血栓通与普伐他汀治疗高脂血症患者的临床研究

目的：研究并比较血栓通与普伐他汀对高脂血症患的疗效。方法：选择90例符合1997年中华心血管病学会提出的中国人的血脂异常防治建议诊断标准的高脂血症患，分为两组；观察组（n=60,采用血栓通）；对照组（n=30,采用普伐他汀），疗程均为4周，分别检测血脂水平变化。结果：两组治疗后血清TC，LDL－C和TG水平均显下降（P＜0．01），HDL－C水平也有较明显升高（P＜0．01），但观察组与对照组比较，无显性差异（P＞0．05）。结论：血栓通治疗高脂血症有明显效果，有广泛前景。     

普伐他汀治疗肾病综合征高脂血症35例临床分析

目的：总结普伐他汀治疗肾病综合征高脂血症的疗效。方法：对35例伴肮脂血症的肾病综合征患者在用强的松、利尿、降压、抗凝治疗的同时，每晚给予普伐他汀10mg，连续1个月。其间停用其他降脂药。治疗前后测定病人血清CH、TG、LDL－C和GDL－C。结果：治疗1个月后血CH、TG、LDL－C均显著下降（P＜0．01），HDL－C则升高（P＜0．05）。未见有不良反应.结论：普伐他汀有显著降血脂作用，特别适用于治疗高胆固醇血症及LDL－C升高者。     

充血性心力衰竭患者运动前后血浆细胞间粘附分子—1含量及临床意义

目的：探讨充血性心力衰竭（CHF）患运动前后血浆细胞间粘附分子－1（ICAM－1）的含量变化及其意义。方法：应用双抗体夹心法测定54例充血性心力衰竭患静息状态及六分钟步行运动后即刻CHF患血浆ICAM－1含量。结果：运动前，CHF患的血浆ICAM－1显高于对照组，且含量与心功能级别密切相关；低钠组CHF患ICAM－1含量明显高于正常血钠组（P＝0．039），运动后CHF患ICAM－1含量较运动前明显增加（O＝0．033），结论：ICAM－1在CHF发生发展中起重要作用。且与病情严重程度相关，CHF患运动后血浆ICAM－1显高于正常人的现象说明CHF患对运动的耐受性明显低于正常人。     

先天性心脏病患者体外循环术后血IL-6及ICAM-1的变化

目的：探讨先天性心脏病（CHD）患体外循环（CPB）术后血浆白细胞介素6（IL－6）及细胞间粘附分子－1（ICAM－1）的变化及其在CPB术后全身炎性反应综合症（SIRS）中的作用。方法：以25例非紫绀型CHD患CPB下手术为研究对象（试验组），10例未作CPB的心血管手术作对照（对照组），酶免法测定手术前、后多时间点外周动脉血中IL－6及ICAM－1水平，同时测定血中性粒细胞数，记录体温。结果：（1）两组术后IL－6水平较术前均明显增高（P＜0．01），但术后各时点的IL－6水平，试验组的比对照组升高更明显（P＜0．01）；（2）术后两组ICMA－1与术前相比无显差异（P＞0．05）；（3）术后两组中性粒细胞水平和体温均升高（P＜0．05），但试验组升高更明显（P＜0．05）。结论：（1）除手术应激外，CBP本身可导致IL－6翻放增加；（2）作为炎性介质，IL－6可能参与CPB后SIRS的发生；（3）单一ICAM－1在CPB心脏手术后SIRS中可能不占重要地位。     

