Expression of platelet endothelial cell adhesion molecule-1 between pancreatic microcirculation and peripheral circulation in rats with acute edematous pancreatitis

OBJECTIVE: To study the ehanges of platelet endothelial cell adhesion molecule-1 (PECAM-1) expression on polymorphonuclear leukocytes (PMNs) in peripheral circulation anti pancreatic microcirculation in rats with acute edematous pancreatitis (AEP). METHODS: The model of AEP was established with 50 Wistar rats, and the changes of PECAM-1 expression on PMNs from the splenic vein and inferior vena cava were determined by flow cytometry. RESULTS: PECAM-I expression on PMNs showed no significant difference between pancreatic microcirculation and peripheral circulation at AEP2h and AEP4h time points. From the AEP4h to the AEP8h time point, PECAM-1 expression in peripheral circulation was up-regulated, but PECAM-1 expression in pancreatic microcirculation was down-regulated. PECAM-1 expression had a significant difference between pancreatic microcirculation and peripheral circulation at the AEP8h time point (P<0.05). CONCLUSION: PECAM-1 expression on PMNs is in a converse way between pancreatic microcirculation and peripheral circulation in AEP.

Effects of TCMP-1 on the changes of platelet endothelial cell adhesion molecule-1 expression in acute edematous pancreatitis

BACKGROUND: Traditional Chinese medicine is a potent agent in the management of clinical and experimental acute pancreatitis (AP), but the molecular mechanism of its the- rapeutic action is unclear. Numerous experimental and clinical studies have shown that platelet endothelial cell ad- hesion molecule-1 (PECAM-1) is pivotal to leukocyte re- cruitment, which results in microcirculatory injury during inflammation, but its role in acute pancreatitis is poorly un- derstood. We investigated the effects of a compound of tra- ditional Chinese medicine pancreatitis-1 (TCMP-1) on the changes of platelet endothelial cell adhesion molecule-1 (PECAM-1) expression on polymorphonuclear leukocytes (PMNs) in acute edematous pancreatitis (AEP). METHODS: The model of acute pancreatitis was estab- lished by subcutaneous injection of caerulein, and TCMP-1 treated groups were given TCMP-1 by catheterization from mouth to stomach (20 ml/kg) immediately after first time subcutaneous injection of caerulein. The changes of expres- sion of PECAM-1 on leukocytes from the blood of the splenic vein and inferior vena cava were determined by flow cytometry. RESULTS: In the AEP group, expression of PECAM-1 on PMNs was not significantly different between pancreatic microcirculation and systemic circulation at AEP2h and AEP4h time point. Then from AEP4h time point to AEP8h time point, expression of PECAM-1 was up-regulated in systemic circulation while it was down-regulated in pancre- atic microcirculation and was significantly different be- tween pancreatic microcirculation and systemic circulation at AEP8h time point (P<0.05). In the TCMP-1 treated group, compared with the AEP group, expression of PE-CAM-1 on PMNs decreased in different levels between pan- creatic microcirculation and systemic circulation and was of significant difference at AEP8h time point (P <0.05). CONCLUSION: Inhibition of PECAM-1 expression on PMNs may prevent PMNs from transmigration through the endo- thelium and may be one of the treatment mechanisms of TCMP-1 decoction on AEP.

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.

Differences in platelet endothelial cell adhesion molecule-1 expression between peripheral circulation and pancreatic microcirculation in cerulein-induced acute edematous pancreatitis

AIM: To investigate the changes of platelet endothelial cell adhesion molecule-1 (PECAM-1) expression on polymorphonuclear leukocytes (PMNs) in peripheral circulation and pancreatic microcirculation in cerulein-induced acute edematous pancreatitis (AEP).METHODS: Fifty Wistar rats were randomly divided into control group (n=10) and AEP group (n=40). A model of AEP was established by subcutaneous injection of cerulein 5.5 and 7.5 μg/kg at 0 and 1 h after the beginning of experiment respectively. PECAM-1 expression on PMNs from splenic vein and inferior vena cava was determined by RT-PCR at mRNA level and determined by flow cytometry at protein level.RESULTS: In experimental rats, an increased PECAM-1mRNA expression was seen from 4 to 8 h of AEP in peripheral circulation (0.77±0.25%, 0.76±0.28%, 0.89±0.30%,1.00±0.21% ), while in pancreatic microcirculation,expression decreased from 2 h and reached the lowest level at 6 h of AEP (0.78±0.29%, 0.75±0.26%, 0.62±0.28%,0.66±0.20%). There were significant differences at 8-h time point of AEP between peripheral circulation and pancreatic microcirculation (1.00±0.21% vs0.66±0.20%, P＜0.05).Meanwhile,the difference at protein level was also found.CONCLUSION: A reverse expression of PECAM-1 on PMNs was found between peripheral circulation and pancreatic microcirculation, suggesting that inhibition of PECAM-1expression may improve the pathological change of AEP.

