系统性红斑狼疮患者血清NGAL、HMGB1、Gal-3与疾病活动度和颈动脉粥样硬化的关系分析

摘要 目的：分析系统性红斑狼疮（SLE）患者血清中性粒细胞明胶酶相关载脂蛋白（NGAL）、高迁移率族蛋白B1（HMGB1）、半乳糖凝集素-3（Gal-3）与疾病活动度和颈动脉粥样硬化（CAS）的关系。方法：选取2020年1月到2023年3月在徐州市中心医院收治的160例SLE患者。采用酶联免疫吸附法检测血清NGAL、HMGB1 、Gal-3水平。根据SLE疾病活动度指数（SLEDAI）评分将患者分为无活动组（n=48）、重度活动组（n=32）中度活动组（n=39）、轻度活动组（n=41）。同时根据颈动脉彩色多普勒超声检查结果将患者分为CAS组（n=56）和无CAS组（n=104）。对比各组血清NGAL、HMGB1、Gal-3水平的差异。SLE发生CAS的影响因素采用多因素logistic回归分析。结果：无活动组、轻度活动组、中度活动组、重度活动组的血清NGAL、HMGB1 、Gal-3的水平依次升高,整体对比差异有统计学意义（P<0.05）。CAS组的血清NGAL、HMGB1、Gal-3的水平高于无CAS组（P<0.05）。多因素logistic回归分析结果显示,高NGAL、高HMGB1 、高Gal-3高、高年龄、SLE病程长是SLE患者发生CAS的危险因素,而规范应用羟氯喹药物治疗是保护因素（P<0.05）。结论：SLE患者血清NGAL、HMGB1 、Gal-3水平升高,且随着疾病严重程度的增加而增加。同时,高NGAL、HMGB1 、Gal-3、年龄以及SLE病程长是SLE患者发生CAS的危险因素。     

血清Gal-3、NT-pro-BNP及hs-CRP水平与慢性心力衰竭超声心动图指标的相关性研究

摘要 目的：探讨血清半乳糖凝聚素-3（Gal-3）、氨基末端脑钠肽前体（NT-pro-BNP）、超敏C反应蛋白（hs-CRP）水平与慢性心力衰竭超声心动图指标的相关性。方法：选择2018年2月～2019年10月我院收治的慢性心功能衰竭患者112例作为研究组,按美国心脏病协会（NYHA）分级分为Ⅱ级组43例、Ⅲ级组39例、Ⅳ级组30例,另选择同期我院体检的健康人员60例作为对照组,比较研究组和对照组及不同心功能分级的慢性心力衰竭患者血清Gal-3、NT-pro-BNP、hs-CRP 水平和超声心动图指标,分析慢性心力衰竭患者上述指标之间的相关性。结果：研究组血清Gal-3、NT-pro-BNP、hs-CRP水平显著高于对照组,E峰与A峰比值（E/A）及左心室射血分数（LVEF）显著低于对照组（P＜0.05）。随NYHA分级增加,慢性心力衰竭患者血清Gal-3、NT-pro-BNP、hs-CRP水平逐渐升高,E/A和LVEF逐渐降低（P＜0.05）。经Pearson相关性分析显示,慢性心功能衰竭患者血清Gal-3、NT-pro-BNP、hs-CRP分别与E/A、LVEF水平呈负相关关系（P＜0.05）。结论：慢性心力衰竭患者血清Gal-3、NT-pro-BNP、hs-CRP水平异常升高,与超声心动图指标相关,检测Gal-3、NT-pro-BNP、hs-CRP有助于慢性心力衰竭的诊断和病情评估。     

