锌原卟啉干预对新生大鼠缺血缺氧性脑损伤的影响

目的 探讨锌原卟啉干预对新生大鼠缺血缺氧性脑损伤的影响。方法 7日龄SD仔鼠125只，随机分为3组，观察各组脑组织HO－1活性、CO和cGMP含量的变化及脑组织的病理改变。结果 （1）缺血缺氧组HO－1活性、cGMP及CO水平升高，与对照组比较有明显差异（P＜0.01)；HI＋Znpp组的HO－1活性，cGMP及CO水平低于HI组（P＜0.01)。（2）HI组及HI＋Znpp组均表现出缺血缺氧的改变但HI组的病理改变明显比HI＋Znpp组严重。结论 缺血缺氧时应用锌原卟啉预处理对新生大鼠缺血缺氧性脑损伤有保护作用。     

左旋四氢巴马汀对大鼠脑微血管内皮细胞缺氧-复氧时细胞间粘附分子-1的影响

目的：探讨左旋四氢巴马汀（L－THP）对缺氧－复氧时脑微血管内皮细胞细胞间粘附分子－1（ICAM－1）表达的影响。方法：采用流式细胞仪检测脑微血管内皮细胞在缺氧、缺氧－复氧及加入L－THP后ICAM－1的阳性细胞百分率。结果：缺氧12h，脑微血管内皮细胞ICAM－1的表达与常氧时差异无显著意义，缺氧12h再给氧12h,ICAM-1的表达明显增加，加入L－THP后，ICAM－1的阳性细胞百分率明显降低。结论：L－THP可减少缺氧－复氧时脑微血管内皮细胞ICAM－1的表达。     

白介素—10和一氧化氮对内毒素诱导肺泡巨噬细胞核因子—кB活化及肿瘤坏死因子释放的调节

目的：探讨白介素－10和外源性一氧化氮（NO）对内毒素（LPS）诱导肺泡巨噬细胞（PAM）核因子－кB（NF－кB）活化及肿瘤坏死因子－α（TNF－α）基因表达的调节，为临床运用提供理论依据。方法：用支气管肺泡灌洗法收集PAM进行培养，分为正常对照组、LPS组、IL－10＋LPS组和NO＋LPS组。用凝胶电泳迁移率改变分析（EMSA）法和酶联免疫吸附（ELISA）法分别检测核提取物中NF－кB活性和细胞培养上清中TNF－α含量。结果：LPS组NF－кB活性和TNF－α含量在刺激后3显著高于对照组；IL－10＋LPS组和NO＋LPS组NF－кB活性和TNF－α含量均显著低于LPS组。结果：LPS诱导PMAM宾NF－кB活化，导致TNF－α基因表达增强；白介素－10和外源性NO可抑制NF－кB活化而减少TNF－α的释放。     

山莨菪碱对脑微血管内皮细胞缺氧-复氧时细胞间黏附分子-1的影响

目的：探讨山莨菪碱（Ani）对缺氧－复氧时脑微血管内皮细胞间黏附分子－1（ICAM－1）表达的影响。方法：采用流式细胞仪检测脑微血管内皮细胞在缺氧、缺氧－复氧及加入Ani后ICAM－1的阳性细胞百分率。结果：缺氧12h，脑微血管内皮细胞ICAM－1的表达与常氧时差异无显著意义，缺氧12h再给氧12h，ICAM－1的表达明显增加，加入Ani后，ICAM－1的阳性细胞百分率明显降低。结论：Ani可减少缺氧－复氧时脑微血管内皮细胞ICAM－1的表达。     

姜黄素对缺氧再给氧大鼠心脏微血管内皮细胞ICAM-1表达的影响

目的：研究姜黄素对缺氧再给氧大鼠心脏微血管内皮细胞粘附分子ICAM－1表达的影响。方法：培养大鼠心脏微血管内皮细胞，建立细胞缺氧再给氧模型，采用酶联免疫吸附试验（ELISA）测定内皮细胞粘附分子ICAM－1的蛋白表达，Northern blot分析测定ICAM－1mRNA的表达。结果：缺氧后内皮细胞ICAM－1的蛋白和mRNA表达明显升高，缺氧再给氧后增高更明显，姜黄素组ICAM－1的蛋白和mRNA的表达较缺氧再给氧组明显下降，呈剂量依赖效应。结论：姜黄素能明显下调缺氧再给氧大鼠心脏微血管内皮细胞ICAM－1的表达，抑制内皮细胞的激活。     