普伐他汀与烟酸肌醇单用和合用对高脂血症的疗效观察

为比较普伐他汀和烟酸肌醇单用和合用对高脂血症病人血脂的影响，将高脂血症患者分成普伐他订组、烟酸肌醇组和联合用药组，观察治疗前后血脂的变化。结果发现，晋代他汀组血清总胆固醇从7．0±1．4降至5．9±1．5mmol／L（P＜0．05），低密度脂蛋白胆固醇从4．6±1．3降至3．6±1．2mmol／L（P＜0．05），而甘油三酯无明显降伏。烟酸肌醇组甘油三酯从2．7±1．2降至2．1±0．9mmol／L（P＜0．05），而总胆固醇和低密度脂蛋白胆固醇无明显降低。两药治疗后高密度脂蛋白均无显著性变化（P＞0．05）。联合用药组治疗后血脂各项指标降低或升高的幅度均比普代他汀组和烟酸肌醇组大，总胆固醇分别降低27.3％、15.6％和7.5％（P＜0．05），甘油三酯分别降低31．9％、7．1％和22．8％（P＜0．05），高密度脂蛋白分别升高11．2％、1．7％和4．49％（P＜0．05）。单一治疗无效的39例高脂血症患者分别联用烟酸肌醇或普伐他汀，观察4周，发现血总胆固醇从6．5±1．4降至4.5±1．3mmol／L（P＜0．01），血甘油三酯从2．6±1．2降至1．9±1．lmmol／L（P＜0．01），高密度脂蛋白从1．16±0．22升至1．27±0．21mmol／L（P＜0．05）。提示普代化汀加烟酸肌醇联合治疗可增强降脂效果，改善血脂组成。     

普伐他汀对冠心病患者血管内皮功能作用的量效关系

目的：探讨不同剂量（10mg，20mg，40mg）的普伐他汀对冠心病病患者血管内皮功能的作用及其量效关系。方法：本研究共入选48例经冠状动脉造影证实为冠心病的男性患者，随机分为4组：对照组（不服用普伐他汀），普伐他汀10mg组、20mg组、40mg组，每组12例，治疗时间为6周。使用上臂肱动脉内皮超声检测内皮依赖性流量介导性扩张（FMD），同时观察血脂水平的变化。结果：治疗6周后，10mg，20mg，40mg的普伐他汀均可显著降低血TC、LDL－C水平（TC分别降低10．96％、16．59％、24．41％，LDL－C分别降低17．19％、26．02％、40．19％；P均＜0．05）。对照组治疗6周前后血脂谱的变化无统计学意义（P＞0．05）。10mg、20mg、40mg的普伐他汀均可显著改善肱动脉血管内皮功能，FDM分别增加3．81％，4．26％、5．44％（P均＜0．05），但三组之间比较无显著差别，且其增加与血TC、LDL－C水平的降低不相关，对照组FMD虽有轻微增加，但无统计学意义（P＞0．05）。结论：普伐他汀10mg／d,20mg／d,40mg／d治疗6周可显著改善冠心病患者血管内皮细胞，但该作用无明显的量效关系。     

麝香、冰片对全脑缺血再灌注大鼠脑微血管内皮细胞ICAM-1表达的影响

目的：研究麝香、冰片对大鼠脑微血管内皮细胞ICAM－1表达的影响。方法：采用Pulsinelli的4血管闭塞法建立大鼠全脑缺血再灌注模型，运用免疫组化染色技术观察微血管内皮细胞ICAM－1表达，并进行半定量分析。结果：模型组、治疗组、尼莫通组缺血区域可见ICAM－1明确表达于脑微血管内皮，而在假手术组脑组织中未见ICAM－1表达，麝香、冰片（治疗组）能明显减少ICAM－1表达，与模型组、尼莫通组比较有统计学意义（P＜0．01）。结论：麝香、冰片可通过抑制ICAM－1的表达，从而抑制多形核白细胞黏附而在脑缺血再灌注损伤的治疗中发挥脑保护作用。     

急性脑梗死患者血清sICAM-1变化及临床意义

为探讨是粘附分子－1（ICAM－1）与急性脑梗死（ACI）发生发展的关系，应用酶联免疫吸附试验（ELISA）以双抗夹心法检测了48例ACI患者发病后24小时内，第3天，第7天，第14天血清内可溶性ICAM－1（sICAM-1）含量的变化，同时采用葡萄糖氧化酶法和硫代巴比妥酸法分别测定了血糖和丙二醛（MDA）水平。结果显示，ACI发病后2周的血清sICAM-1含量明显高于正常对照组（P＜0．05），发病后24小时内即见血清sICAM-1水平增高，至第3天达最高水平，以后逐渐降低。血sICAM-1水平与MDA和血糖呈正相关。认为ICAM－1参与了ACI的病理损伤过程，氧化应激和高血糖可能是加重这一病理损伤过程的重要因素。     

