芜菁多糖对哮喘大鼠炎症反应的影响

目的 探讨芜菁多糖对哮喘大鼠炎症反应的影响.方法 将40只Wistar大鼠编辑并按随机数字表法分为正常对照组、模型组、芜菁小剂量组和芜菁大剂量组;模型组和芜菁大、小剂量组制作哮喘大鼠模型;芜菁大、小剂量组分别按5 mg/kg和2.5 mg/kg的剂量给予芜菁多糖灌胃;正常对照组和模型组给予蒸馏水灌胃,共持续2周.检测各组哮喘大鼠血清炎症因子水平和支气管肺泡灌洗液(BALF)中细胞数目.结果 芜菁小剂量和大剂量组哮喘大鼠血清肿瘤坏死因子-α(TNF-α)、IL-6、IL-2及C反应蛋白(CRP)水平均明显低于模型对照组[(90.33±5.90) pg/ml、(92.01±3.26) pg/ml vs(136.43±7.81) pg/ml,(19.08±1.27) pg/ml、(18.33±2.09) pg/ml vs (25.14±2.31)pg/ml,(115.36±7.27) pg/ml、(110.72±10.05) pg/ml vs(193.16±12.33) pg/ml,(70.58±14.85)μg/ml、(71.69±12.11)μg/ml vs(93.21±17.25)μg/ml],差异具有统计学意义(t =3.144～17.188,P＜0.01);芜菁小剂量和大剂量组哮喘大鼠BALF中细胞总数、嗜酸性粒细胞比例及淋巴细胞比例明显低于模型对照组[(1.58±0.67)×109/L、(1.55 ±0.89)×109/L vs (3.05 ±1.21)×109/L,(20.31±4.27)％、(21.06±3.53)％ vs (26.35±5.91)％,(16.77±5.47)％、(15.89±6.03)％vs (23.56±4.81)％],差异具有统计学意义(t=2.430 ～3.158,P＜0.05,P＜0.01).结论 芜菁多糖可以有效抑制哮喘大鼠体内各类炎症因子的分泌,减轻炎症反应大发生.     

氯氰菊酯对人乳腺癌细胞MCF-7 Akt/NF-κB/caspase 9信号通路作用研究

目的 研究氯氰菊酯对人乳腺癌细胞MCF-7 Akt/NF-κB/caspase-9信号通路的影响,探讨氯氰菊酯对MCF-7的作用机制。方法 用0和1.0×10-6 mol·L-1浓度氯氰菊酯染毒MCF-7细胞24 h,应用Western Blot法测定p-Akt、p-NF-κB p65和caspase 9蛋白表达水平。结果 与0 mol·L-1对照组相比,1.0×10-6 mol·L-1氯氰菊酯染毒组作用细胞后,p-Akt蛋白表达量(对照组:0.12±0.0081,染毒组:0.19±0.0167)上调,差异有统计学意义(t=-5.777,P=0.004)、p-NF-κB p65蛋白表达量(对照组:0.32±0.0342,染毒组:0.57±0.0964)上调,差异有统计学意义(t=-4.249,P=0.013)。caspase-9蛋白表达量(对照组:0.52±0.0069,染毒组:0.45±0.02068)下调,差异有统计学意义(t=5.285,P=0.006)。结论 氰菊酯通过对MCF-7细胞Akt/NF-κB/caspase-9信号通路产生影响发挥拟雌激素作用。     

PI3K/Akt信号通路在不同类型乳腺癌细胞系中的表达及机制

目的分析PI3K/Akt信号通路在不同类型乳腺癌细胞系中的表达及机制。方法通过MTT研究不同浓度的紫杉醇对不同类型的乳腺癌细胞系的不同抑制时间,采用蛋白印迹法检测PI3K/Akt的蛋白表达情况。结果在紫杉醇的作用下,随着剂量和时间的改变,灵敏度最高为MCF-7 (20190809),MDA-MB-453 (20190801)细胞的抑制效果最明显,抑制效果最差的为T47D (201900703)。Western Blot结果显示,MCF10A、MDA-MB-453的PI3K/Akt信号蛋白水平显著高于T47D和MCF-7,各蛋白的表达水平与β-actin比较,差异有统计学意义(P0. 05)。结论紫杉醇对不同类型的乳腺癌细胞具有良好的疗效,发挥作用的机制可能是通过介导PI3K/Akt信号通路中的PI3K和ILK蛋白。     