Platelet-activating factor mediates hydrogen peroxide induced endothelial-leukocyte adhesion

The effects of hydrogen peroxide（H2O2）on endothelial-polymorphonuclear leuko-cyte（EC-PMN）adhesion and their mechanisms were studied in cultured bovine pulmonaryartery endothelial monolayers in vitro.H2O2 at various concentrations(10-3,10-2,10-1mol/Lrespectively)stimulated EC-dependent PMN adhesion,of which 10-2mol/L H2O2 was the mostpotent one,increasing adhesion to 2.3 times that of the control.Pretreatment of PMNs with SRI63-441,a platelet-activating factor（PAF）receptor antagonist,had no inhibition effect on H2O2induced EC-PMN adhesion.Pretreatment of ECs with SRI 63-441 before H2O2 exposure signifi-cantly decreased PMN adherence to ECs.Pretreatment of ECs with phospholipase A2 inhibitorp-bromophenacyl-bromide or calmodulin antagonist chlorpromazine and calcium ion chelate EG-TA obviously decreased H2O2 induced increment of EC-PMN adhesion.These results suggestthat H2O2 may activate ECs,causing the inflow of extracellular calcium or the release of calciumfrom intracellular deposits.Increased intracellar Ca2+may bind with calmodulin to activate phos-pholipase A2,thus initiating PAF synthesis and promoting EC-PMN adhesion.

Integrin binding peptides facilitate growth and interconnected vascular-like network formation of rat primary cortical vascular endothelial cells in vitro

Neovascularization and angiogenesis in the brain are important physiological processes for normal brain development and repair/regeneration following insults. Integrins are cell surface adhesion receptors mediating important function of cells such as survival, growth and development during tissue organization, differentiation and organogenesis. In this study, we used an integrin-binding array platform to identify the important types of integrins and their binding peptides that facilitate adhesion, growth, development, and vascular-like network formation of rat primary brain microvascular endothelial cells. Brain microvascular endothelial cells were isolated from rat brain on post-natal day 7. Cells were cultured in a custom-designed integrin array system containing short synthetic peptides binding to 16 types of integrins commonly expressed on cells in vertebrates. After 7 days of culture, the brain microvascular endothelial cells were processed for immunostaining with markers for endothelial cells including von Willibrand factor and platelet endothelial cell adhesion molecule. 5-Bromo-2′-dexoyuridine was added to the culture at 48 hours prior to fixation to assess cell proliferation. Among 16 integrins tested, we found that α5β1, αvβ5 and αvβ8 greatly promoted proliferation of endothelial cells in culture. To investigate the effect of integrin-binding peptides in promoting neovascularization and angiogenesis, the binding peptides to the above three types of integrins were immobilized to our custom-designed hydrogel in three-dimensional(3 D) culture of brain microvascular endothelial cells with the addition of vascular endothelial growth factor. Following a 7-day 3 D culture, the culture was fixed and processed for double labeling of phalloidin with von Willibrand factor or platelet endothelial cell adhesion molecule and assessed under confocal microscopy. In the 3 D culture in hydrogels conjugated with the integrin-binding peptide, brain microvascular endothelial cells formed interconnected vascular-like network with clearly discernable lumens, which is reminiscent of brain microvascular network in vivo. With the novel integrin-binding array system, we identified the specific types of integrins on brain microvascular endothelial cells that mediate cell adhesion and growth followed by functionalizing a 3 D hydrogel culture system using the binding peptides that specifically bind to the identified integrins, leading to robust growth and lumenized microvascular-like network formation of brain microvascular endothelial cells in 3 D culture. This technology can be used for in vitro and in vivo vascularization of transplants or brain lesions to promote brain tissue regeneration following neurological insults.

The role of adhesion molecules in gastri c ulcer healing

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Correlation of PECAM-1 gene C373G locus polymorphism with endothelial injury and placental pathological damage in patients with preeclampsia

Objective:To study the correlation of PECAM-1 gene C373G locus polymorphism with endothelial injury and placental pathological damage in patients with preeclampsia.Methods:Pregnant women with preeclampsia and healthy pregnant women delivering in Obstetrics Department of Yibin Second People's Hospital between May 2014 and September 2016 were selected and enrolled in PE group and control group respectively. Peripheral blood was collected to determine PECAM-1 gene C373G polymorphism as well as the contents of endothelial injury molecules sEng, PAR-1, sFlt-1 and ET-1;placenta tissue was collected to determine the contents of pathological damage molecules Gadd45 , TIMP2, Fas, Apaf-1 and caspase-3.Results:PECAM-1 gene C373G locus GC and GG genotype constituent ratio and allele G constituent ratio in peripheral blood of PE group were significantly higher than those of control group while CC genotype constituent ratio and allele C constituent ratio were significantly lower than those of control group. sFlt-1, sEng, PAR-1 and ET-1 contents in serum as well as Gadd45 , TIMP2, Fas, Apaf-1 and caspase-3 contents in placenta of PE group were significantly higher than those of control group;sFlt-1, sEng, PAR-1 and ET-1 contents in serum as well as Gadd45 , TIMP2, Fas, Apaf-1 and caspase-3 contents in placenta of PE patients with PECAM-1 gene C373G locus GC and GG genotypes were higher than those of PE patients with CC genotype.Conclusion: Increased allele G in PECAM-1 gene C373G loci is closely correlated with endothelial injury and placental pathological damage in patients with preeclampsia.

