急性坏死性胰腺炎模型大鼠血清脂联素表达水平及意义

目的观察急性坏死性胰腺炎模型大鼠血清脂联素表达变化及与胰腺损伤程度的相关性在急性坏死性胰腺炎发病中的意义。方法40只雄性Sprague-Dawley大鼠随机分为正常对照组(CON组)8只及急性坏死性胰腺炎组(ANP组)32只。CON组剖腹后只翻动十二指肠及胰腺后关腹。ANP组逆行胰胆管内注射1.5%去氧胆酸钠制备ANP模型。术后6、12、24、48 h处死大鼠,观察胰腺组织病理改变并评分,检测血清淀粉酶、脂联素、TNF-α和IL-6水平变化。结果 ANP组大鼠胰腺病理学评分及血清淀粉酶、TNF-α、IL-6水平均较CON组升高(P<0.05),血清脂联素在发病早期下降缓慢,24 h后迅速下降,48 h较24 h显著降低(P<0.01),并与胰腺病理学评分及TNF-α水平呈高度负相关(r=-0.846、-0.789,P<0.05)。结论血清脂联素在ANP发生发展中呈现一定的变化规律,并且与胰腺严重程度呈负相关,可能在ANP的发病机制中起重要作用。     

肝硬化大鼠小肠黏膜形态结构改变与内毒素血症

目的研究药物和胆汁淤积引起的肝硬化大鼠小肠黏膜形态结构改变和血浆内毒素水平。方法分别以硫代乙酰胺(TAA)(n=10)诱导和行胆管结扎术后(BDL)(n=7)的肝硬化大鼠为模型组,另以正常大鼠(n=12)作为正常对照组,分别观察光镜和透射电镜下小肠黏膜的形态,并采用鲎试剂基质显色法测定腹主动脉血浆内毒素含量。结果光镜下观察到模型组肝硬化大鼠小肠肠黏膜绒毛稀疏、萎缩,上皮细胞坏死,黏膜水肿伴有炎性细胞浸润;电镜下观察到模型组大鼠小肠壁超微结构有明显改变,肠黏膜绒毛破坏,减少,变短,倒伏,缺失,肠黏膜紧密间隙增宽,肠黏膜杯状细胞分泌减少,肠黏膜上皮细胞内线粒体和内质网肿胀。正常对照组大鼠的小肠黏膜绒毛形态及超微结构没有明显改变。模型组大鼠的血浆内毒素水平明显高于正常对照组(P<0.01)。结论模型组肝硬化大鼠都存在小肠黏膜结构的改变和内毒素水平的增高,提示肝硬化大鼠小肠黏膜的损伤与肠源性内毒素血症密切相关。     

Tumor necrosis factor-α and interleukin-6 in cirrhotic patients with spontaneous bacterial peritonitis