扩张型心肌病患者LVSI、MHR及Gal-3的临床意义及其与NYHA心功能分级的相关性分析

摘要 目的：研究扩张型心肌病（DCM）患者左心室球形指数（LVSI）、单核细胞计数与高密度脂蛋白胆固醇（HDL-C）比值（MHR）和血清半乳糖凝集素-3（Gal-3）的变化,并分析其与DCM患者心功能的关系。方法：选择2018年1月-2022年10月在我院接受治疗的DMC患者68例作为研究组,并选取同期50例健康体检者作为对照组。研究组患者根据出院6个月份是否发生主要不良心血管事件分为MACE组和No-MACE组。比较各组间左心室射血分数（LVEF）、左心室舒张末期内径（LVEDD）、左室收缩末期内径（LVESD）、LVSI、单核细胞计数、HDL-C、MHR以及血清Gal-3。结果：（1）研究组患者LVEF显著低于对照组,而研究组患者LVEDD、LVESD以及LVSI均显著高于对照组（P<0.05）。（2）研究组患者单核细胞计数、HDL-C、MHR以及Gal-3均显著高于对照组（P<0.05）。（3）不同心功能分级DCM患者LVEF、LVEDD、LVESD、单核细胞计数和HDL-C组间比较无显著差异（P>0.05）,但LVSI、MHR和血清Gal-3组间比较差异显著（P<0.05）。（4）MACE组患者LVSI、MHR和Gal-3均显著高于No-MACE组患者（P<0.05）。结论：LVSI、MHR和血清Gal-3在扩张型心肌病患者中升高,并与患者心功能分级有关,可作为DCM患者心功能恶化评价指标。     

Role for Hepatic and Circulatory ST6Gal-1 Sialyltransferase in Regulating Myelopoiesis

Recent findings have established a role for the ST6Gal-1 sialyltransferase in modulating inflammatory cell production during Th1 and Th2 responses. ST6Gal-1 synthesizes the Sia(α2,6) to Gal(β1,4)GlcNAc linkage on glycoproteins on cell surfaces and in systemic circulation. Engagement of P1, one of six promoter/regulatory regions driving murine ST6Gal-1 gene expression, generates the ST6Gal-1 for myelopoietic regulation. P1 utilization, however, is restricted to the liver and silent in hematopoietic cells. We considered the possibility that myelopoiesis is responsive to the sialylation of liver-derived circulatory glycoproteins, such that reduced α2,6-sialylation results in elevated myelopoiesis. However, 2-dimensional differential in gel electrophoresis (2D-DIGE) analysis disclosed only minimal alterations in the sialylation of sera glycoproteins of ST6Gal-1-deficient mice when compared with wild-type controls, either at baseline or during an acute phase response when the demand for sialylation is greatest. Furthermore, sera from ST6Gal-1-deficient animals did not enhance myelopoietic activity in ex vivo colony formation assays. Whereas there was only minimal consequence to the α2,6-sialylation of circulatory glycoproteins, ablation of the P1 promoter did result in strikingly depressed levels of ST6Gal-1 released into systemic circulation. Therefore, we considered the alternative possibility that myelopoiesis may be regulated not by the hepatic sialyl glycoproteins, but by the ST6Gal-1 that was released directly into circulation. Supporting this, ex vivo colony formation was notably attenuated upon introduction of physiologic levels of ST6Gal-1 into the culture medium. Our data support the idea that circulatory ST6Gal-1, mostly of hepatic origin, limits myelopoiesis by a mechanism independent of hepatic sialylation of serum glycoproteins.     