丙泊酚对脂多糖诱导的大鼠肺微血管内皮细胞AQP-1表达的影响

目的 观察丙泊酚对脂多糖（LPS）刺激的大鼠肺微血管内皮细胞水通道蛋白-1（AQP-1）表达的影响，阐明其减轻急性肺损伤的可能机制。方法 大鼠肺微血管内皮细胞体外培养后随机分为7组，每组5份：①C组（对照组）；②LPS0.1组（脂多糖终浓度为0、1μg／mL）；③LPS，组（脂多糖终浓度为1μg/mL）；④LPS10组（脂多糖终浓度为10μg／mL）；⑤P4（丙泊酚终浓度为4μg／mL＋LPS10组；⑥P40（丙泊酚终浓度为40μg／mL）＋LPS10组；⑦L40（脂质溶剂的体积和浓度同P40＋LPS10组。按上述分组，在相应组中分别加入不同浓度丙泊酚、等量脂肪乳剂或培养液，于37℃5％CO2培养箱中孵育30min，再在相应组中加入LPS,置于培养箱继续孵育6h。收集细胞并测定下列指标：AQP一1（免疫细胞化学和Westernblotting）和蛋白质渗透压反射系数（σ）。结果 LPS可浓度依赖性减少内皮细胞AQP-1的表达和（值P〈0．01）。与LPS10组比较，P4＋LPS10及P40＋LPS10两组能显著增加内皮细胞AQP-1的表达和（值P〈0．01），而140＋LPS10组变化不明显（P〉0．05）。结论 丙泊酚可通过调节AQP-1的表达和盯变化，从而减轻ALI／ARDS肺水肿的形成。     

一氧化氮对内毒素刺激肺泡巨噬细胞核因子-κB的影响

目的：探讨一氧化氮（NO）在内毒素刺激肺泡巨噬细胞（PAM）对核因子－kB(NF-kB)活性的影响。方法：用支气管肺泡灌洗法收集PAM进行培养，分正常对照组、脂多糖（LPS）组和NO＋LPS组。用凝胶电泳迁移率改变分析（EMSA）法和酶联免疫吸附（ELISA）法分别检测核提取物中NF－kB活性和细胞培养上清中肿瘤坏死因子－α（TNF-α）含量。结果：LPS组NF－kB活性和TNF－α含量在刺激后1小时明显高于正常对照组；NO＋LPS组NF－kB活性和TNF－α含量在刺激后1小时均显著低于LPS组。结论：LPS诱导PAM的NF－kB活化，导致TNF－α大量释放；NO可抑制NF－kB活化而减少TNF－α的基因表达。     

抑制一氧化氮合成对犬感染性休克的影响

目的：探讨一氧化氮（NO）在感染性休克中的作用机制，及抑制NO合成的治疗学意义。方法：10只健康杂种狗予戊巴比妥麻醉，大肠杆菌内毒素（LPS）60μg·kg-1·h-1×30min静脉滴注，继以生理盐水（NS）15ml·kg-1·h-1维持。随机分成两组。组Ⅰ、组Ⅱ在LPS开始注射后60min分别单剂注射NS30ml、NS30ml＋L-硝基精氨酸（LNNA）20mg·kg-1。观察血液动力学、氧动力学、尿NO3/NO2（NOx）、血浆内皮素（ET）变化。结果：LPS注射后60min两组动物均呈典型高动力状态，平均动脉压（MAP）、体循环阻力（SVRI）明显下降，心脏指数（CI）轻度增加。LPS使氧输送（DO2）、氧耗（VO2）增加。尿NOx升高。LNNA使MAP恢复至基础水平，SVRI、PVRI显著升高且超过基础值；CI下降，DO2、VO2减少，PvO2上升，尿NOx低于组Ⅰ，而ET明显高于组Ⅰ。结论：LPS诱导的犬感染性休克的血液动力学异常与NO过多释放有关，NO抑制LPS引起的ET释放。LNNA虽可逆转低血压，但对感染性休克的整体治疗不利。     