柴胡皂苷D对SGC-7901细胞生长及迁移抑制作用

目的探讨柴胡皂苷D对胃癌SGC-7901细胞生长、迁移抑制作用及机制。方法实验设对照组、低、中、高剂量柴胡皂苷组(5、10、20μmol/L柴胡皂苷D);采用四甲基偶氮唑蓝(MTT)法检测各组细胞24、48和72 h细胞增殖情况;采用原位末端转移酶标记法(TUNEL)检测各组细胞凋亡;Transwell检测各组细胞迁移能力;实时定量荧光PCR技术(real time PCR)检测各组细胞中norrin及livin表达;蛋白印迹法检测各组细胞norrin、livin、p57和cyclin E表达。结果 MTT结果显示,与对照组比较,低、中、高剂量柴胡皂苷组SGC-7901细胞增殖受到明显抑制,呈剂量效应关系(P<0.05);Transwell结果显示,与对照组[(190±7)个/视野]比较,低、中、高剂量柴胡皂苷组细胞迁移数量[分别为(114±9)、(87±6)、(38±4)个/视野]均减少(均P<0.05);与对照组(4.94±1.14)比较,低、中、高剂量柴胡皂苷组SGC-7901细胞凋亡指数[分别为(8.46±1.18)、(11.76±2.85)、(34.34±7.74)]均增加(均P<0.05);与对照组比较,中、高剂量柴胡皂苷组SGC-7901细胞中norrin、livin mRNA及蛋白表达均减少(均P<0.05),各剂量组SGC-7901细胞中cyclinE蛋白表达均明显减少,p57表达明显增加,且呈剂量效应关系(均P<0.05)。结论柴胡皂苷D对胃癌细胞生长、迁移具有抑制作用,其机制可能与柴胡皂苷D减少norrin、livin表达,延长细胞周期、促进细胞凋亡有关。     

不同剂量瑞舒伐他汀对ox-LDL诱导的人单核-巨噬细胞组织因子表达的影响及机制

目的 研究不同剂量瑞舒伐他汀对氧化修饰低密度脂蛋白(ox-LDL)诱导的人单核-巨噬细胞组织因子(TF)表达的影响及可能机制.方法 实验分七组:空白对照组、ox-LDL对照组、多聚肌苷酸组、不同剂量(0.01、0.1、1、5μmol/L)瑞舒伐他汀组.RT-PCR检测各组血凝素样氧化低密度脂蛋白受体-1(LOX-1)mRNA、TF mRNA的表达水平,ELISA检测各组TF蛋白含量的表达.结果 不同剂量瑞舒伐他汀对ox-LDL诱导后人单核-巨噬细胞LOX-1 mRNA、TF mRNA和TF表达的影响:七组之间比较,差异均有统计学意义(F =91.334,58.833,103.552,P＜0.05).ox-LDL组与空白组比较,LOX-1 mRNA、TF mRNA、TF的表达均增加[(3.25156±0.15772) vs(1±0);(2.522451±0.138967) vs(1±0);(207.7233±1.154701)ng/L vs(184.8467±0.871799) ng/L],差异有统计学意义(P＜0.05);多聚肌苷酸组、各瑞舒伐他汀组与ox-LDL组比较,三者表达均下降,且不同剂量瑞舒伐他汀组表达呈剂量依赖性减少,差异均有统计学意义(P＜0.05);不同剂量瑞舒伐他汀组之间进行两两比较时,各组间差异有统计学意义(均P ＜0.05).结论 LOX-1介导的ox-LDL可使人单核-巨噬细胞TF表达增加,瑞舒伐他汀可通过ox-LDL途径,且呈剂量依赖性下调单核-巨噬细胞LOX-1 mRNA、TFmRNA的表达,使TF蛋白表达减少.     