AIM: To evaluate the role of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in cirrhotic patients who have hepatic and renal impairment with spontaneous bacterial peritonitis (SBP).METHODS: We prospectively studied 120 cirrhotic patients with SBP and 80 cirrhotic patients with sterile ascitic fluid. They included 144 males and 56 females with ages ranging between 34 and 62 years. The diagnosis of cirrhosis was established by clinical and laboratory criteria that did not require histological confirmation. The severity of underlying liver disease was evaluated using Pugh’s modification of Child’s criteria (Child-Pugh scores). Ascitic fluid was sent to the laboratory for cell count, culture, sensitivity testing, and measurement of chemical elements (i.e., albumin, glucose). Specimens were inoculated into aerobic and anaerobic blood culture bottles. Serum and ascitic fluid were also collected in sterile tubes at study entry (before the initiation of antibiotic treatment) and 48 h later. Assays for TNF-α and IL-6 in the serum and ascitic fluid were performed with an immunoenzymometric assay using manufacture’s instructions.RESULTS: Cytokine levels in serum and ascitic fluid were significantly higher in the patients with SBP. (plasma TNF-α: 135.35 ng/mL ± 11.21 ng/mL vs 92.86 ng/mL ± 17.56 ng/mL, P < 0.001; plasma IL-6: 32.30 pg/mL ± 7.07 pg/mL vs 12.11 pg/mL ± 6.53 pg/mL, P < 0.001; ascitic fluid TNF-α: 647.54 ± 107.11 ng/mL vs 238.43 ng/mL ± 65.42 ng/mL, P < 0.001); ascitic fluid IL-6: 132.84 ng/mL ± 34.13 vs 40.41 ± 12.85 pg/mL, P < 0.001). About 48 (40%) cirrhotic patients with SBP developed renal and hepatic impairment and showed significantly higher plasma and ascitic fluid cytokine levels at diagnosis of infection. [(plasma TNF-α: 176.58 ± 17.84 vs 135.35 ± 11.21 ng/mL) (P < 0.001) and (IL-6: 57.83 ± 7.85 vs 32.30 ± 7.07 pg/mL) (P < 0.001); ascitic fluid TNF-α: 958.39 ± 135.72 vs 647.54 ± 107.11 ng/mL, (P < 0.001), ascitic fluid IL-6: 654.74 ± 97.43 vs 132.84 ± 34.13 pg/mL, (P < 0.001)]. Twenty nine patients (60.4%) with SBP and renal impairment died whereas, only four patients (5.55%) with SBP but without renal impairment died from gastrointestinal hemorrhage (P < 0.0005).CONCLUSION: It appears that TNF-α production may enhance liver cell injury and lead to renal impairment. This correlated well with the poor prognosis and significantly increased mortality associated with SBP in cirrhotic patients.     

VSL#3 can prevent ulcerative colitis-associated carcinogenesis in mice

AIM To investigate the effects of VSL#3 on tumor formation, and fecal and intestinal mucosal microbiota in azoxymethane/dextran sulfate sodium(AOM/DSS) induced mice model. METHODS C57 BL/6 mice were administered AOM/DSS to develop the ulcerative colitis(UC) carcinogenesis model. Mice were treated with 5-ASA(75 mg/kg/d), VSL#3(1.5 × 109 CFU/d), or 5-ASA combined with VSL#3 by gavage from the day of AOM injection for three months(five days/week). The tumor load was compared in each group, and tumor necrosis factor(TNF-α) and interleukin(IL)-6 levels were evaluated in colon tissue. The stool and intestinal mucosa samples were collected to analyze the differences in the intestinal microbiota by 16 s rDNA sequencing method.RESULTS VSL#3 significantly reduced the tumor load in AOM/DSS-induced mice model and decreased the level of TNF-α and IL-6 in colon tissue. The model group had a lower level of Lactobacillus and higher level of Oscillibacter and Lachnoclostridium in fecal microbiota than the control group. After the intervention with 5-ASA and VSL#3, Bacillus and Lactococcus were increased, while Lachnoclostridium and Oscillibacter were reduced. 5-ASA combined with VSL#3 increased the Lactobacillus and decreased the Oscillibacter. The intestinal mucosal microbiota analysis showed a lower level of Bifidobacterium and Ruminococcaceae_UCG-014 and higher level of Al oprevotel a in the model group as compared to the control group. After supplementation with VSL#3, Bifidobacterium was increased. 5-ASA combined with VSL#3 increased the level of both Lachnoclostridium and Bifidobacterium. CONCLUSION VSL#3 can prevent UC-associated carcinogenesis in mice, reduce the colonic mucosal inflammation levels, and rebalance the fecal and mucosal intestinal microbiota.     