2型糖尿病合并冠心病患者血清IL-6、PCT、CatS、Gal-3与糖脂代谢、胰岛素抵抗和心功能的相关性分析

摘要 目的：探讨2型糖尿病（T2DM）合并冠心病患者血清白介素-6（IL-6）、降钙素原（PCT）、组织蛋白酶S（CatS）、半乳糖凝集素3（Gal-3）与糖脂代谢、胰岛素抵抗和心功能的相关性。方法：选择我院2019年2月～2021年2月收治的102例T2DM患者,将其根据是否伴有冠心病分成单纯T2DM组（n=62）和T2DM合并冠心病组（n=40）。另取同期健康体检人员50例作为对照组。比较三组血清IL-6、PCT、CatS、Gal-3水平。对比单纯T2DM组与T2DM合并冠心病组间糖脂代谢、胰岛素抵抗和心功能指标差异,并分析血清IL-6、PCT、CatS、Gal-3与上述指标的相关性。结果：单纯T2DM组、T2DM合并冠心病组的血清IL-6、PCT、CatS、Gal-3水平均高于对照组,且T2DM合并冠心病组上述各项指标水平均高于单纯T2DM组（P＜0.05）。T2DM合并冠心病组空腹血糖（FPG）、低密度脂蛋白胆固醇（LDL-C）水平以及胰岛素抵抗指数（HOMA-IR）均高于单纯T2DM组（P＜0.05）,而两组间餐后2 h血糖（2hPG）、糖化血红蛋白（HbA1c）、甘油三酯（TG）、总胆固醇（TC）、高密度脂蛋白胆固醇（HDL-C）、空腹胰岛素（FINS）水平比较无统计学差异（P>0.05）。T2DM合并冠心病组左心室射血分数（LVEF）、左心室收缩末期容积（LVESV）及左心室舒张末期容积（LVEDV）均低于单纯T2DM组（P＜0.05）。Pearson相关性分析结果显示：T2DM合并冠心病患者的血清IL-6、PCT、CatS、Gal-3水平与LDL-C水平、HOMA-IR均呈正相关,而与LVEF、LVESV、LVEDV均呈负相关（P＜0.05）。结论：T2DM合并冠心病患者血清IL-6、PCT、CatS、Gal-3水平呈异常高表达,且和糖脂代谢、胰岛素抵抗和心功能密切相关,对患者病情具有一定辅助评估价值。     

Degeneration of dystrophic or injured skeletal muscles induces high expression of Galectin-1

Muscle degenerative diseases such as Duchenne Muscular Dystrophy are incurable and treatment options are still restrained. Understanding the mechanisms and factors responsible for muscle degeneration and regeneration will facilitate the development of novel therapeutics. Several recent studies have demonstrated that Galectin-1 (Gal-1), a carbohydrate-binding protein, induces myoblast differentiation and fusion in vitro, suggesting a potential role for this mammalian lectin in muscle regenerative processes in vivo. However, the expression and localization of Gal-1 in vivo during muscle injury and repair are unclear. We report the expression and localization of Gal-1 during degenerative-regenerative processes in vivo using two models of muscular dystrophy and muscle injury. Gal-1 expression increased significantly during muscle degeneration in the murine mdx and in the canine Golden Retriever Muscular Dystrophy animal models. Compulsory exercise of mdx mouse, which intensifies degeneration, also resulted in sustained Gal-1 levels. Furthermore, muscle injury of wild-type C57BL/6 mice, induced by BaCl(2) treatment, also resulted in a marked increase in Gal-1 levels. Increased Gal-1 levels appeared to localize both inside and outside the muscle fibers with significant extracellular Gal-1 colocalized with infiltrating CD45(+) leukocytes. By contrast, regenerating muscle tissue showed a marked decrease in Gal-1 to baseline levels. These results demonstrate significant regulation of Gal-1 expression in vivo and suggest a potential role for Gal-1 in muscle homeostasis and repair.     

Galectin-3 exacerbates ox-LDL-mediated endothelial injury by inducing inflammation via integrin β1-RhoA-JNK signaling activation