血管紧张素Ⅱ受体拮抗剂对大鼠内毒素性急性肺损伤的保护作用

目的 研究血管紧张素Ⅱ（AngⅡ）受体拮抗剂对大鼠内毒素性急性肺损伤（ALI）的保护作用。方法 取Wistar大鼠印只，雌雄不拘，随机分为三组：（1）正常对照组（10只），给予大鼠静注等量生理盐水；（2）大肠肝菌脂多糖（LPS）组，分为3、6、12和24h四个观察组（每组均10只），分别给大鼠注射LPS（10mg／kg），间隔不同的时间后将大鼠放血活杀，取肺组织待测；（3）LPS＋AngⅡ受体拮抗剂组（10只），先给予大鼠静注AngⅡ受体拮抗剂[Sar^1，Ile^8]AngⅡ（20μg/kg）处理，然后观察6h，放血活杀后取肺组织待测。分别以肺湿／干重比、伊文思蓝法测定肺微血管通透性和肺组织病理变化，观察LPS对大鼠肺组织的急性损伤作用以及AngⅡ受体拮抗剂对该损伤作用的影响。结果 与对照组比较，LPS组各时相点大鼠肺组织W／D值显著升高（P〈0．01），致大鼠肺血管中伊文思蓝染料向组织中渗漏显著增多（P〈0．01），LPS组出现炎性细胞浸润、水肿等损伤表现，总病理评分达（12．00±2．45）分；LPS＋AngⅡ受体拮抗剂组大鼠肺组织湿／干重比、肺微血管蛋白渗出量和组织形态学变化均较LPS组显著好转。结论 AngⅡ受体拮抗剂对大鼠内毒素性ALI有保护作用。     

老年大鼠心肌再灌注时ICAM-1表达变化规律及艾司洛尔的影响

目的：探讨细胞间粘附分子－1（ICAM－1）表达与老年大鼠心肌缺血再灌注损伤（IRI）的关系，并观察艾司洛尔（ES）对IRI的影响。方法：大鼠116只，分设缺血再灌注（IR）组，IR＋ES组和假手术对照组，并分设缺血1h，再灌注3、6、12、24h时相点，取缺血心肌用原位杂交和免疫组织化学方法检测ICAM－1 mRNA及其蛋白质表达水平，用酶法测定中性粒细胞（PMNs)浸润数，硫代巴比妥酸比色法测定心肌组织丙二醛（MDA），用黄嘌呤过氧化物酶法测定过氧化物歧化酶（SOD）活性，TTC染色法测定梗死范围。结果：心肌IR时，ICAM－1表达、MDA含量、PMNs浸润数均明显增高，SOD活性明显降低；ICAM－1蛋白表达水平、PMNs浸润与心肌梗死范围呈显著正相关，但ICAM－1 mRNA、MDA、SOD与梗死范围无明显相关性。IR＋ES组上述指标于再灌注时虽也明显增高，但比IR组明显减轻。结论：心肌IR时，ICAM－1参与介导了PMNs对组织细胞的粘附、浸润和IRI的发生、发展；ES可通过抑制ICAM－1的表达而产生心肌保护作用。     

Effect of berberine on hepatocyte proliferation,inducible nitric oxide synthase expression,cytochrome P450 2E1 and 1A2 activities in diethylnitrosamine- and phenobarbital-treated rats