检测细胞间粘附分子-1对原发性肝癌的诊断意义

1资料与方法：患者血清标本-80℃保存,HCC44例,LC30例,健康献血员30例。组织标本：经病理证实的HCC标本35例,正常肝组织6例。smICAM－1检测用免疫组织化学给台多媒体彩色病理图文分析系统分析,ICAM－1用相对定量,即ICAM－1量＝（样品灰度－本底灰度）×样品面积。血清sICAM－1应用ELISA法检测。统计学分析用t检验及直线相关分析。2.sICAM－1测检的结果：（1）LC组（242.3±96.1）U／ml与HCC组（286.4±83．4）U／mlsICAM－1水平均明显高于正常对照组（90.6±397）U／ml（P＜0．01）HCC组sICAM－l水平高于LC组（…     

L-精氨酸抑制高胆固醇饮食诱发的大鼠动脉血管细胞间粘附分子表达

目的：观察L-精氨酸抗动脉粥样硬化的作用是否与其抑制大鼠动脉血管细胞间粘附分子（intercellularadhesionmolecule,ICAM－1）的表达有关。方法：Wistar大鼠24只,随机分为NC组（普通饲料及饮水）,CC组（饲料中含4％胆固醇,1％胆酸）,AC组（饲料中含4％胆固醇,1％胆酸,饮水中含3％L-精氨酸盐酸盐）;每组8只。8周后采血,处死Wistar大鼠取其主动脉作ICAM－1的免疫组织化学及信使核糖核酸（mRNA）NorthernBlot分析。结果：AC及CC组大鼠的血清胆固醇浓度无显著差异,但明显高于NC组。NC及CC组大鼠血清L-精氨酸浓度无明显差异,但明显低于AC组（P＜0．01）。L-精氨酸抑制高胆固醇膳食诱发的大鼠动脉ICAM－1表达。结论：L-精氨酸抑制动脉ICAM－1表达作用可能是其抑制高胆固醇膳食诱发的动脉粥样硬化的分子机制之一。     

细胞间黏附分子-1基因K469E多态性与冠状动脉支架置入后再狭窄相关性的初步探讨

目的　炎症反应是冠状动脉支架置入后再狭窄的重要因素 ,细胞间黏附分子 1(ICAM 1)是介导白细胞在血管内皮细胞表面紧密黏附的重要黏附分子。本研究的目的在于探索ICAM 1基因多态性与中国北方汉族人群中冠状动脉支架置入后再狭窄的相关性。方法　收集冠状动脉支架术后行冠状动脉造影随访的患者 12 4例 ,同时收集传统危险因素、手术相关因素信息。应用PCR RFLP方法确定ICAM 1K4 6 9E基因型。结果　入选的 12 4例患者中再狭窄者 72例 ,无再狭窄者 5 2例 ;12 4例中ICAM 1K4 6 9E基因型频率为 :KK纯合子 5 0 8% ,EE纯合子 7 3% ,EK杂合子 4 1 9%。再狭窄患者中KK纯合子和E等位基因携带基因型的频率分别为 5 8 3%、4 1 7% ;无再狭窄患者中二者的频率分别为 4 0 4 %、5 9 6 %。二者分布差异有显著性 (P =0 0 4 9)。调整混杂因素后显著性差异更为明显 ,KK纯合子OR值为 2 6 ,95 %可信区间为 1 2～ 5 8(P =0 0 18)。危险因素分层发现在肥胖 (体重指数≥ 2 7)、高脂血症患者KK纯合子的再狭窄危险更高 ,OR值分别为 9 3、3 7(P值均小于 0 0 5 )。结论　ICAM 14 6 9KK纯合子冠状动脉支架置入后再狭窄危险性较高 ,且在肥胖或高脂血症患者中作用更为显著。     