血小板内皮细胞黏附分子1和平滑肌肌动蛋白对瘢痕疙瘩综合治疗预后的影响

目的:探究瘢痕疙瘩血管内血小板内皮细胞黏附分子1(platelet endothelial cell adhesion molecule-1,PECAM-1)与平滑肌肌动蛋白(smooth muscle actin,SMA)的表达水平对瘢痕疙瘩综合治疗预后的影响。方法:回顾性分析2020年8月至2022年6月江苏大学附属医院皮肤科门诊收治的瘢痕疙瘩患者61例,共计69处瘢痕疙瘩,均接受手术切除与^(90)Sr同位素敷贴综合治疗,免疫组织化学染色检测手术切除瘢痕疙瘩标本血管内PECAM-1及SMA表达水平,电话及门诊随访6个月。结果:19处(27.5%)瘢痕疙瘩6个月内复发,11处(15.9%)在^(90)Sr同位素敷贴治疗后发生不良反应,复发组PECAM-1与SMA的高表达率均高于未复发组(χ^(2)=7.496,P=0.006;χ^(2)=5.197,P=0.023);治疗后不良反应发生率与PECAM-1及SMA的表达水平无明显关系(χ^(2)=0.172,P=0.935;χ^(2)=1.110,P=0.484)。结论:瘢痕疙瘩血管内PECAM-1及SMA的表达水平与综合治疗预后呈负相关,二者可能是判断瘢痕疙瘩预后的潜在指标。

ACI患者血清APN、Lp-PLA2、PECAM-1水平与出院后一年认知功能障碍的相关性探讨

目的 探讨急性脑梗死(ACI)患者出院时血清脂联素(APN)、脂蛋白相关磷脂酶A2(Lp-PLA2)、血小板内皮细胞黏附分子-1 (PECAM-1)水平与长期认知功能障碍(PSCI)的相关性,为临床预测PSCI提供相关标志物。方法 选取新疆维吾尔自治区人民医院2020年8月至2022年1月ACI患者108例,根据出院后1年时是否存在PSCI,分为认知正常组(77例)与认知障碍组(31例)。比较两组临床基本资料及入院时、出院时血清APN、Lp-PLA2、PECAM-1水平,分析血清APN、Lp-PLA2、PECAM-1水平与长期PSCI的相关性。结果 认知障碍组出院后1年简易精神状态评价量表(MMSE)评分为(22.13±2.06)分,低于认知正常组(29.14±0.31)分(P<0.05);两组年龄、神经功能缺损程度、合并糖尿病、糖化血红蛋白(HbAlc)、同型半胱氨酸(Hcy)水平差异有统计学意义(P<0.05);认知障碍组出院时血清APN水平低于认知正常组,Lp-PLA2、PECAM-1水平高于认知正常组(P<0.05);出院时血清APN水平与出院后1年MMSE评分呈正相关,Lp-PLA2、PECAM-1水平与出院后1年MMSE评分呈负相关(r=0.727、-0.667、-0.750,均P<0.05);Logistic回归分析,将其他因素校正前后,出院时血清APN、Lp-PLA2、PECAM-1水平均与ACI患者长期PSCI独立相关(P<0.05);出院时血清APN、LpPLA2、PECAM-1水平预测ACI患者长期PSCI的AUC分别为0.783 (95%CI:0.693~0.857)、0.736 (95%CI:0.643~0.817)、0.827 (95%CI:0.743~0.893),联合预测ACI患者长期PSCI的AUC为0.936 (95%CI:0.872~0.974),优于3者单独预测。结论 ACI患者出院时血清APN、Lp-PLA2、PECAM-1水平与长期PSCI独立相关,可作为临床早期预测指标,且联合预测价值可靠。