This study investigated the effect of berberine on the early phase of hepatocarcinogenesis stimulated by diethylnitrosamine (DEN, 150 mg/kg, 4 weeks) plus phenobarbital (PB, 75 mg/kg, 7 days) in rats. The expressions of proliferating cell nuclear antigen (PCNA) and inducible nitric oxide synthase (iNOS) were evaluated by immunohistochemistry. The activities of CYP isoenzymes were analyzed using different probe drugs including chlorzoxazone (CYP2E1) and phenacetin (CYP1A2) by high-performance liquid chromatography (HPLC) in vivo or in vitro. Results showed that the expressions of PCNA and iNOS were induced by DEN plus PB in liver tissues. Oral administration of berberine (50 mg/kg) inhibited the hepatocyte proliferation and iNOS expression, decreased cytochrome P450 content, inhibited activities of CYP2E1 and CYP1A2 in DEN-plus-PB-treated rats in vivo. Moreover, berberine (10, 50 and 100 μM) inhibited the activities of CYP2E1 and CYP1A2 in microsomes isolated from DEN-plus-PB-treated rats in vitro, suggesting that anti-hepatocarcinogenetic potential of berberine might be due to inhibiting oxidative metabolic activities of CYP 2E1 and CYP1A2, and decreasing NO production in rats.     

雌二醇化学发光免疫测定法的建立

目的　建立灵敏度高 ,测定范围宽的检测人血清雌二醇 (E2 )的化学发光免疫分析法 (CLIA)。方法　采用竞争抑制法 ,用碱性磷酸酶标记抗原 ,金刚烷 (CSPD)增敏化学发光体系作为酶底物。结果　敏感度为 2 .0pg/ml;在 10～ 10 0 0pg/ml之间可以准确定量 ;用不同浓度的E2 质控血清测定精密性 ,批内变异 <8% (n =2 0 ) ,批间变异 <10 % (n =2 0 )。与雌醇、雌酮、雌三醇(E3 )的交叉反应 <1% ,与睾酮、可的松等无交叉反应。试剂具有良好的稳定性 ,在 4℃保存 14个月其整体变化幅度 <10 %。与BeckmanAccessTm及其配套试剂比较有较好的相关性。结论　方法灵敏度高 ,特异性强 ,稳定性好 ,检测范围宽 ,准确性和重复性好。     

The Expression of Heme Oxygenase-1 Induced by Lansoprazole

Our previous studies have demonstrated that lansoprazole inhibits acute inflammatory reactions as well as intestinal mucosal injuries induced by ischemia-reperfusion or indomethacin administration in rats. Thus, proton pump inhibitors such as lansoprazole have been demonstrated to prevent gastrointestinal mucosal injury by mechanisms independent of acid inhibition. In our in vitro study, lansoprazole induced the expression of heme oxygenase-1 (HO-1) on rat gastric epithelial cells (RGM-1 cells), and exerted anti-inflammatory effect on the dependent of HO-1 expression. Furthermore, NF-E2-related factor-2 (Nrf2) played an important role in HO-1 expression induced by lansoprazole. In this review, we focused on lansoprazole-induced HO-1 expression, its anti-inflammatory action, and the role of Nrf2 in its expression.     

胸腺肽联合血必净对老年肺部感染合并脓毒症患者的免疫调节作用

目的探讨胸腺肽联合血必净在老年肺部感染合并脓毒症患者中,通过改变辅助性T细胞1/2（Th1/Th2）、调节性T细胞（Treg细胞）的表达而发挥免疫调节作用。方法收集2012-01～2014-01南京医科大学附属南京医院ICU老年肺部感染合并脓毒症患者60例作为治疗组,应用胸腺肽联合血必净免疫调节治疗,采集入院时和第7天留取外周血,用流式细胞仪检测Th1、Th2细胞和Treg细胞,同时送检降钙素原（ PCT）、C-反应蛋白（ CRP）;以7 d死亡为终点将治疗组再分成两组,其中17例死亡患者为死亡组,存活的43例为生存组。以同期住ICU的老年肺部感染合并脓毒症未用胸腺肽和血必净治疗的19例患者为对照组。结果①治疗组第7天Th1、Th2细胞高于入院时及对照组治疗前后（P均＜0．05）;治疗组第7天Th1/Th2高于入院时及对照组治疗前后（P均＜0．01）;治疗组第7天Treg细胞低于入院时（P＜0．01）,与对照组治疗前后比较差异无统计学意义（ P＞0．05）。②生存组治疗第7天Th1、Th2细胞高于死亡组（ P分别＜0．01、＜0．05）,Treg细胞低于死亡组（P＜0．01）。③60例患者入院时CRP、PCT和APACHEⅡ评分与对照组比较差异无统计学意义（P＞0．05）。④治疗组住ICU时间短于对照组（P＜0.05）;两组病死率比较差异无统计学意义（P＞0．05）。结论老年肺部感染合并脓毒症患者早期外周血Th1、Th2细胞和Treg细胞表达异常,胸腺肽联合血必净治疗可改善机体的免疫状态。     