吡咯烷二硫代氨基甲酸酯联合霉酚酸酯保护糖尿病大鼠肾脏机制的实验研究

目的 探讨吡咯烷二硫代氨基甲酸酯(PDTC)联合霉酚酸酯(MMF)对糖尿病大鼠肾脏协同保护作用及机制.方法 链脲佐菌素(STZ)诱导糖尿病大鼠34只,并随机分为糖尿病未治疗组(D组),PDTC治疗组(P组), MMF治疗组(M组)和PDTC联合MMF治疗组(P+M组),以正常同龄大鼠作为对照组(C组).8周后测定血糖、血尿素氮、肌酐及24 h尿蛋白.处死动物后,称肾重并计算肾重指数(KI);光镜、电镜观察肾脏病理改变;免疫组化检测肾小球白细胞介素18(IL-18)、细胞间黏附分子1(ICAM-1)、肿瘤坏死因子的表达.结果 D组及各治疗组血糖、血尿素氮、肌酐、24 h尿蛋白、KI均高于C组(P＜0.05);各治疗组与D组相比,除血糖外,上述各指标均有明显改善(P＜0.05);P+M组24 h尿蛋白低于P和M组(P＜0.05).D组大鼠肾小球体积增大、系膜细胞增生、毛细血管基底膜增厚、足突融合, 各治疗组上述病理改变有不同程度减轻.D组IL-18、 ICAM-1、 TNF-α在肾小球的表达较C组增高(P＜0.05),各治疗组较D组表达下降(P＜0.05),其中P+M组IL-18、ICAM-1、TNF-α表达较M组下降显著(P＜0.05),IL-18、TNF-岜泶锝螹组下降(P＜0.05).结论 PDTC和MMF对糖尿病大鼠肾脏均有保护作用,二者联用较单药效果更好,其机制可能与抑制肾内炎性细胞因子表达有关.     

培哚普利和依那普利对ApoE基因敲除小鼠动脉粥样硬化进展的影响

目的 探讨血管紧张素转换酶抑制剂(ACEI)对ApoE基因敲除小鼠动脉粥样硬化病变进程的影响,特别是对斑块成分的影响,并比较培哚普利与依那普利的疗效.方法 ApoE基因敲除小鼠随机分为培哚普利组、依那普利组及对照组3组.对主动脉根部斑块进行定量分析,并评估斑块胶原含量及脂核面积.以冰冻切片进行免疫荧光检查,观察斑块内单核细胞/巨噬细胞-2(MOMA-2)、细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子(VCAM-1)、基质金属蛋白酶-9(MMP-9)的表达.结果 各实验组之间的血压、血脂差异无统计学意义.与对照组比较,培哚普利组与依那普利组的斑块面积分别少了25.33%和22.86%(P均＜0.01),但是两组ACEI的斑块面积差异无统计学意义.培哚普利组与依那普利组减小脂核面积(分别为52.98%及38.98%,P均＜0.01)及MOMA-2(分别为88.38%及52.16%,P均＜0.01)、ICAM-1(分别为80.87%及49.59%,P均＜0.01)、VCAM-1(分别为77.56%及56.44%,P均＜0.01)、MMP-9(分别为86.93%及55.56%,P均＜0.01)的表达,并增加斑块胶原含量(分别为298.36%及168.14%,P均＜0.01),而且培哚普利组在这些方面均显著优于依那普利组(P均＜0.05).结论 ACEI在不影响血脂和血压的情况下可以抑制ApoE基因敲除小鼠动脉粥样硬化斑块的炎症并延缓动脉粥样硬化的进展.尽管培哚普利和依那普利在减少斑块面积方面差异无统计学意义,但是培哚普利在稳定斑块方面优于依那普利.     

膳食碘对高脂血症小鼠甲状腺功能及脂代谢的影响

目的 研究碘摄入量对高脂血症小鼠甲状腺功能及血脂代谢的影响.方法 将4周龄雌性c57BL/6J小鼠50只随机分为重度低碘组(SID)、轻度低碘组(MID)、适碘组(NI)、10倍碘过量组(10HI)、50倍碘过量组(50HI),每组10只.均用高脂、高胆固醇、低碘(碘含量为20～40 μg/kg)饲料喂养.SID组饮用...     

Phase tissue intercellular adhesion molecule-1 expression in nude mice human liver cancer metastasis model

AIM To study the phase cancer tissue intercellular adhesion molecule-1 (ICAM-1) expression of human cancer metastasis model in nude mice, and to analyze the relationship between ICAM-1 expression and the metastasis and recurrence of hepatocellular cancinoma (HCC).METHODS HCC tissues from liver cancer metastasis model in nude mice (LCI-D20) was orthotopically implanted, and ICAM-1 expression in HCC tissues at different growing time were detected by immunodot blot. Tumor size, intrahepatic and extrahepatic metastasis foci were observed by naked eyes and under light microscope.RESULTS ICAM-1 was positively correlated to the tumor growing time (r=0.88, P＜0.01) and tumor size r=0.5, P＜0.05). It was higher in metastatic HCC than in nonmetastatic HCC (8.24±0.95 vs 3.03±0.51, P＜0.01). ICAM-1 content in cancer tissues increased suddenly after metastasis occurred and then maintained in a high level. ICAM-1 was also higher in multimetastasis group than in monometastasis group (10.05±1.17 vs 5.48±0.49, P＜0.05).CONCLUSION Tissue ICAM-1 could predict not only the metastasis of human liver cancer metastasis model in nude mice early and sensitively, but also the metastasis degree. So tissue ICAM-1 may be a potential index indicating the status of metastasis of HCC patients.     