Oxidized low-density lipoprotein (Ox-LDL)-induced endothelial cell injury plays a crucial role in the pathogenesis of atherosclerosis (AS). Plasma galectin-3 (Gal-3) is elevated inside and drives diverse systemic inflammatory disorders, including cardiovascular diseases. However, the exact role of Gal-3 in ox-LDL-mediated endothelial injury remains unclear. This study explores the effects of Gal-3 on ox-LDL-induced endothelial dysfunction and the underlying molecular mechanisms. In this study, Gal-3, integrin β1, and GTP-RhoA in the blood and plaques of AS patients were examined by ELISA and western blot respectively. Their levels were found to be obviously upregulated compared with non-AS control group. CCK8 assay and flow cytometry analysis showed that Gal-3 significantly decreased cell viability and promoted apoptosis in ox-LDL-treated human umbilical vascular endothelial cells (HUVECs). The upregulation of integrinβ1, GTP-RhoA, p-JNK, p-p65, p-IKKα, and p-IKKβ induced by ox-LDL was further enhanced by treatment with Gal-3. Pretreatment with Gal-3 increased expression of inflammatory factors (interleukin [IL]-6, IL-8, and IL-1β), chemokines(CXCL-1 and CCL-2) and adhesion molecules (VCAM-1 and ICAM-1). Furthermore, the promotional effects of Gal-3 on NF-κB activation and inflammatory factors in ox-LDL-treated HUVECs were reversed by the treatments with integrinβ1-siRNA or the JNK inhibitor. We also found that integrinβ1-siRNA decreased the protein expression of GTP-RhoA and p-JNK, while RhoA inhibitor partially reduced the upregulated expression of p-JNK induced by Gal-3. In conclusion, our finding suggests that Gal-3 exacerbates ox-LDL-mediated endothelial injury by inducing inflammation via integrin β1-RhoA-JNK signaling activation.     

Galectin-3 in Patients with Atrial Fibrillation Undergoing Radiofrequency Catheter Ablation

Background

Galectin-3 (Gal-3) is an emerging biomarker in heart failure that is involved in fibrosis and inflammation. However, its potential value as a prognostic marker in atrial fibrillation (AF) is unknown. The aim of this study was to assess the impact of AF catheter ablation on Gal-3 and evaluate its prognostic impact for predicting rhythm outcome after catheter ablation.

Methods

Gal-3 was measured at baseline and after 6 months using specific ELISA. AF recurrences were defined as any atrial arrhythmia lasting longer than 30 sec within 6 months after ablation.

Results

In 105 AF patients (65% males, age 62±9 years, 52% paroxysmal AF) undergoing catheter ablation, Gal-3 was measured at baseline and after 6 months and compared with an AF-free control cohort (n=14, 50 % males, age 58±11 years). Gal-3 was higher in AF patients compared with AF-free controls (7.8±2.9 vs. 5.8±1.8, ng/mL, p=0.013). However, on multivariable analysis, BMI (p=0.007) but not AF (p=0.068) was associated with Gal-3. In the AF cohort, on univariable analysis higher Gal-3 levels were associated with female gender (p=0.028), higher BMI (p=0.005) and both CHADS2 (p=0.008) and CHA2DS2-VASC (p=0.016) scores, however, on multivariable analysis only BMI remained significantly associated with baseline Gal-3 (p=0.016). Gal-3 was similar 6 months after AF catheter ablation and was not associated with sinus rhythm maintenance.

Conclusions

Although galectin-3 levels are higher in AF patients, this is driven by cardiometabolic co-morbidities and not heart rhythm. Gal-3 is not useful for predicting rhythm outcome of catheter ablation.     

Low-dose cyclophosphamide modulates galectin-1 expression and function in an experimental rat lymphoma model

In recent years, one of the most important insights into tumor immunity was provided by the identification of negative regulatory pathways and immune escape strategies that greatly influence the magnitude of antitumor responses. Galectin-1 (Gal-1), a member of a family of highly conserved β-galactoside-binding proteins, has been recently shown to contribute to tumor cell evasion of immune responses by modulating survival and differentiation of effector T cells. However, there is still scarce information about the regulation of Gal-1 expression and function in vivo. Here we show that administration of a single low-dose cyclophosphamide (Cy), which is capable of restraining metastasis in the rat lymphoma model L-TACB, can also influence Gal-1 expression in primary tumor, metastasis, and spleen cells and modulate the effects of this protein on T cell survival. A time-course study revealed a positive correlation between Gal-1 expression and tumor volume in primary tumor cells. Conversely, Gal-1 expression was significantly reduced in spleen cells and lymph node metastasis throughout the period studied. Interestingly, cyclophosphamide treatment was capable of restoring the basal levels of Gal-1 expression in primary tumors and spleens. In addition, this antimetastatic agent rendered spleen T cells from tumor-bearing animals resistant to Gal-1-induced cell death. Our results suggest that, in addition to other well-known functions of cyclophosphamide, this immunomodulatory agent may also modulate Gal-1 expression and function during tumor growth and metastasis with critical implications for tumor-immune escape and immunotherapy.Mariano F. Zacarías Fluck and María J. Rico contributed equally to this work.     