Nurse Practitioner–Directed Cardio-Diabetes Pilot Program

Historically, antihyperglycemics for patients with Type 2 diabetes have not been managed by cardiology clinicians. This paradigm has shifted after the release of cardiovascular (CV) outcome trials using 2 new classes of antihyperglycemics agents, sodium-glucose cotransporter-2 inhibitors or glucagon-like peptide 1 receptor agonists, which demonstrated a decrease in all-cause mortality, CV death, and stroke. The purpose of this pilot program was to translate this trial data into practice by developing a protocol for cardiology-based nurse practitioners (NPs) to initiate these agents. Cardiology NPs demonstrated the feasibility of initiating these agents within a cardiology practice using a shared decision-making, patient-centric framework.     

α-甘露糖苷贮积症的分子遗传学及其在临床诊断与防治方面的意义

MAN281基因突变导致α-甘露糖苷酶缺乏或活性降低是引起α-甘露糖苷贮积症的根本内因。对MAN2BI基因、LAMAN酶的结构和功能的研究、基因型与表现型的相关性研究以及诊防治方面的研究近年来都取得了诸多新进展。本文重点围绕这几方面作一综述。     

Down-regulation of sphingosine kinase 2 (SphK2) increases the effects of all-trans-retinoic acid (ATRA) on colon cancer cells

Sphingosine kinase 2 (SphK2) is a type of sphingosine kinase, which express highly in most of cancers. SphK2 produce sphingosine-1-phosphate (S1P) and then accumulate in cancer cells. Our previous study showed that S1P antagonized the effects of all-trans-retinoic acid (ATRA) via the receptor-dependent and independent pathway. In this study, we aimed to investigate the roles of SphK2 in affecting ATRA's activity in human colon cancer cells. Cell proliferation was estimated by the clonogenic assay. The distribution of cell cycle was analyzed by flow cytometry assay. The apoptotic cells were determined by Annexin V-FITC/PI staining method. Western blotting assay was performed to analyze the levels of the proteins related to apoptosis and cell cycle. The mRNA levels of SphK2 and RARβ were evaluated by real-time PCR assay. RNA interference assay was performed to evaluate SphK2 activity. S1P antagonized the effect of ATRA on HT-29 cell proliferation, the ATRA-induced RARβ expression, the arrest of cell cycle in G₁-phase, and induction of apoptosis. Down-regulation of SphK2 resulted in the reverse actions on the S1P-induced antagonistic effects on ATRA. Western blotting analysis indicated that down-regulation of SphK2 might activate apoptotic proteins, regulation of p53/p21^Waf1/Cip1 and EGFR and PI3K/AKT signaling pathways. In conclusion, down-regulation of SphK2 increased the effects of ATRA on colon cancer cells.     