胃肿瘤患者循环可溶性细胞间粘附分子-1和血管细胞粘附分子-1

AIM To elucidate the biological and clinical significance of sICAM-1 and sVCAM-1 in patients with gastric cancer.METHODS The serum levels of soluble ICAM-1 and VCAM-1 were measured with sandwith enzyme immunoassay.RESULTS In gastric cancer patients, soluble ICAM-1 and VCAM-1 concentrations were significantly elevated in comparision with those of healthy subjects (289.23μg/L±32.69μg/L vs 190.44μ/L±35.92μg/L,1430.88μg/L±421.71μg/L vs 727.24μg/L±157.68μg/L, respectively, P＜0.01). The increment in serum sICAM-1 and sVCAM-1 concentrations correlated well with the staging of gastric cancer. The serum levels of sICAM-1 and sVCAM-1 in patients of Ⅲ-Ⅳ stages were higher than those of Ⅰ-Ⅱ stages (346.60μg/L±92.10μg/L vs 257.54μg/L±32.77μg/L, 1800.60μg/L±510.76μg/L vs 1262.81μg/L±236.73μg/L). The levels of sICAM-1 and sVCAM-1 were correlated significantly (r=0.49,P＜0.01). The sICAM-1 and sVCAM-1 levels correlated positively with alkaline phophatase (r=0.63,0.71,P＜0.001) and white cell count (r=0.52,0.43, P＜0.01); but correlated negatively with serum albumin (r=-0.41, -0.49, P＜0.01).CONCLUSION The measurement of circulating ICAM-1 and VCAM-1 may bring additional prognostic information for patients with gastric cancer in varying stages.INTRODUCTIONTumor growth and metastasis involves a variety of cell-cell and cell-extracellular matrix interactions mediated by cell adhesion molecules. Currently, a number of cell adhesion molecules, such as intercellular adhesion molecules-1 (ICAM-1), vascular cell adhesion molecules-1 (VCAM-1), etc. have been found.ICAM-1 and VCAM-1 are members of the immunoglobulin supergene family which are cytokine-induced glycoproteins (IL-1, TNFα and IFNγ). Both of them have five or seven extracellular immunoglobulin-like domains, a single transmembranous domain and a short cytoplasmic tail[1,2]. The natural ligand of ICAM-1 or VCAM-1 is LFA-1 (CD11a) and Mac-1 (CD11b) or VLA-4, respectively[3]. ICAM-1 is a widely distributed protein on a variety of tissues, and can be detected in many cells such as macrophage, T- and B-cells, or fibroblasts, endothelial and epithelial cells. VCAM-1 is also a widely distributed protein and is constitutively expressed on tissue macrophage, dentritic cells in lymphoid tissue and skin, as well as on bone marrow fibroblasts and epithelial cells. Expression of VCAM-1 is inducible on vascular endothelial cells under pathological conditions[4].Recently, soluble forms of several adhesion molecules including ICAM-1 and VCAM-1 were found in serum of normal donors[5]. Abnormally high levels of them have been described in some solid malignant tumors, leukemia, autoimmune disease, infectious disease, etc.The present study was carried out to measure the circulating levels of sICAM-1 and sVCAM-1 in gastric cancer before treatment was given and to study their correlation with clinical, histological and routine laboratory parameters.     