葡多酚对人乳腺癌细胞增殖的抑制作用研究

目的研究葡多酚(GPC)对人乳腺癌(MCF-7)细胞增殖活性的影响及雌激素受体(ER)的调节作用。方法将GPC与MCF-7细胞共同培养,共设肿瘤细胞对照组、高、中、低(200、100、10μg/ml)剂量GPC组、ER阻断剂对照组(ICI10-6mol/L)和ER阻断剂(ICI10-6mol/L)+GPC(200μg/ml)6个组。用MTT法测定各组乳腺癌细胞的增殖活性水平,用免疫组化方法检测乳腺癌细胞中增殖细胞核抗原(PCNA)和Bax蛋白的表达水平。结果与肿瘤细胞对照组比,高剂量GPC组乳腺癌细胞的增殖活性水平和PCNA阳性表达率降低,Bax蛋白阳性表达率升高(P<0.05);ER阻断剂+GPC组乳腺癌细胞的增殖活性水平、PCNA阳性表达率,均较高剂量GPC组升高,Bax蛋白阳性表达率降低,各项差别均有显著性意义(P<0.05)。结论GPC可有效抑制人乳腺癌细胞的增殖,并促进其凋亡;其作用与ER调节有密切关系。     

钙激活蛋白酶抑制剂对高糖诱导乳鼠心肌细胞凋亡的作用机制

目的 探讨钙激活蛋白酶(Calpain)抑制剂对高糖诱导的乳鼠心肌细胞凋亡的作用机制.方法 分离培养SD乳鼠心肌细胞,实验分为3组:(1)对照组;(2)高糖(35 mmol/L)组,刺激72 h;(3)高糖(35 mmol/L)+ ALLN(25 mol/L)组.MTT测定各组心肌细胞的生长活力,激光共聚焦显微镜观察和检测心肌细胞线粒体通透性和膜电位,Western blot法检测激活型caspase-3蛋白的表达.结果 MTT结果分析显示高糖刺激72 h后,心肌细胞生存率下降(55％±11％),ALLN预处理组生存率为(70％±15％),与高糖组比较差异具有统计学意义(P＜0.05).高糖可以刺激心肌细胞线粒体通透性增加,mPTP孔开放,降低心肌细胞线粒体膜电位,而ALLN预处理可以抑制高糖对心肌细胞的这种作用(相对荧光强度:30％±15％ vs 60％±11％,P＜0.05).高糖刺激可以导致心肌细胞激活型caspase-3的表达增加,加入ALLN预处理后可以抑制激活型caspase-3的表达,差异有统计学意义(0.42 ±0.11 vs 0.21±0.12,P＜0.05).结论 Calpain抑制剂对高糖诱导的乳鼠心肌细胞凋亡的作用存在保护效应.     

镉通过类雌激素样作用促进人乳腺癌MCF-7细胞增殖

[目的]研究镉对人乳腺癌MCF-7细胞增殖及雌激素受体(estrogen receptor,ER)蛋白表达水平的影响及其可能机制。[方法]用1×10~(-6)、1×10~(-7)、1×10~(-8)、1×10~(-9)、1×10~(-10)、1×10~(-11) mol/L的17β-雌二醇(后称雌激素)培养不同来源的A、B两株MCF-7细胞4 d,应用CCK8法筛选敏感细胞株并确定雌激素促细胞增殖作用最强的浓度。用1×10~(-6)、1×10~(-7)、1×10~(-8)、1×10~(-9)、10~(-10)、1×10~(-11) mol/L的镉溶液染毒敏感细胞株,确定镉促进细胞增殖的最大浓度。设置阴性对照组(去雌激素培养液)、实验组(1×10~(-8) mol/L镉)、阳性对照组(1×10~(-9) mol/L雌激素),通过克隆形成实验检测镉对MCF-7细胞集落形成能力的影响。利用ER抑制剂(ICI182780)初步探讨镉致细胞增殖的可能机制,增设实验抑制剂组(1×10~(-8) mol/L镉+1×10~(-7) mol/L ER抑制剂)、阳性抑制剂组(1×10~(-9) mol/L雌激素+1×10~(-7) mol/L ER抑制剂),通过CCK8法、流式细胞术和Western blot分别检测各组的细胞增殖率、细胞周期S期比例和ER表达水平。[结果]实验所用B株MCF-7细胞为雌激素敏感细胞株,且当雌激素浓度为1×10~(-9) mol/L时,对MCF-7细胞的促进增殖作用[(203.55±36.65)%]最大(P0.001)。与阴性对照组(100%)相比,1×10~(-8)~1×10~(-10) mol/L镉溶液可促进MCF-7细胞增殖[(163.78±31.90)%~(176.88±10.06)%](P0.001)。1×10~(-8) mol/L镉可促进细胞集落形成(P0.05),增加细胞S期比例(P0.001),提高细胞ER蛋白表达水平(P0.001)。与实验组相比,加入ER抑制剂能够抑制镉对MCF-7细胞的促增殖作用[由(135.17±23.96)%降至(107.66±7.64)%](P0.01),抑制镉诱导的细胞S期比例增加[由(24.17±0.53)%降至(12.36±0.43)%](P0.001),拮抗镉诱导的ER表达增加[由(56.19±3.67)%降至(38.84±1.04)%](P0.05)。[结论]镉可以促进人乳腺癌细胞MCF-7增殖和ER表达,这种作用可被ER抑制剂所抑制,提示镉可能具有雌激素样作用。     