脓毒症大鼠肺基质金属蛋白酶-2/9表达与血必净干预

目的 观察创伤弧菌脓毒症大鼠肺基质金属蛋白酶(MMP)-2/9和组织型金属蛋白酶抑制剂(TIMP)-1/2的动态表达及血必净干预.方法 温州医学院生命科学院实验室,清洁级SD大鼠110只,随机(随机数字法)分为正常对照组(A组,n=10)、创伤弧菌脓毒症组(B组,n=50,采用大鼠左下肢皮下注射创伤弧菌悬液制作创伤弧菌脓毒症大鼠模型)及血必净干预组(C组,n=50,感染后0.5 h腹腔注射血必净4 mL/kg).B、C组大鼠于染菌后1,6,12,24,48 h麻醉后活杀,留取右肺标本.观察大鼠行为学变化,采用考马斯亮蓝法测肺通透性,采用逆转录-聚合酶链式反应(RT-PCR)法测肺MMP-2/9,TIMP-1/2 mRNA的表达,免疫组化法和双抗体夹心酶联免疫吸附法(ELISA)测肺MMP-2/9和TIMP-1/2的表达.数据采用单因素方差分析,并用LSD-t法进行组间两两比较,以P＜0.05为差异有统计学意义.结果 B组和C组肺通透性显著高于A组,C组显著低于B组.B组和C组MMP-2/9,TIMP-1/2mRNA显著升高,B组分别于6 h(0.344±0.108),6 h(1.230±0.377),12 h(0.523±0.098),12 h(0.280±0.070)达高峰(P＜0.05),C组分别于12 h(0.256±0.074),6 h(0.968±0.225),12 h(0.746±0.316),12 h(0.356±0.035)达高峰(P＜0.05),C组MMP-2/9mRNA升高趋势显著低于B组(P＜0.05),TIMP-1/2mRNA显著高于B组(P＜0.05).B组和C组MMP-2/9,TIMP-1/2蛋白也升高,B组分别于12 h(0.692±0.191),12 h(0.061±0.017),24 h(1384.42±91),24 h(41.04±3.60)达高峰(P＜0.05);C组分别于24 h(0.217±0.065),12 h(0.045±0.013),24 h(1617.22±103),24 h(47.66±3.58)达高峰(P＜0.05);C组MMP-2/9蛋白升高趋势低于B组(P＜0.05),TIMP-1/2蛋白早期与B组差别不大,后期显著高于B组(P＜0.05).结论 MMP/TIMP比例失衡是创伤弧菌脓毒症大鼠肺损伤机制之一,血必净可促进MMP/TIMP比例恢复平衡,对创伤弧菌脓毒症大鼠肺损伤具有保护作用.

Abstract：

Objective To detect the expression of MMP-2/9 and TIMP-1/2 in the lung of Vibrio vulnificus sepsis rats and observe the intervention of Xuebijing injection. Method One hundred and ten SD rats of clean grade were randomly(random number) divided into normal control group (group A, n = 10),Vibrio vulnificus sepsis group (group B, n = 50. Sepsis was reproduced in rats with subcutaneous injection in left lower limb with Vibrio vulnificus) and Xuebijin intervention group ( group C, n = 50. Rats were intraperitoneal(ip) with the dose of Xuebijing 4mL/kg at the time of 30 min later after infection). The rats in group B and C were sacrificed at 1 h, 6 h, 12 h, 24 h, 48 h after infection, the expression of MMP-2/9 and TIMP-1/2 were examined by PCR, Immunohistochemistry or ELISA methods, the lung permeability were measured by Coomassie Brilliant Blue method. Experimental data used single factor analysis of variance, and between groups by LSD method for pairwise comparison,P ＜0.05 statistically significant difference. Results The lung permeability increased both in group B and C compared with group A,and in group B were relatively higher. The lung MMP-2/9, TIMP-1/2mRNA expression in groups B and C compared with in group A was markedly higher, and reached the peak at 6 h(0. 344 ± 0. 108 ),6 h ( 1. 230 ± 0.377 ), 12 h (0.523 ±0.098),12 h(0.280±0.070) (P＜0.05) in group B while at 12 h(0.256 ±0.074),6 h(0.968±0.225) ,12 h(0.746 ±0. 316) ,12 h(0.356 ±0.035) (P ＜0. 05) in group C; the MMP-2/9mRNA expression in group C decreased(P＜0. 05) compared with the group B while the TIMP-1/2mRNA expression increased(P＜0. 05). The lung MMP-2/9, TIMP-1/2 protein expression in groups B and C compared with the group A(0.345±0.109) also increased, and the peak was at 12 h (0. 692 ± 0. 191 ), 12 h (0. 061 ±0.017) ,24 h(1384.42 ±91) ,24 h(41.04 ±3.60)in group B while at 24 h(0. 217 ±0.065) ,12 h(0. 045± 0. 013 ) ,24 h ( 1617.22 ± 103 ) ,24 h (47.66 ± 3.58 )in group C, the MMP-2/9 protein expression in group C was lower than in group B(P＜0.05), the TIMP-1/2 protein expression in group C was similar to in group B early while marked increased(P＜0.05)later. Conclusions MMP/TIMP imbalance was one of the mechanisms of the lung injury in the rats with Vibrio vulnificus sepsis, Xuebijing could restore the balance of MMP/TIMP ratio.     