TNF-α和IL-6血清检测在儿童急性病毒性心肌炎诊断中的价值

目的探讨急性病毒性心肌炎患儿血清肿瘤坏死因子-α（TNF-α）及白介素-6（IL-6）水平变化及其临床价值。方法应用放射免疫法（RIA）和酶联免疫法（EIISA）,检测53例急性病毒性心肌炎患儿及20名健康儿童血清中TNF—α及IL-6含量。结果心肌炎组血清TNF—α和IL-6水平分别为（526．7±32．9）mg／L和（3．23±0．53）mg/L,而健康组分别为（383．1±27．5）mg／L和（1．63±0．22）mg／L,二者相比差异有统计学意义（P〈0．05）;临床治愈后,心肌炎组TNF—α及IL-6分别降至（407．3±34．4）mg／L和（1．97±0．29）mg／L,与正常组相比差异无统计学意义（P〉0．05）。结论检测TNF—α及IL-6血清水平及其变化,有助于判断急性病毒性心肌炎患儿病情及心肌损害程度。     

卡托普利注射液对充血性心力衰竭细胞因子的干预作用

目的　探讨血管紧张素转换酶抑制剂 (ACEI)对心力衰竭 (CHF)患者血清肿瘤坏死因子 -α(TNF-α) ,白细胞介素 - 6 (IL- 6 ) ,白细胞介素 - 10 (IL- 10 ) ,一氧化氮 (NO)的干预影响。方法　将 5 5例 CHF患者分为治疗组和常规组。常规组采用常规治疗 ,治疗组在常规治疗基础上用卡托普利注射液治疗 1周 ,在治疗前与治疗后测定 TNF-α,IL- 6 ,IL- 10 ,NO的变化。结果　治疗后两组血清 TNF- α,IL- 6 ,NO水平均明显下降 (P<0 .0 5 ,P<0 .0 1,P<0 .0 1) ;治疗前血清 IL - 10水平较对照组升高无显著性差异 (P>0 .0 5 ) ,治疗后 IL - 10水平明显升高 (P<0 .0 5 ) ;治疗组治疗后上述指标降低或升高的幅度显著高于常规组治疗后降低或升高的幅度 (P<0 .0 5 )。结论　 ACEI可能通过调控细胞因子的浓度来改善心功能 ,为其治疗心力衰竭进一步提供理论依据     

细胞因子对肺癌H460细胞MMP表达的影响及地塞米松的干预作用

目的 在肺癌H460细胞的三维立体培养过程中,直接观察细胞因子[肿瘤坏死因子α（TNF-α）和IL-1β]对肺癌H460细胞关于基质金属蛋白酶-2（MMP-2）和MMP-9表达的诱导作用及地塞米松的干预作用.方法 在肺癌H460细胞三维立体培养过程中加入细胞因子TNF-α和IL-1β来诱导MMP的表达,同时加入地塞米松干预MMP-2和MMP-9的表达;用明胶酶谱法测定MMP-2、MMP-9,同时在培养5d后测定胶原含量大小.结果 TNF-α和IL-1β诱导培养在立体胶原内的肺癌H460细胞产生大量MMP-2和MMP-9,并促进其活化,引起大量胶原降解,地塞米松抑制了MMP-2及MMP-9的表达及活化,进而抑制了胶原的降解,对抗了细胞因子TNF-α和IL-1β对胶原的降解作用.结论 细胞因子TNF-α和IL-1β可诱导MMP的表达,MMP可直接降解肺内胶原,进而促进肺癌的侵袭或转移;地塞米松通过抑制MMP的表达与活化对抗MMP对肺组织的破坏作用,进而抑制了肺癌的侵袭与转移.     

Protective effect of omeprazole on gastric mucosal of cirrhotic portal hypertension rats

Objective:To observe the protective effect of omeprazole on gastric mucosal of cirrhotic portal hypertension rats.Methods:All rats were randomly divided into normal control group,cirrhosis and treatment group.Thioacetamide was used to establish rat model of cirrhotic portal hypertension.The necrotic tissue of gastric mucosa ulcer focus,degree of neutrophils infiltration at the ulcer margin,portal pressure,portal venous flow,abdominal aortic pressure,abdominal aortic blood flow at front end,gastric mucosal blood flow(GMBF),glycoprotein(GP)of gastric mucosa,basal acid secretion,H' back-diffusion,gastric mucosal damage index,NO,prostaglandin E_2(PGE_2) and tumor necrosis factor-α(TNF-α) were determined respectively,and the pathological changes of gastric mucosa were also observed by microscope.Results:Compared with cirrhosis group and the control group,the ulcer bottom necrotic material,gastric neutrophil infiltration and UI of the treatment group were all decreased significantly(P0.01),GMBF value,GP values,serum NO,PGE_2,TNF- a were all significantly increased.Conclusions:Omeprazole has an important protective effect on gastric mucosal and it can increase gastric mucosal blood flow and related to many factors.     