老年代谢综合征患者血清炎性因子及脂联素水平与轻度认知功能障碍的关系

目的 探讨老年代谢综合征(metabolic syndrome,MS)患者血清基质金属蛋白酶(MMP)-9、细胞间黏附因子(ICAM-1)、脂联素水平与认知功能的相关性.方法 采用多种神经心理学量表对MS患者74例和健康对照者30例进行认知功能评定,并测量其体质指数(BMI)、腹围、血压及检测空腹血糖(FBG)、血脂等代谢指标;将MS患者再分为MS+轻度认知功能障碍(MCI)组(39例)和MS组(35例);测定所有受试者的MMP-9、ICAM-1和脂联素水平.结果 (1)MS+MCI组的BMI、收缩压、FBG、三酰甘油(TG)水平均高于MS组及对照组(P＜0.05).MS+MCI组、MS组血清MMP-9、ICAM-1的水平明显高于对照组(P＜0.01),而脂联素水平明显低于对照组(x2=26.62,P＜0.01);MS+MCI组血清MMP-9水平明显高于MS组(Z=-4.61,P＜0.05),脂联素水平明显低于MS组(Z=-5.77,P＜0.05);(2)Spearman直线相关分析显示,MS+MCI组、MS组血清MMP-9(r=-0.794,P＜0.001)、ICAM-l(r=-0.501,P＜0.001)与脂联素显著负相关,MMP-9与ICAM-1之间显著正相关(r=0.481,P=0.006);(3)多重线性回归分析显示,蒙特利尔认知评估量表(MoCA)评分与MMP-9(β=-3.438,P=0.001)、脂联素(β=1.337,P=0.006)、收缩压(β=-0.058,P=0.003)、FBG(β=-0.227,P=0.049)具有线性相关关系;(4)多因素Logisic逐步回归分析结果显示,高MMP-9(OR=1.007)、低脂联素(OR=0.359)水平是老年MS患者发生认知功能障碍的危险因素.结论 老年MS患者存在认知功能损害;MCI患者血清炎症因子表达增加,且与代谢异常存在相关性;MMP-9可能促进神经退行性变,而脂联素在这一过程中起到保护作用,表明炎性反应参与老年MS患者MCI的病理过程.

Abstract：

Objective To evaluate the relationships of the serum levels of matrix metalloproteinase-9 (MMP-9), intercellular adhesion molecule-1 (ICAM-1) and adiponectin with the mild cognitive impairment (MCI) in senile metabolic syndrome (MS)patients. Methods The 74 cases with MS and 30 health controls (control group) were enrolled. Mini-mental state examination (MMSE), montreal cognitive assessment (MoCA), digit-symbol test (DST), auditory verbal memory test (AVMT), trail making test(TMT), sunderland clock drawing test (CDT) and verbal fluency test (VFT) were applied to evaluate cognitive function. Based on the cognitive assessment, MS patients were divided into two groups: 39 cases with MCI (MS+MCI group) and 35 cases without cognitive impairment (MS group). The levels of MMP-9, ICAM-1 and adiponectin were measured by ELISA. Biochemical variables were measured by routine methods in all subjects. Results (1)MS+MCI group showed the higher levels of BMI, SBP, FBG and MMP-9 (all P＜0.05) and lower level of adiponectin (P＜0.05) than did the MS group. And MS group had higher levels of MMP-9 and ICAM-1 (P＜0.01) and lower adiponectin level (P＜0.01) than did the control group. (2)Spearman's correlation analysis showed that the serum levels of MMP-9 (r=-0.794, P＜0.001) and ICAM-l (r=-0.501, P＜0.001) were negatively correlated with adiponectin. However, MMP-9 was positively correlated with ICAM-1 (r=0.481, P=0.006). (3)Multiple linear regression analysis indicated that there was linear relationship of MoCA with MMP-9 (β=-3.438, P=0.0019), adiponectin (β=1.337, P=0.006), SBP (β=-0.058, P=0.003) and FBG (β=-0.227, P=0.049). (4)Stepwise logistic analysis showed that both high MMP-9 (OR=1.007) and low adiponectin (OR=0.359) were risk factors for the decline of cognitive function. Conclusions Elderly patients with MS may show deterioration in memory, calculation and visuospatial perception. Elevated inflammatory factors might contribute, in combination with abnormal metabolism, to MCI. MMP-9 might contribute to neuronal degeneration. However, adiponectin could strongly counteract the risk factors for cognitive impairment.     