Mice deficient in galectin-1 exhibit attenuated physiological responses to chronic hypoxia-induced pulmonary hypertension

Pulmonary hypertension (PH) is characterized by sustained vasoconstriction, with subsequent extracellular matrix (ECM) production and smooth muscle cell (SMC) proliferation. Changes in the ECM can modulate vasoreactivity and SMC contraction. Galectin-1 (Gal-1) is a hypoxia-inducible beta-galactoside-binding lectin produced by vascular, interstitial, epithelial, and immune cells. Gal-1 regulates SMC differentiation, proliferation, and apoptosis via interactions with the ECM, as well as immune system function, and, therefore, likely plays a role in the pathogenesis of PH. We investigated the effects of Gal-1 during hypoxic PH by quantifying 1) Gal-1 expression in response to hypoxia in vitro and in vivo and 2) the effect of Gal-1 gene deletion on the magnitude of the PH response to chronic hypoxia in vivo. By constructing and screening a subtractive library, we found that acute hypoxia increases expression of Gal-1 mRNA in isolated pulmonary mesenchymal cells. In wild-type (WT) mice, Gal-1 immunoreactivity increased after 6 wk of hypoxia. Increased expression of Gal-1 protein was confirmed by quantitative Western analysis. Gal-1 knockout (Gal-1(-/-)) mice showed a decreased PH response, as measured by right ventricular pressure and the ratio of right ventricular to left ventricular + septum wet weight compared with their WT counterparts. However, the number and degree of muscularized vessels increased similarly in WT and Gal-1(-/-) mice. In response to chronic hypoxia, the decrease in factor 8-positive microvessel density was similar in both groups. Vasoreactivity of WT and Gal-1(-/-) mice was tested in vivo and with use of isolated perfused lungs exposed to acute hypoxia. Acute hypoxia caused a significant increase in RV pressure in wild-type and Gal-1(-/-) mice; however, the response of the Gal-1(-/-) mice was greater. These results suggest that Gal-1 influences the contractile response to hypoxia and subsequent remodeling during hypoxia-induced PH, which influences disease progression.     

Nuclear export of phosphorylated galectin-3 regulates its antiapoptotic activity in response to chemotherapeutic drugs

Galectin-3 (Gal-3), a member of the beta-galactoside binding protein family containing the NWGR antideath motif of the Bcl-2 protein family, is involved in various aspects of cancer progression. Previously, it has been shown that the antiapoptotic activity of Gal-3 is regulated by the phosphorylation at Ser(6) by casein kinase 1 (CK1). Here we questioned how phosphorylation at Ser(6) regulates Gal-3 function. We have generated serine-to-alanine (S6A) and serine-to-glutamic acid (S6E) Gal-3 mutants and transfected them into the BT-549 human breast carcinoma cell line, which does not express Gal-3. BT-549 cell clones expressing wild-type (wt) and mutant Gal-3 were exposed to chemotherapeutic anticancer drugs. In response to the apoptotic insults, phosphorylated wt Gal-3 was exported from the nucleus to the cytoplasm and protected the BT-549 cells from drug-induced apoptosis while nonphosphorylated mutant Gal-3 neither was exported from the nucleus nor protected BT-549 cells from drug-induced apoptosis. Furthermore, leptomycin B, a nuclear export inhibitor, increased the cisplatin-induced apoptosis of Gal-3 expressing BT-549 cells. These results suggest that Ser(6) phosphoryaltion acts as a molecular switch for its cellular translocation from the nucleus to the cytoplasm and, as a result, regulates the antiapoptotic activity of Gal-3.     