Interleukin-17 gene expression in patients with rheumatoid arthritis

Abstract

Interleukin-17 is a proinflammatory cytokine. Recent animal studies have shown that IL-17 plays a role in the initiation and progression of arthritis. However, whether IL-17 has a prominent role in human rheumatoid arthritis (RA) or not remains unclear. Here we investigated the role of IL-17 in patients with RA. cDNA was prepared from knee joint synovial tissues of RA (n = 11) and osteoarthritic (OA, n = 10) patients and PBMC of RA (n = 52) and healthy subjects (n = 34). IL-17 gene expression level was measured by real-time PCR, and was compared with various clinical parameters. IL-17 gene expression in synovial tissues of RA was similar to that in OA. IL-17 gene expression level in PBMC of RA patients was significantly higher than in the control. The response (changes in DAS) to two-week treatment with anti-TNF-α blockers (infliximab or etanercept) did not correlate with changes in IL-17 gene expression levels. The IL-17/TNF-α gene expression ratio at baseline (before treatment) tended to be lower in responders to the treatment. Expression of IL-17 gene in PBMC may be associated with the inflammatory process of RA. IL-17/TNF-α expression ratio is a potentially suitable marker of response to anti-TNF-α therapy.     

溃疡性结肠炎患者血清TNF-α、IL-10表达与肠道菌群分布的相关性

目的 观察溃疡性结肠炎(UC)患者肠道菌群分布情况,分析血清肿瘤坏死因子-α(TNF-α)、白细胞介素-10(IL-10)水平与肠道菌群的关系,为未来该类疾病临床干预方案的制定提供参考依据.方法 回顾性分析2017年1月至2020年6月南京医科大学附属南京医院(南京市第一医院)完成治疗的29例活动期UC患者,作为观察组...     

PM2．5急性暴露对大鼠凝血功能的影响及其机制

目的探讨PM2．5暴露对大鼠凝血功能的影响及机制。方法24只雌性SD大鼠随机分为4组：对照组、PM2.53．75mg／kg组、PM257．5mg／kg组、PM2s15mg／kg组。将大鼠暴露于不同剂量PM2．5,24h后处死大鼠,取大鼠血浆检测凝血酶原时间（PT）、活化的部分凝血活酶时间（APTT）、纤维蛋白原（FIB）,取BALF显微镜下细胞计数及分类,大鼠肺脏石蜡切片HE染色观察病理改变,酶联免疫吸附试验法检测BALF中IL-6、肿瘤坏死因子α（TNFd）含量、肺组织丙二醛（MDA）含量及血清血管性血友病因子（vWF）含量,蛋白免疫电泳法（Westernblot）检测血管紧张素Ⅱ的1型受体（ATl）蛋白表达。结果PM2.57．5mg／kg组、PM2.5 15mg／kg组PT、APTT值较对照组及PM2.53．75mg／kg组缩短（P〈0．05）,各组血浆FIB值均无统计学差异（P〉0．05）。PM2.5各剂量组BALF中细胞总数及中性粒细胞比例均明显高于对照组（P〈0．05）,且随着PM2.5剂量增加而呈剂量依赖性升高。PM2.57．5mg／kg组和PMzs15mg／kg组BALF中II-6、TNF-α含量、肺组织MDA含量、血清vwF含量及肺组织ATl受体蛋白表达明显高于对照组及PM2.53．75mg／kg组（P〈0．05）。结论PM2.5暴露可导致PT、APTT缩短,诱发血液高凝,其机制可能与炎症反应及血管内皮损伤相关。     