氯胺酮对乳腺癌细胞迁移及NET-1、RhoA表达的影响

目的探究氯胺酮对乳腺癌细胞迁移及神经上皮细胞转化基因1(NET-1)、RHo A表达的影响。方法以乳腺癌细胞系MDA-MB-231为研究对象,根据于培养基中添加不同浓度的氯胺酮分为4组:空白对照组(0μg/ml)、氯胺酮低剂量组(5μg/ml)、氯胺酮中剂量组(10μg/ml)、氯胺酮高剂量组(20μg/ml);采用Transwell迁移实验及细胞划痕实验观察各组细胞迁移情况;应用荧光实时定量PCT(qRT-PCR)检测各组乳腺癌MDA-MB-231细胞中NET-1、RhoA基因表达情况;应用蛋白免疫印记(Western blot)法检测各组乳腺癌MDA-MB-231细胞中NET-1、RhoA蛋白表达情况。结果与空白对照组相比,氯胺酮组MDA-MB-231细胞的迁移数目明显降低(P0.05),且随着氯胺酮剂量的增加,迁移数目逐渐降低;与空白对照组相比,氯胺酮组MDA-MB-231细胞的迁移超出划痕部分明显减少(P0.05),且随着氯胺酮剂量的增加,迁移部分逐渐减少;与空白对照组相比,氯胺酮组MDA-MB-231细胞中NET-1、RhoA基因及蛋白的表达水平均显著下调(P0.05),且随着氯胺酮剂量的增加,NET-1、RhoA基因的表达及蛋白表达水平均逐渐下调。结论氯胺酮可能通过下调NET-1、RhoA基因及蛋白的表达,抑制乳腺癌细胞的迁移,达到治疗或缓解乳腺癌病症的目的。     

缬沙坦/氨氯地平和依贝沙坦/双氢克尿噻联合治疗老龄高血压疗效的研究

Objective To compare the clinical effect of valsartan/amlodipine combination or irbesartan/hydrochlorothiazide(HCTZ)combination in very elderly hypertensives.Methods After a 4-week placebo period,94 hypertensives,aged 75-89 years were random given valsartan 160 mg/amlodipine 5 mg or irbesartan 300 mg/HCTZ 12.5 mg for 24 weeks according to a rospective study.After 4 weeks,amlodipine or HCTZ was doubled in non-responders.Patients were checked every 4 weeks.At each visit,sitting,lying and standing blood pressure(BP),systolic BP(SBP)and diastolic BP(DBP)were measured. At the end of placebo period and treatment period,electrolytes and uric acid were evaluated.Results Blood pressure was significantly decreased in both treatment groups,however,there was no statistical significance between two groups.BP changes from lying to standing position were significantly greater in the irbosartan/HCTZ group(-17.2/-9.1 mmHg)than that in the valsartan/amlodipine group(-10.1/-1.9 mmHg,t=2.14,P＜0.05 for SBP and t=3.11,P＜0.01 for DBP vs.irbesartan/HCTZ).Potassium significantly decreased and uric acid significantly increased(-0.4 mmol/L,t = 2.33,P＜ 0.05 and+29.7μ mol/L,t =2.54,P＜0.05 vs.baseline,respectively)only in the irbesartan/HCTZ group.Conclusions Both combinations had similarly effective in reducing clinical BP in very elderly hypertensives.However,valsartan/amlodipine offered some advantage and less pronounced BP orthostatic changes and absence of metabolic adverse effects.     