基于VEGF/PI3K/Akt通路基因表达探讨骨坏死康复丸对激素性股骨头坏死大鼠血管新生的影响

【目的】观察骨坏死康复丸对激素性股骨头坏死(SONFH)大鼠的治疗作用及机制。【方法】将60只大鼠随机分为空白组,模型组,仙灵骨葆胶囊组及骨坏死康复丸低、中、高剂量组,每组10只。除空白组,其他各组大鼠采用脂多糖联合糖皮质激素诱导法建立SONFH模型。干预结束后,分别进行股骨头的血管造影观察骨髓内微血管变化、苏木素-伊红(HE)染色并计算空骨陷窝率、Micro-CT扫描分析、压缩实验,采用实时定量聚合酶链反应(RT-qPCR)法检测全血磷脂酰肌醇3-激酶(PI3K)、蛋白激酶B(Akt)1、血管内皮生长因子(VEGF)、血小板内皮细胞黏附分子1(CD31)基因表达。【结果】与空白组比较,模型组股骨头髓腔内血供差,空骨陷窝率增加(P<0.05),骨密度、骨体积分数显著降低(P<0.05),股骨头最大载荷及弹性模量降低(P<0.05),全血Akt1、PI3K、VEGF、CD31 mRNA表达水平降低(P<0.05);与模型组比较,骨坏死康复丸高剂量组和仙灵骨葆胶囊组股骨头髓腔内血供较好,空骨陷窝率减少(P<0.05),骨密度、骨体积分数、骨小梁数量、骨小梁厚度显著升高(P<0.05)及骨小梁分离度显著减小(P<0.05),股骨头最大载荷及弹性模量升高(P<0.05),全血Akt1、PI3K、VEGF、CD31 mRNA表达水平升高(P<0.05);骨坏死康复丸高剂量组上述各指标与仙灵骨葆胶囊组比较,差异均无统计学意义(P>0.05)。【结论】骨坏死康复丸可改善大鼠激素性股骨头坏死,其机制与促进VEGF/PI3K/Akt通路基因表达,进而促进血管新生有关。

Nrf2、LTBP2、PECAM1与NSCLC患者EGFR靶向治疗反应性关系及意义

目的:探讨血清核因子E2相关因子2(Nrf2)、转化生长因子结合蛋白2(LTBP2)、血小板内皮细胞黏附分子1(PECAM1)与非小细胞肺癌(NSCLC)患者表皮生长因子受体(EGFR)靶向治疗反应性关系及意义。方法:选取我院2021年1月—2023年1月收治的95例NSCLC患者为研究对象,根据EGFR靶向治疗3个月后的治疗反应性分为有效组(54例)、无效组(41例)。比较2组治疗前及治疗1个月、2个月后血清Nrf2、LTBP2、PECAM1水平,分析治疗1个月、2个月后血清Nrf2、LTBP2、PECAM1水平与NSCLC患者EGFR靶向治疗反应性相关性,偏回归分析治疗无效的影响因素,受试者工作特征曲线(ROC)分析治疗1个月、2个月后血清Nrf2、LTBP2、PECAM1水平联合检测对NSCLC患者EGFR靶向治疗效果的预测价值。结果:治疗1个月、2个月后无效组血清Nrf2、LTBP2、PECAM1水平均高于有效组(P<0.05);相关性分析发现,治疗1个月、2个月后血清Nrf2、LTBP2、PECAM1水平与治疗反应性均呈负相关(P<0.05);Logistic回归分析发现,治疗1个月、2个月后血清Nrf2、LTBP2、PECAM1水平为NSCLC患者EGFR靶向治疗效果的影响因素(P<0.05);ROC曲线分析发现,治疗1个月、2个月后血清Nrf2、LTBP2、PECAM1水平联合预测治疗无效的曲线下面积(AUC)分别为0.761、0.816,最佳预测敏感度、特异度分别为(85.37%、66.67%)、(92.68%、70.37%),高于单一指标预测(P<0.05)。结论:血清Nrf2、LTBP2、PECAM1水平与NSCLC患者EGFR靶向治疗反应性密切相关,并在预测治疗效果方面具有较高效能。