生长抑素联合乌司他丁对急性胰腺炎患者血清白细胞介素-6及肿瘤坏死因子-α水平的影响

目的 探讨生长抑素联合乌司他丁对急性胰腺炎（AP）的临床疗效及对患者血清白细胞介素-6（IL-6）及肿瘤坏死因子（TNF）-α水平的影响.方法 收集我院2010年1月～2012年1月收治的急性胰腺炎患者184例,并将其随机分为对照组90例,给予乌司他丁;联合用药组94例,在对照组的基础上加用生长抑素.两组均以10天为1个疗程,观察两组患者治疗后临床疗效、IL-6及TNF-α水平及临床症状（腹痛缓解时间、通便时间、血淀粉酶、胃肠功能评分）改善情况.结果 （1）联合用药组总有效率为94.7％ （89/94）,对照组为85.6％ （77/90）,联合用药组临床疗效显著优于对照组,两组比较差异有统计学意义（P＜0.05）.（2）两组患者治疗后IL-6及TNF-α水平与同组治疗前比较,差异有统计学意义（P＜0.05）,治疗后两组患者炎性水平均改善.联合用药组IL-6及TNF-α水平改善显著优于对照组（P＜0.05）.（3）联合用药组患者腹痛缓解时间、胃肠功能评分、通便时间、血淀粉酶显著优于对照组（P＜0.05）.结论 生长抑素联合乌司他丁治疗急性胰腺炎疗效确切,改善IL-6与TNF-α水平,可有效改善患者临床症状.     

慢性阻塞性肺疾病的炎症相关生物标志物研究进展

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)已被广泛认为系一种慢性炎症反应性疾病,不仅累及肺,还可引起一系列肺外效应,很多炎症分子参与其中,它们是COPD发病机制的重要组成部分,与COPD患者的预后有着一定联系.本文综述了若干与COPD相关的炎症标志物的近期研究进展.     

慢性阻塞性肺疾病大鼠模型中骨骼肌蛋白降解机制的研究

目的 研究慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)大鼠模型的骨骼肌蛋白降解机制,为有效防治COPD患者骨骼肌蛋白高分解,功能障碍等难题提供科学理论和依据.方法 成年雄性SD大鼠30只,分为模型组18只,对照组12只,采用反复熏香烟和气管内注入脂多糖复制COPD大鼠模型.酶联免疫吸附法(ELISA)测定血清和膈肌组织中的白介素6(IL-6),肿瘤坏死因子α(TNF-α),γ干扰素(IFN-γ)等含量.蛋白免疫印迹法测定大鼠膈肌和腓肠肌内的E2-14K、MAFbx、MuRF-1的蛋白表达.结果 在模型组中,血清和膈肌内的IL-6、TNF-α均较对照组显著升高,IFN-γ则较对照组显著降低.Western blot的结果显示:膈肌组织中E2-14K、MAFbx、MuRF-1均较对照组表达明显增强(各蛋白的相对表达量分别为0.96±0.12 vs 0.53±0.09、0.99±0.10 vs 0.53士0.08、0.95±0.08 vs 0.51±0.16,P＜0.0l).腓肠肌中E2-14K、MAFbx、MuRF-1亦较对照组表达增强(各蛋白的相对表达量分别为0.98±0.06 vs 0.83士0.05、1.00±0.04 vs 0.81±0.05、0.92±0.05 vs0.71±0.05,P＜0.05).体质量与TNF-α呈显著负相关(血清r=-0.84,膈肌r=-0.75,P值均＜0.01),与IFN-γ呈正相关(血清r=-0.71,膈肌r=-0.69,P值均＜0.01);中性粒细胞百分比与1L-6呈正相关(血清r =0.82,膈肌r=0.91,P值均＜0.01);膈肌组织中,IL-6、TNF-α的水平与膈肌的E2-14K、MAFbx、MuRF-1灰度值呈显著正相关,相关系数分别为r=0.86、r=0.94、r=0.89,P＜0.01和r=0.84、r=0.83、r=0.84,P＜0.01;IFN-y与E2-14K、MAFbx、MuRF-1灰度值呈显著负相关,相关系数为r =0.81、r=0.80、r=0.78,P＜0.01.结论 在COPD大鼠模型中,炎症因子、免疫调节因子的表达失衡和骨骼肌内泛素及泛素化蛋白的过度表达可能是引起骨骼肌蛋白降解加快的重要原因.     