Functional and structural bases of a cysteine-less mutant as a long-lasting substitute for galectin-1

Galectin-1 (Gal-1), a member of the beta-galactoside-binding animal lectin family, has a wide range of biological activities, which makes it an attractive target for medical applications. Unlike other galectins, Gal-1 is susceptible to oxidation at cysteine residues, which is troublesome for in vitro/vivo studies. To overcome this problem, we prepared a cysteine-less mutant of Gal-1 (CSGal-1) by substituting all cysteine residues with serine residues. In the case of wild-type Gal-1, the formation of covalent dimers/oligomers was evident after 10 days of storage in the absence of a reducing agent with a concomitant decrease in hemagglutination activity, while CSGal-1 did not form multimers and retained full hemagglutination activity after 400 days of storage. Frontal affinity chromatography showed that the sugar-binding specificity and affinity of Gal-1 for model glycans were barely affected by the mutagenesis. Gal-1 is known to induce cell signaling leading to an increase in the intracytoplasmic calcium concentration and to cell death. CSGal-1 is also capable of inducing calcium flux and growth inhibition in Jurkat cells, which are comparable to or more potent than those induced by Gal-1. The X-ray structure of the CSGal-1/lactose complex has been determined. The structure of CSGal-1 is almost identical to that of wild-type human Gal-1, showing that the amino acid substitutions do not affect the overall structure or carbohydrate-binding site structure of the protein. These results indicate that CSGal-1 can serve as a stable substitute for Gal-1.     

Galectin-1 sensitizes resting human T lymphocytes to Fas (CD95)-mediated cell death via mitochondrial hyperpolarization, budding, and fission

Galectins have emerged as a novel family of immunoregulatory proteins implicated in T cell homeostasis. Recent studies showed that galectin-1 (Gal-1) plays a key role in tumor-immune escape by killing antitumor effector T cells. Here we found that Gal-1 sensitizes human resting T cells to Fas (CD95)/caspase-8-mediated cell death. Furthermore, this protein triggers an apoptotic program involving an increase of mitochondrial membrane potential and participation of the ceramide pathway. In addition, Gal-1 induces mitochondrial coalescence, budding, and fission accompanied by an increase and/or redistribution of fission-associated molecules h-Fis and DRP-1. Importantly, these changes are detected in both resting and activated human T cells, suggesting that Gal-1-induced cell death might become an excellent model to analyze the morphogenetic changes of mitochondria during the execution of cell death. This is the first association among Gal-1, Fas/Fas ligand-mediated cell death, and the mitochondrial pathway, providing a rational basis for the immunoregulatory properties of Gal-1 in experimental models of chronic inflammation and cancer.     

In vitro gene delivery to HepG2 cells using galactosylated 6-amino-6-deoxychitosan as a DNA carrier

A chitosan derivative, 6-amino-6-deoxy chitosan (6ACT), was galactosylated and was investigated as a gene carrier. A series of galactose-modified 6ACT (Gal-6ACT) with degrees of substitution (d.s.) ranging from 3% to 50% per pyranose were prepared by reductive alkylation with lactose. DNA retardation assays showed that the electrostatic interaction between Gal-6ACT and plasmid DNA was not changed by galactose modification up to 50% per pyranose of 6ACT. Gal-6ACT with a d.s. of 38% was bound to galactose-recognizing lectin, RCA120. A significant increase in transfection efficiency for HepG2 cells was observed at degree of substitutions ranging from 18% to 50% and at N/P values ranging from 1.5 to 2.5. Under optimum conditions, Gal-6ACT showed about 10 times higher efficiency than 6ACT. However, a slight uptake by the galactose receptors on hepatocytes was observed by flow cytometric analysis. Moreover, Gal-6ACT with a d.s. of 38% mediated efficient gene transfer into both A549 and HeLa cells lacking the galactose receptor. These results suggest that the enhancement of transfection efficiency of Gal-6ACT was not due to the increase of receptor-mediated cellular uptake. In addition, the enhanced gene transfer efficiency was not specific to the galactose modification because the efficiency of glucose-modified 6ACT for HepG2 cells was similar as that of Gal-6ACT.     