PECAM-1、心室重构与急性心肌梗死冠脉介入术后合并重度心力衰竭的相关性及预后预测

目的探讨血小板内皮细胞黏附分子-1(PECAM-1)、心室重构与急性心肌梗死冠脉介入术后合并重度心力衰竭的相关性及预后预测价值。方法选取2020年5月—2023年5月内蒙古包钢医院收治的80例急性心肌梗死冠脉介入术后合并心力衰竭患者作为研究对象,应用Killip分级来评价患者心力衰竭严重程度并进行分组,将其分为Ⅰ级组16例,Ⅱ级组23例,Ⅲ级组20例,Ⅳ级组21例,另选取同期来内蒙古包钢医院体检的30名健康志愿者作为对照组。对比五组患者PECAM-1与心室重构指标水平,应用Spearman相关分析PECAM-1、心室重构与急性心肌梗死冠脉介入术后合并重度心力衰竭的相关性。随后将80例急性心肌梗死冠脉介入术后合并心力衰竭患者中院内死亡者分为死亡组(n=20),将其余患者分为存活组(n=60),对比两组患者临床一般情况,并分析PECAM-1、心室重构对急性心肌梗死冠脉介入术后合并心力衰竭预后的预测价值。结果Ⅳ级患者PECAM-1、左心室质量指数(LVMI)明显高于Ⅲ级、Ⅱ级、Ⅰ级和对照组,左心室重构指数(LVRI)低于Ⅲ级、Ⅱ级、Ⅰ级和对照组(P<0.05);Spearman相关分析结果显示:PECAM-1、LVMI与急性心肌梗死冠脉介入术后合并重度心力衰竭呈正相关,LVRI与急性心肌梗死冠脉介入术后合并重度心力衰竭呈负相关(P<0.05);存活组与死亡组患者Killip分级、合并陈旧性心肌梗死、PECAM-1、LVRI、LVMI水平对比,差异有统计学意义(P<0.05);logistic回归分析结果表明:PECAM-1(OR=2.458,95%CI:1.359~3.257)、LVRI(OR=2.546,95%CI:1.364~3.475)、LVMI(OR=2.774,95%CI:1.876~4.010)为急性心肌梗死介入术后合并心力衰竭的独立预测指标(P<0.05)。结论PECAM-1、心室重构与急性心肌梗死冠脉介入术后合并重度心力衰竭具有明显相关性,且能够通过PECAM-1与心室重构情况来预测急性心肌梗死冠脉介入术后合并重度心力衰竭的预后情况。

腔隙性脑梗死患者血清PECAM-1、GDF11、FGF21与脑动脉血流动力学和颈动脉粥样硬化的关系

目的 分析腔隙性脑梗死患者血清血小板内皮细胞黏附分子-1(PECAM-1)、生长分化因子11(GDF11)、成纤维细胞生长因子21(FGF21)与脑动脉血流动力学和颈动脉粥样硬化的关系。方法 选取2020年1月—2022年1月陕西省人民医院神经内科收治腔隙性脑梗死患者160例为脑梗死组,并根据颈动脉内膜中层厚度(IMT)分为颈动脉粥样硬化亚组、颈动脉正常亚组,另选取同期健康体检者100例为健康对照组,比较2组血清PECAM-1、GDF11、FGF21水平和脑动脉血流动力学参数,采用Pearson线性相关性分析腔隙性脑梗死患者血清PECAM-1、GDF11、FGF21与脑动脉血流动力学参数的相关性。采用Logistic多因素回归分析腔隙性脑梗死患者发生颈动脉粥样硬化的影响因素,绘制受试者工作特征曲线(ROC)分析血清PECAM-1、GDF11、FGF21水平对颈动脉粥样硬化的诊断价值。结果 脑梗死组血清PECAM-1、FGF21高于健康对照组,血清GDF11低于健康对照组(t=8.386、17.511、6.795,P<0.001)。脑梗死组大脑中动脉、基底动脉搏动指数均高于健康对照组(t=16.928、7.686,P<0.001)。腔隙性脑梗死患者血清PECAM-1、FGF21水平与大脑中动脉、基底动脉搏动指数呈正相关(PECAM-1:r=0.537、0.462,P<0.001;FGF21:r=0.569、0.503,P<0.001),血清GDF11与大脑中动脉、基底动脉搏动指数呈负相关(r=-0.512、-0.498,P<0.001)。Logistic多因素回归分析结果显示,高血压史、低密度脂蛋白胆固醇(LDL-C)高、PECAM-1高、FGF21高是腔隙性脑梗死患者颈动脉粥样硬化发生的危险因素[OR(95%CI)=3.654(1.601~8.343)、2.481(1.508~4.085)、1.073(1.032~1.114)、1.024(1.011~1.038),P<0.01],血清高密度脂蛋白胆固醇(HDL-C)高、GDF11高是其保护因素[OR(95%CI)=0.781(0.613~0.995)、0.992(0.987~0.997),P<0.05];ROC曲线显示,血清PECAM-1、GDF11、FGF21及三者联合评估颈动脉粥样硬化发生风险的曲线下面积(AUC)分别为0.798、0.716、0.813、0.909,三者联合评估效能高于单项指标预测(Z/P=2.097/0.036,2.290/0.022,2.005/0.045)。结论 腔隙性脑梗死患者血清PECAM-1、GDF11、FGF21水平与脑动脉血流动力学参数有关,对颈动脉粥样硬化的评估具有重要意义。