慢性乙型肝炎合并高脂血症患者应用阿托伐他汀后血清CRP、TNF-α、IL-6及IL-10的变化

目的探讨阿托伐他汀对慢性乙型肝炎合并高脂血症患者血清CRP、TNF-α、IL-6及IL-10的影响。方法回顾性分析慢性乙型肝炎合并高脂血症患者127例,按照在治疗过程中是否加入阿托伐他汀分为两组,未加入阿托伐他汀的组别为对照组,观察组为加用阿托伐他汀20 mg/次口服,检测两组患者治疗前后C反应蛋白(CRP)、肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-10(IL-10)、丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、总胆红素(TBIL)的水平。结果治疗前两组的ALT、AST、TBIL相比,差异均无明显统计学意义(P0.05);治疗后,对照组的ALT、AST、TBIL均出现下降趋势,而观察组的ALT、AST、TBIL均出现上升趋势,与治疗前相比,差异有统计学意义(P0.05);治疗后两组的ALT、AST、TBIL相比,差异有统计学意义(P0.05)。两组患者治疗后CRP、TNF-α、IL-6均较治疗前明显下降,IL-10升高(P0.05);治疗后观察组TNF-α、IL-6均较对照组下降更为显著,IL-10升高更为显著(P0.05)。结论阿托伐他汀有助于降低慢性乙型肝炎合并高脂血症患者血清CRP、TNF-α、IL-6水平,提高IL-10水平,但能升高ALT、AST、TBIL水平,临床上对于慢性乙型肝炎合并高脂血症应用阿托伐他汀降脂治疗的同时,对肝脏损伤尚需进一步观察。     

高原地区慢性阻塞性肺疾病急性加重期合并慢性肺心病抗氧化治疗的研究

目的探讨高原慢性阻塞性肺疾病急性加重期（AECOPD）合并慢性肺心病（CCP）患者抗氧化治疗措施。方法将126例高原（海拔2260～3500m）AECOPD合并CCP患者随机分为红景天治疗组（A组）、氨溴索治疗组（B组）和对照组（C组）,每组42例。3组患者均给予抗感染、祛痰、平喘、吸氧等常规治疗。在常规治疗基础上,A组给予口服藏药红景天胶囊,每次2．0g,3次／d,共28d;B组给予盐酸氨溴索30mg静脉滴注,2次／d,共28d。C组仅给予常规治疗。3组均在治疗前和治疗28d后,分别测血清8-异前列腺素F2α（8-iso—PGF2α）、超氧化物歧化酶（SOD）、还原型谷胱甘肽（GSH）、丙二醛（MDA）、总抗氧化能力（T—AOC）、1s用力呼气容积占预计值百分比（FEV1％pred）、FEV．与用力肺活量比值（FEV1／FVC）、动脉血氧分压（PaO2）、动脉血二氧化碳分压（PaCO2）。结果治疗前,3组间血清8-iso—PGF2α、SOD、GSH、MDA、T—AOC水平、FEV1％pred、FEV1／FVC、PaO2、PaCO2差异无显著性（均P〉0．05）。治疗后,3组血清8-iso PGF2α、MDA水平、PaCO2较治疗前显著降低（均P〈0．01）,SOD、GSH、T—AOC水平、FEV1％pred、FEV1／FVC、PaO2较治疗前显著升高（均P〈0．01）;A组和B组各项指标与对照组比较差异均有统计学意义,且A组各项指标均较B组为优（8-iSO—PGF2α：6．21±1．42比8．62±1．45,SOD：89．56±7．61比79．33±7．25,GSH：42．76±4．52比35．26±4．22,MDA：5．26±1．52比7．33±1．68,T—AOC：24．60±3．46比21．67±2．78,FEV1％pred：44．33±6．05比39．84±5．88,FEV1／FVC：47．85±5．36比43．78±5．04,PaO2：53．81±5．60比48．58±5．47,PaCO2：42．82±5．18比47．67±5．54,均P〈0．01）。126例患者治疗前,血清8-iso—PGF2α、MDA与FEV1％pred、FEV1／FVC、PaO：呈显著负相关（分别r=-0．754、-0．788、-0．812和-0．777、-0．654、-0．752,均P〈0．01）,与PaCO,呈显著正相关（分别r=0．726、0．685,均P〈0．01）,SOD、GSH、T—AOC与FEV1％pred、FEVI／FVC、PaO2呈显著正相关（分别r=0．685、0．716、0．733,0．805、0．746、0．657和0．635、0．702、0．733,均P〈0．01）,与PaCO2呈显著负相关（r=-0．716、-803、-0．752,均P〈0．01）。结论氧化／抗氧化比例失衡参与了高原AECOPD合并CCP的发病;红景天和氨溴索在高原AECOPD合并CCP患者的治疗中具有较好的抗氧化作用,红景天的效果优于氨溴索。     