Possible involvement of galectin-3 in microglial activation in the hippocampus with trimethyltin treatment

Trimethyltin (TMT) is an organotin neurotoxicant with effects that are selectively localized to the limbic system (especially the hippocampus), which produces memory deficits and temporal lobe seizures. Galectin-3 (Gal-3) is a beta-galactoside-binding lectin that is important in cell proliferation and regulation of apoptosis. The present study evaluated the temporal expression of Gal-3 in the hippocampus of adult BALB/c mice after TMT treatment (i.p., 2.5 mg/kg). Western blotting analyses showed that Gal-3 immunoreactivity began to increase 2 days after treatment; the immunoreactivity peaked significantly within 4 days after treatment but significantly declined between days 4 and 8. Immunohistochemical analysis indicated that Gal-3 expression was very rare in the hippocampi of vehicle-treated controls. However, Gal-3 immunoreactivity appeared between 2 and 8 days after TMT treatment and was primarily localized to the hippocampal dentate gyrus (DG), in which neuronal degeneration occurred. The immunoreactivity was detected predominantly in most of the Iba1-positive microglia and in some GFAP-positive astrocytes of the hippocampal DG. Furthermore, Gal-3 expression co-localized with the pro-inflammatory enzymes cyclooxygenase-2 and inducible nitric oxide synthase in the hippocampal DG. Therefore, we suggest that Gal-3 is involved in the inflammatory process of neurodegenerative disorder induced by organotin intoxication.     

2型糖尿病患者血清尿酸、胱抑素C、半乳糖凝集素-3、丝氨酸蛋白酶抑制剂B1与血糖及颈动脉粥样硬化的关系研究

摘要 目的：研究2型糖尿病（T2DM）患者血清尿酸（UA）、胱抑素C（CysC）、半乳糖凝集素-3（Gal-3）、丝氨酸蛋白酶抑制剂B1（Serpin B1）与血糖及颈动脉粥样硬化（CAS）的关系。方法：选取2020年4月-2022年4月青岛市中医医院内分泌科收治的110例T2DM患者,根据有无CAS分为CAS组36例和非CAS组74例,检测并对比两组血清UA、CysC、Gal-3、Serpin B1水平。通过Pearson/Spearman相关系数分析T2DM患者血清UA、CysC、Gal3、Serpin B1水平与血糖指标的相关性。收集患者基础资料,采用多因素Logistic回归分析T2DM患者发生CAS的影响因素。结果：CAS组血清UA、CysC、Gal-3、Serpin B1水平均明显高于非CAS组（P＜0.05）。CAS组平均年龄大于非CAS组,吸烟史患者比例、空腹血糖、糖化血红蛋白（HbA1c）、胰岛素抵抗指数（HOMA-IR）、低密度脂蛋白胆固醇（LDL-C）水平高于非CAS组（P＜0.05）。相关性分析显示,T2DM患者血清UA、CysC、Gal-3、Serpin B1水平与HbA1c、HOMA-IR呈正相关（P＜0.05）。多因素Logistic回归分析显示,年龄较大、HbA1c、HOMA-IR、血清UA、CysC、Gal3、Serpin B1水平较高是T2DM患者发生CAS的危险因素（P＜0.05）。结论：血清UA、CysC、Gal-3、Serpin B1水平升高与T2DM患者血糖水平有关,同时也是T2DM患者发生CAS的影响因素。