血清CXC趋化因子受体5和血小板内皮细胞黏附分子-1对胃癌的诊断和预后评估价值

目的探讨血清CXC趋化因子受体5(CXCR5)和血小板内皮细胞黏附分子-1(PECAM-1)对胃癌的诊断和预后评估价值。方法选取2014年1月至2015年10月淮安市洪泽区人民医院收治的经病理确诊的102例胃癌患者为研究组,另选取同期性别和年龄相匹配的80例体检健康者为对照组。采用酶联免疫吸附试验法检测血清CXCR5和PECAM-1水平,采用受试者工作特征曲线(ROC曲线)分析CXCR5和PECAM-1对胃癌的诊断效能,以及与胃癌临床病理特征的关系。定期随访胃癌患者5年,比较存活组和死亡组血清CXCR5和PECAM-1水平,采用ROC曲线分析CXCR5和PECAM-1对胃癌死亡的预测效能,采用多因素Cox回归分析影响死亡的危险因素,比较CXCR5和PECAM-1高表达与低表达患者5年总生存率的差异。结果研究组血清CXCR5和PECAM-1水平明显高于对照组,差异有统计学意义(t=8.562、21.235,P<0.05)。ROC曲线结果显示,CXCR5、PECAM-1和两者联合诊断胃癌的曲线下面积(AUC)分别为0.829、0.874和0.912(P<0.05)。TNM分期为Ⅲ~Ⅳ期患者CXCR5和PECAM-1水平明显高于Ⅰ~Ⅱ期,低分化患者CXCR5和PECAM-1水平高于中高分化,淋巴结转移患者CXCR5和PECAM-1水平高于无淋巴结转移,肿瘤最大径>5 cm患者CXCR5和PECAM-1水平高于肿瘤最大径≤5 cm,差异均有统计学意义(P<0.05)。随访胃癌患者5年后,生存率为53.9%(55/102),死亡组血清CXCR5和PECAM-1水平明显高于存活组,差异有统计学意义(t=10.235、24.235,P<0.05)。ROC曲线结果显示,CXCR5、PECAM-1和两者联合诊断预测胃癌死亡的AUC分别为0.754、0.801和0.866(P<0.05)。Cox回归分析显示,TNM分期、淋巴结转移、肿瘤最大径、CXCR5和PECAM-1是影响胃癌预后的危险因素(P<0.05)。生存分析显示,CXCR5高表达患者5年总生存率比CXCR5低表达患者明显降低(χ^(2)=6.416,P=0.011);PECAM-1高表达患者5年总生存率比PECAM-1低表达患者明显降低(χ^(2)=16.052,P<0.001)。结论血清CXCR5和PECAM-1高表达可能参与胃癌的发生和临床预后,有望成为胃癌诊断和预后评估的重要指标,CXCR5和PECAM-1高表达与胃癌多个病理特征(TNM分期、分化程度和肿瘤最大径及淋巴结转移)密切相关。

PECAM-1、E-选择素和TSP-1对妊娠期高血压疾病发生妊娠结局不良的诊断价值

目的观察血小板内皮细胞黏附分子-1(PECAM-1)、E-选择素和血小板反应蛋白-1(TSP-1)对妊娠期高血压疾病(HDCP)患者发生妊娠结局不良的诊断效能。方法选取2020年1月至2022年1月在该院住院治疗的95例HDCP患者作为HDCP组,另选取同期在该院孕期保健检查的48例孕妇作为正常妊娠组。比较两组及不同严重程度HDCP患者血清PECAM-1、E-选择素和TSP-1水平,分析妊娠结局不良的影响因素,以及HDCP患者血清PECAM-1、E-选择素和TSP-1水平对妊娠结局不良的诊断效能。结果HDCP组血清PECAM-1水平明显低于正常妊娠组,其水平随着HCDP患者严重程度升高而降低,而HDCP组血清E-选择素和TSP-1水平均明显高于正常妊娠组,并且随着HDCP严重程度升高而升高,差异均有统计学意义(P<0.05)。妊娠结局不良组发病孕周、分娩孕周和血清PECAM-1水平均明显低于妊娠结局良好组,差异均有统计学意义(P<0.05);妊娠结局不良组血清E-选择素和TSP-1水平均明显高于妊娠结局良好组,差异均有统计学意义(P<0.05);妊娠结局不良组年龄、初产妇、孕前体质量指数、心率、收缩压和舒张压与妊娠结局良好组比较,差异均无统计学意义(P>0.05)。多因素Logistic回归分析结果显示,血清PECAM-1水平降低,血清E-选择素和TSP-1水平升高是HDCP患者发生妊娠结局不良的独立危险因素(P<0.05)。血清PECAM-1、E-选择素和TSP-1水平对HDCP患者发生妊娠结局不良具有较高的诊断效能,3项指标联合检测的灵敏度为82.2%,特异度为96.0%,曲线下面积为0.945,明显高于PECAM-1(Z=2.157,P=0.031)、E-选择素(Z=3.617,P<0.05)和TSP-1(Z=3.326,P=0.001)单项检测。结论血清PECAM-1、E-选择素和TSP-1是反映HDCP病情严重程度的指标,是HDCP患者发生妊娠结局不良的独立影响因素,3项指标联合检测对HDCP患者发生妊娠结局不良具有较高的诊断效能。