白介素15与慢性阻塞性肺疾病大鼠骨骼肌降解的相关性研究

目的 研究慢性阻塞性肺疾病(COPD)大鼠模型骨骼肌降解途径——泛素-蛋白酶体途径与白介素15(IL-15)的相关关系,为有效防治COPD患者骨骼肌蛋白高分解提供理论与依据.方法 成年雄性SD大鼠45只,分为模型组30只,健康组15只,采用反复熏香烟加气管内注入脂多糖法复制COPD大鼠动物模型.实时荧光定量PCR法和Western blot法分别检测大鼠膈肌、腓肠肌和肋间肌中E2-14K、MAFbx、Ub基因和蛋白表达.ELISA法检测大鼠血清、膈肌、腓肠和肋间肌中IL-15和肿瘤坏死因子α(TNF-α)的含量.结果 COPD模型大鼠膈肌、腓肠肌和肋间肌中E2 14K、MAFbx、Ub基因和蛋白表达分别较健康组升高.COPD模型组大鼠血清、膈肌、腓肠肌和肋间肌中IL-15、TNF-α的水平较健康组升高.大鼠血清、膈肌、腓肠肌和肋间肌中IL-15和TNF-α水平呈正相关(血清r=0.75;膈肌r =0.81;腓肠肌r=0.82;肋间肌r=0.78,P值均＜0.05).膈肌、腓肠肌和肋间肌中IL-15均与E2-14K、MAFbx、Ub相对表达量呈正相关(膈肌r=0.88、r=0.86、r=0.87;腓肠肌r=0.85、r=0.87、r=0.76;肋间肌r=0.85、r =0.80、r=0.84,P值均＜0.05).大鼠造模结束后体质量净增长与血清、膈肌、腓肠肌和肋间肌中IL-15呈负相关(血清r=-0.90,膈肌r=-0.85,腓肠肌r=-0.82,肋间肌r=-0.82,P＜0.05).结论 在COPD模型大鼠中,IL-15可能通过TNF-α共同作用于泛素-蛋白酶体途径影响骨骼肌降解的作用.     