地塞米松对大鼠光气急性肺损伤血管生成素-1、2的影响

目的 探讨地塞米松对大鼠光气急性肺损伤(ALI)血管生成素-1、2(Ang-1,2)表达的影响.方法 采用大鼠光气吸入性肺损伤动物模型.36只SD大鼠随机(随机数字法)分为3组:正常对照组(吸入与光气染毒组同等流量的空气)、光气染毒组(吸入8.33 mg/L纯度为100％的光气5min)、地塞米松处理组(尾静脉注入2.5 mg/kg地塞米松1h后,吸入同等剂量的光气).染毒2h后收集支气管肺泡灌洗液(BALF)测定中性粒细胞细胞数、蛋白含量和肺湿/干质量比(W/D).采用双抗体夹心酶标免疫分析法(ELISA法)测定各组血清和BALF中Ang-1,2水平.RT-PCR法对肺脏组织中Ang-1,2和Tie-2mRNA的水平进行半定量研究.Western blot技术检测肺脏组织中Ang-1,2和Tie-2蛋白含量.结果 与正常对照组比较,光气染毒组肺W/D、BALF中中性粒细胞数和蛋白含量明显升高,差异具有统计学意义(P＜0.01);与光气染毒组比较,地塞米松处理组的肺W/D、BALF中中性粒细胞数和蛋白含量明显降低,差异具有统计学意义(P＜0.01).与正常对照组比较,光气染毒组血清、BALF及肺组织中Ang-1和Tie-2表达明显下降,差异具有统计学意义(P＜0.01);与光气染毒组比较,地塞米松处理组Ang-1和Tie-2表达明显升高,差异具有统计学意义(P＜0.01).与正常对照组比较,光气染毒组血清、BALF及肺组织中Ang-2表达明显升高,差异具有统计学意义(P＜0.01);与光气染毒组比较,地塞米松处理组Ang-2表达明显下降,差异具有统计学意义(P ＜0.05,P＜0.01).结论 地塞米松可能通过抑制Ang-2表达并促进Ang-1和Tie-2表达来有效地保护大鼠光气吸入性急性肺损伤.     

急性脑梗死患者血浆血栓素B2、6-酮-前列腺素F1α及其比值水平的动态变化与临床意义

目的通过测定急性脑血管病患者血浆血栓素B₂(TXB₂),6-酮-前列腺素F_1α(6-keto-PGF_1α)的含量及其动态变化,了解血小板功能变化。方法检测205例急性脑梗死患者发病后24 h内、1周时、2周时的血浆TXB₂和6-keto-PGF_1α含量及其比值(T/6-K),并与正常对照组(n=40)进行比较。结果急性脑梗死患者发病后24 h内、1周时、2周时的血浆TXB₂和6-keto-PGF_1α的含量均明显高于正常正对照组(P<0.01);TXB₂在1周时达峰值,至2周时下降;6-keto-PGF_1α逐渐增高,至2周时达峰值;T/6-K在发病后24 h内、1周时均明显高于正常正对照组(P<0.01),1周时达峰值,至2周时下降,基本与正常对照组相似(P>0.05)。结论TXB₂、6-keto-PGF_1α及T/6-K的测定有助于了解急性脑梗死患者血小板功能的变化,保持TXB₂与6-keto-PGF_1α的平衡对维持血流通畅有重要意义。