电针预处理对脑缺血再灌注损伤大鼠神经功能及缺血半暗带区VEGF、CD31表达的影响

目的通过观察电针预处理对脑缺血再灌注损伤大鼠神经功能、脑梗死体积及半暗带区脑组织血管内皮生长因子(vascular endothelial growth factor,VEGF)、血小板-内皮细胞黏附分子(platelet endothelial cell adhesion molecule-1,CD31)表达的影响,判断电针预处理对半暗带区血管新生的影响,探索电针预处理改善脑缺血再灌注损伤的可能作用机制。方法将36只SD大鼠按照随机数字表法分为假手术组、模型组、电针预处理组,每组12只。电针预处理组予以电针百会、水沟、大椎,每天1次,共7次;假手术组、模型组仅捆绑,不予电针处理。实验第8天,参照Zea Longa方法对模型组、电针预处理组进行大脑动脉栓塞(medial cerebral artery occlusion,MCAO)造模后灌注,假手术组仅切开皮肤暴露颈动脉,不做手术。造模24 h后,对各组大鼠进行神经功能缺损评分(neurological severity scores,NSS)法评估神经功能,评分后取大鼠梗死侧脑半球行红四氮唑(2,3,5-Triphenyltetrazolium Chloride,TTC)染色检测脑梗死面积,取脑缺血半暗带区组织进行HE染色观察脑组织形态变化,免疫组织化学法测定VEGF、CD31表达。结果假手术组未见梗死以及任何神经功能损伤,细胞形态正常;模型组半暗带区细胞损伤显著增加,排列紊乱,呈肿胀状,毛细血管管腔塌陷;电针预处理组损伤程度减轻,排列轻度紊乱,细胞肿胀不明显。与假手术组比较,模型组大鼠神经功能缺损评分明显升高(P<0.01),脑梗死面积明显增加(P<0.01),缺血半暗带区VEGF、CD31表达明显增加(P<0.01);与模型组比较,电针预处理组大鼠神经功能缺损评分降低(P<0.05),脑梗死面积明显减少(P<0.01),缺血半暗带区VEGF、CD31表达明显增加(P<0.01)。结论电针预处理可能通过促进缺血半暗带区血管新生,从而改善脑缺血再灌注损伤大鼠神经功能损伤、降低脑梗死体积。

藏药二十五味松石丸抑制血管生成和上皮间充质转化改善四氯化碳-酒精诱导的大鼠肝纤维化研究

目的研究二十五味松石丸是否通过抑制血管生成和上皮间充质转化改善四氯化碳(CCl_(4))-酒精诱导的大鼠肝纤维化模型。方法SPF级健康雄性SD大鼠30只,随机分为正常组,模型组,二十五味松石丸低、中和高[88、176、352 mg/(kg·d)]剂量组,每组6只。采用50%CCl_(4)橄榄油腹部皮下左右交替注射,同时以5%酒精饮料喂养建立肝纤维化模型;正常组皮下注射同体积橄榄油以蒸馏水喂养,持续8周,造模的同时按照分组灌胃相应的药物和0.4%羧甲基纤维素钠治疗。HE和Masson染色检测大鼠肝脏组织病理变化和胶原纤维增生;生化试剂盒测定血清谷丙转氨酶(ALT)、谷草转氨酶(AST),酶联免疫分析测定肿瘤坏死因子(TNF-α)、透明质酸(HA)和层黏连蛋白(LA)水平;免疫组化检测血小板内皮细胞黏附分子-1(CD31)、α-平滑肌肌动蛋白(α-SMA)、转化生长因子β1(TGF-β1)、E-钙黏蛋白(E-cadherin)和波形蛋白(Vimentin)表达;免疫印迹法检测α-SMA、TGF-β1、E-cadherin和Vimentin蛋白表达。结果与正常组相比,模型组大鼠肝组织病理损伤严重,胶原纤维明显增生;模型组中大鼠血清中ALT、AST活性明显升高,TNF-α含量明显增加,HA和LN含量明显升高;模型组大鼠肝组织内CD31、α-SMA、TGF-β1和Vimentin蛋白表达明显增加,E-cadherin蛋白表达明显降低。与模型组相比,二十五味松石丸各剂量组均能改善大鼠肝组织病理损伤、降低肝功能和肝纤维化指标,降低大鼠血清中TNF-α水平及肝组织内CD31、α-SMA、TGF-β1和Vimentin蛋白表达,增加E-cadherin蛋白表达。结论二十五味松石丸可改善CCl_(4)酒精复合因素诱导的大鼠肝纤维化,其作用可能与抑制血管新生和上皮间充质转化相关。