慢性阻塞性肺疾病患者血清白介素6、肿瘤坏死因子α水平与肺功能的相关性研究

目的 探讨慢性阻塞性肺疾病(COPD)患者血清白介素6(IL-6)、肿瘤坏死因子α(TNF-α)水平与肺功能相关性的临床意义.方法 选取我院收治的COPD患者84例和健康体检者45例.血常规检测外周血中性粒细胞占白细胞总数百分比(Neu/Leu％),采用ELISA方法测定COPD患者和健康体检者血清IL-6和TNF-α浓度,同时计算第1秒用力呼气容积占预计值百分比(FEV1 ％pred)检测肺功能指标.结果 COPD稳定期组、急性加重期组的外周血Neu/Leu％,血清IL-6、TNF-α水平均高于对照组,急性加重期组较稳定期组进一步升高,差异均有统计学意义(P＜0.05).FEV1％ pred值在正常对照组以及COPD稳定期组、急性加重期组则呈递减趋势,组间两两比较差异均有统计学意义(P＜0.05).血清IL-6、TNF-α水平与FEV1％ pred均呈负相关(P＜0.05),与Neu/Leu％均呈正相关(P＜0.05).结论 IL-6、TNF-α、中性粒细胞密切参与了COPD的炎症反应过程,与肺功能密切相关,可作为评估病情严重程度的辅助指标.     

脉搏波速与冠状动脉炎症状态的关系研究

目的检测冠心病患者脉搏波速（Pulse Wave Velocity,PWV）及血清炎症因子高敏C反应蛋白（Hs-CRP）、白介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）,探讨PWV与冠状动脉炎症状态的相互关系。方法采用对照、单盲、条件分组,非随机的方法。以2009年3月—2010年3月我院心内科住院冠心病（CHD）患者140例为研究对象,检测PWV,抽清晨血查Hs-CRP、IL-6、TNF-α。结果 PWV正常与异常组Hs-CRP、IL-6、TNF-α比较,差异均有统计学意义（P〈0.05）。PWV正常组的Hs-CRP为（1.37±0.77）mg/L,PWV异常组的Hs-CRP为（5.97±5.39）mg/L,Hs-CRP与PWV呈正相关,直线回归和相关分析（r=0.573,P〈0.01）;PWV正常组的IL-6为（49.1±30.1）ng/L,PWV异常组的IL-6为（77.2±55.5）ng/L,IL-6与PWV呈正相关,直线回归和相关分析（r=0.387,P〈0.01）;PWV正常组的TNF-α为（1063±343）ng/L,PWV异常组的TNF-α为（1517±668）ng/L,TNF-α与PWV呈正相关（r=0.327 P〈0.01）。结论 PWV与炎症因子关系密切,二者呈正相关关系,可互相反映。当PWV大于正常时,炎症因子浓度增高,当Hs-CRP接近6.0mg/L,IL-6〉80ng/L,TNF-α〉1500ng/L时,PWV增加,提示动脉僵硬度增高。     

The aqueous extract from Toona sinensis leaves inhibits microglia-mediated neuroinflammation

The leaves of Toona sinensis, a well-known traditional oriental medicine, have been prescribed for the treatment of enteritis and infection. Recently, aqueous extracts of Toona sinensis leaves (TSL-1) have demonstrated many biological effects both in vitro and in vivo. In the central nervous system, microglial activation and their proinflammatory responses are considered an important therapeutic strategy for neuroinflammatory disorders such as cerebral ischemia, Alzheimer's disease, and Parkinson's disease. The present study attempted to validate the effect of TSL-1 on microglia-mediated neuroinflammation stimulated by lipopolysaccharide (LPS). As inflammatory parameters, the production of nitric oxide (NO), inducible NO synthase, and tumor necrosis factor-α were evaluated. Our results demonstrate that TSL-1 suppresses LPS-induced NO production, tumor necrosis factor-α secretion, and inducible NO synthase protein expression in a concentration-dependent manner, without causing cytotoxicity. In addition, the inhibitory effects of TSL-1 in LPS-stimulated BV-2 microglia were extended to post-treatment suggesting the therapeutic potential of TSL-1. Therefore, this work provides the future evaluation of the role of TSL-1 in the treatment of neurodegenerative diseases by inhibition of inflammatory mediator production in activated microglia.