Migration inhibitory factor up-regulates vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 via Src, PI3 kinase, and NFkappaB

Cell adhesion molecules are critical in monocyte (MN) recruitment in immune-mediated and hematologic diseases. We investigated the novel role of recombinant human migration inhibitory factor (rhMIF) in up-regulating vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) and their signaling pathways in human MNs. rhMIF-induced expression of VCAM-1 and ICAM-1 was significantly higher compared with nonstimulated MNs. rhMIF induced MN VCAM-1 and ICAM-1 expression in a concentration-dependent manner (P < .05). Antisense oligodeoxynucleotides (ODNs) and inhibitors of Src, PI3K, p38, and NFkappaB significantly reduced rhMIF-induced MN VCAM-1 and ICAM-1 expression (P < .05). However, Erk1/2 and Jak2 were not involved. Silencing RNA directed against MIF, and inhibitors of Src, PI3K, NFkappaB, anti-VCAM-1, and anti-ICAM-1 significantly inhibited rhMIF-induced adhesion of HL-60 cells to human dermal microvascular endothelial cells (HMVECs) or an endothelial cell line, HMEC-1, in cell adhesion assays, suggesting the functional significance of MIF-induced adhesion molecules (P < .05). rhMIF also activated MN phospho-Src, -Akt, and -NFkappaB in a time-dependent manner. rhMIF induced VCAM-1 and ICAM-1 up-regulation in 12 hours via Src, PI3K, and NFkappaB as shown by Western blotting and immunofluorescence. MIF and MIF-dependent signaling pathways may be a potential target for treating diseases characterized by up-regulation of cell adhesion molecules.     

辛伐他汀对高脂血症大鼠心肌梗死后心室重构的影响

目的研究高脂血症对心肌梗死(AMI)后心室重构的影响,以及辛伐他汀对心梗大鼠心室重构的作用。方法高脂饲料喂养SD大鼠15d后结扎冠脉,造成高脂血症心肌梗死复合模型,分为假手术组、心梗组、高脂假手术组、高脂心梗组、辛伐他汀大剂量和小剂量共6组,术后48h给药,观察48h和4周死亡率,高频超声心动图于术后4周观察心脏结构功能及梗死心肌范围。结果高脂组大鼠AMI后48h死亡率高于正常血脂AMI组(P<0.05)。术后4周高脂假手术组较正常血脂假手术组FS降低(P<0.05);且血清TC、LDL-C水平分别与FS、EF和LVDs呈直线相关(P<0.01)。辛伐他汀大、小剂量均能降低LVDd、LVDs(P<0.05,0.01),降低LVEDV、LVESV(P<0.01),升高EF、FS(P<0.05)。结论高脂血症能损害心功能,增加AMI后急性期死亡率,高脂AMI动物较正常血脂AMI动物心室重构和心功能损伤均有加重趋势。辛伐他汀不仅降低血脂水平,还可减轻心室扩张,改善心功能。     

外周血单个核细胞中与慢性乙型肝炎重症化进程有关的免疫分子表达

目的 筛选慢性乙型肝炎(CHB)患者外周血单个核细胞(PBMC)中与肝炎重症化相关的免疫分子.方法 采用荧光定量PCR技术检测各型CHB患者PBMC中39个免疫分子(包括白细胞分化抗原、趋化因子受体、凋亡相关配体和受体、黏附分子、Toll样受体等)mRNA的相对表达水平.多组间两两比较采用单因素方差分析中的Scheffe法,相关性检验采用Spearman等级相关分析.结果 荧光定量结果显示,39个免疫分子中与肝炎严重程度相关的分子共有9个,即肿瘤坏死因子相关凋广诱导配体(TRAIL)、TRAIL受体(TRAIL-R)2、CD64、CD30、CD27、CD28、L-选择素(CD62L)、细胞间黏附分子-1(ICAM-1)和CXC型趋化因子受体(CXCR)2,与健康对照组相比,这9种免疫分子在CHB重度组的表达量增高倍数分别为3.88、4.37、2.51、2.22、2.97、2.53、4.07、4.29和4.25倍(F=1.96、2.13、1.33、1.16、1.57、2.14、2.03、2.10、2.08,均P＜0.05).其中TRAIL、TRAIL-R2、CD64、CD30、CD27的表达量与IFNγ的表达量呈显著正相关(r=0.816、0.572、0.462、0.697、0.793,均P＜0.01).TRAIL-R2、CD64、CD30、CD62L、ICAM-1表达量与TNF-α的表达量呈显著正相关(r=0.494、0.588、0.568、0.968、0.976,均P＜0.01).结论 TRAIL、TRAIL-R2、CD64、CD30、CD27、CD28、CD62L、ICAM-1和CXCR2的异常表达与肝脏炎性反应和肝炎重症化相关.