统计学意义(P<0.05);认知障碍组、认知正常组血清sICAM-1水平均高于对照组,且认知障碍组高于认知正常组,差异有统计学意义(P<0.05);Pearson相关性分析结果显示,血清ESM-1水平与认知功能呈正相关(r>0,P<0.05);血清sICAM-1水平与认知功能呈负相关(r<0,P<0.05);ROC曲线结果显示,血清ESM-1、sICAM-1水平单项及联合预测PD患者发生认知障碍的曲线下面积分别为0.643、0.605、0.911,其中联合检测预测价值最高。结论:血清ESM-1水平与认知功能呈正相关,血清sICAM-1水平与认知功能呈负相关,且血清ESM-1、sICAM-1水平联合检测预测PD患者发生认知障碍的价值高于两者单项检测预测价值。