H型高血压合并急性脑梗死患者血清L_(p)-PLA2、SAA、PECAM-1水平与病情程度和疾病预后的关系

目的 分析血清脂蛋白磷脂酶A2(L_(p)-PLA2)、淀粉样蛋白A(SAA)和血小板内皮细胞黏附分子-1(PECAM-1)水平与急性脑梗死(ACI)病情程度和疾病预后的相关性。方法 选择2021年7月—2022年6月海安市人民医院急诊科收治的高血压合并ACI患者180例,根据血清同型半胱氨酸(Hcy)水平分为观察组124例(H型高血压)和对照组56例(单纯高血压)。观察组再根据颈部超声检查结果分为非易损斑块亚组45例和易损斑块亚组79例,根据发病72 h内美国国立卫生院卒中量表(NIHSS)评分较入院时的变化值分为非早期神经功能恶化亚组(非END亚组)53例和END亚组71例,根据发病后90 d的改良Rankin量表(mRS)评分分成预后良好亚组89例和预后不良亚组35例。比较各组血清L_(p)-PLA2、SAA、PECAM-1水平。Pearson分析血清L_(p)-PLA2、SAA、PECAM-1水平与Hcy水平、Alberta卒中项目早期CT(ASPECTS)评分、急性生理与慢性健康状况评分系统Ⅱ(APACHEⅡ)评分的相关性;绘制受试者工作特征曲线(ROC)分析血清L_(p)-PLA2、SAA、PECAM-1评估H型高血压合并ACI的效能。结果 血清L_(p)-PLA2、SAA、PECAM-1水平比较,观察组高于对照组(t/P=6.481/0.005、8.154/<0.001、7.462/<0.001),易损斑块亚组高于非易损斑块亚组(t/P=7.628/<0.001、8.319/<0.001、8.615/<0.001),END亚组高于非END亚组(t/P=7.854/<0.001、8.627/<0.001、9.825/<0.001),预后不良亚组高于预后良好亚组(t/P=7.915/<0.001、8.968/<0.001、8.763/<0.001)。Pearson分析显示,血清L_(p)-PLA2、SAA、PECAM-1水平与Hcy、APACHEⅡ评分均呈正相关(Hcy:r/P=0.691/<0.001、0.725/<0.001、0.674/<0.001;APACHEⅡ评分:r/P=0.591/<0.001、0.640/<0.001、0.683/<0.001),与ASPECTS评分呈负相关(r/P=-0.598/<0.001、-0.703/<0.001、-0.629/<0.001)。血清L_(p)-PLA2、SAA、PECAM-1及三者联合检测评估H型高血压合并ACI的曲线下面积(AUC)分别为0.681、0.709、0.754、0.924,三者联合检测评估效能高于单项检测(Z=6.863、7.418、7.905,P均<0.001)。结论 血清L_(p)-PLA2、SAA、PECAM-1在H型高血压合并ACI中呈高表达,与患者的颈动脉斑块稳定性、疾病严重程度和预后密切相关,三者联合检测的临床价值更高。

参麦注射液联合拉贝洛尔治疗妊娠期高血压的疗效及对患者PECAM-1、sVEGFR-1和VEGF水平的影响

目的观察参麦注射液联合拉贝洛尔治疗妊娠期高血压的疗效及对患者血清血小板内皮细胞黏附分子-1(PECAM-1)、人可溶性血管内皮生长因子受体-1(sVEGFR-1)和血管内皮生长因子(VEGF)水平的影响。方法选取2018年6月—2019年12月麻城市中医医院收治的妊娠期高血压患者99例,应用随机数字表法分为观察组49例和对照组50例。对照组患者予以拉贝洛尔治疗,观察组患者在对照组基础上联合参麦注射液治疗,2组患者均持续治疗7 d。比较2组患者临床疗效,治疗前后血压、脐动脉血流动力学参数[阻力指数(RI)、搏动指数(PI)、收缩末期血流速度最大值(SV)/舒张末期血流速度最大值(DV)(S/D)]及血清PECAM-1、sVEGFR-1、VEGF水平,并统计2组妊娠结局及不良反应。结果观察组患者治疗总有效率为93.88%,高于对照组的78.00%(χ^(2)=5.138,P=0.023)。治疗7 d后,2组患者收缩压、舒张压均显著低于治疗前;2组患者RI、PI、S/D均明显低于治疗前,且观察组低于对照组(P均<0.01);2组患者PECAM-1水平较治疗前升高,sVEGFR-1、VEGF水平较治疗前降低,且观察组上述指标变化较对照组更显著(P<0.05或P<0.01)。观察组早产率、剖宫率均低于对照组(P<0.05);2组新生儿窒息、新生儿死亡发生率比较差异无统计学意义(P>0.05)。结论参麦注射液联合拉贝洛尔治疗妊娠期高血压能更好地控制血压,调节胎盘血流,调节PECAM-1、sVEGFR-1与VEGF水平,改善妊娠结局,且安全性好。