乙酰半胱氨酸对肥胖哮喘小鼠气道炎症和重建的作用

目的探讨乙酰半胱氨酸对哮喘气道炎症和重建的影响。方法60只雌性C57／6J小鼠按随机数字表法分为哮喘组（A组）,肥胖哮喘组（B组）,治疗组（C组）,对照组（D组）,每组15只。经腹腔注射与雾化吸入卵蛋白（OVA）制作慢性哮喘模型,高脂饮食制造肥胖模型。计数支气管肺泡灌洗液（BALF）中细胞总数及分类,ELISA法测定肺组织匀浆中IL-6和8-异前列腺素F2α（8-iso-PGF2α）水平,肺组织切片观察各组小鼠病理变化,并测定气管壁面积（WAt）、气管平滑肌面积（WAm）、管腔基底膜周长（Pbm）。结果,A组、B组小鼠BALF中白细胞总数及嗜酸性粒细胞比例、肺组织IL-6水以及病理切片中气管壁厚度（WAt／Pbm）、气管平滑肌厚度（WAm／Pbm）均较D组明显增加,且B组IL-6和WAt／Pbm较A组进一步增加（P〈0．05）。C组小鼠BALF中白细胞总数、IL-6和WAt／Pbm均较B组明显下降（P〈0．05）。四组小鼠肺组织匀浆8-iso—PGF2α水平按D组、C组、A组、B组依次升高,各组差异有统计学意义（F=101．8,P〈0．01）。Pearson相关分析表明,8-iso—PGF2α水平与肺组织IL-6水平和WAt／Pbm和呈正相关（r=0．817、0．737,P〈0．01）。结论乙酰半胱氨酸能够通过抑制氧化应激反应,抑制哮喘小鼠的气道炎症和气道重建。     

脂多糖对人皮肤成纤维细胞胶原代谢的影响

目的探讨脂多糖（1ipopolysaccharide,LPS）对人皮肤成纤维细胞胶原代谢的影响,以了解LPS在增生性瘢痕形成中的生物学作用。方法取正常皮肤行成纤维细胞培养后,分为1个对照组及6个实验组。实验组分别与终浓度为0．005、0．010、0．050、0．100、0．500和1．000μg／ml大肠杆菌LPS（Ecoli055：B5）培养,对照组DMEM培养。用逆转录-聚合酶链反应（RT-PCR）法测定成纤维细胞Ⅰ、Ⅲ型前胶原mRNA及胶原酶mRNA的表达,并以同一个体相同代数的瘢痕组织成纤维细胞做对照。结果与对照组比较,LPS刺激浓度在0．005-0．1μg／ml时,促进正常皮肤成纤维细胞Ⅰ、Ⅲ型前胶原mRNA表达（0．323±0．041,0．303±0．063,0．391±0．071,0．344±0．086,0．488±0．059,0．401±0．087,0．616±0．107,0．434±0．084,0．823±0．092,0．542±0．082）,抑制胶原酶mR-NA表达（0．598±0．068,0．556±0．049,0．441±0．043,0．372±0．083,0．260±0．027）,且呈一定的剂量依赖性;当LPS刺激浓度为0．5μ／ml,上述作用下降（0．451±0．063,0．374±0．072,0．360±0．062）;而当LPS刺激浓度到达1．0μg/ml时,抑制正常皮肤成纤维细胞Ⅰ、Ⅲ型前胶原mRNA表达（0．162±0．025,0．171±0．061）,促进胶原酶mRNA表达（0．444±0．114）。LPS刺激浓度在0．1μg／ml时,成纤维细胞（0．823±0．092,0．542±0．082,0．260±0．027）Ⅰ、Ⅲ型前胶原mRNA和胶原酶mRNA表达与同一个体增生性瘢痕组织成纤维细胞（0．829±0．049,0．569±0．038,0．277±0．059）近似。结论LPS对人皮肤成纤维细胞Ⅰ、Ⅲ型前胶原mRNA和胶原酶mRNA的表达,其直接调节可能是参与增生性瘢痕形成的重要机制。     

异丙酚对大鼠肺缺血/再灌注损伤的保护作用

Objective To study the protective effects of propofol against ischemia/reperfusion injury in rat lung. Methods Rat model of pulmonary ischemia/reperfusion injury was used in this study. Rats were randomly divided into three groups, including sham opera-tion group (group A), iachemia/reperfusion group (group B) and propofol group (group C), 15 rats in each group. The concentration of tumor necrosis factor -α and interleukin-6 in bronchoalveolar lavage fluid (BALF) were measured by enzyme linked immunosorbent assay (ELISA). Then blood gas analysis, lung wet/dry (W/D) weight ratio were detected in each group. Results Propofol could significantly improve PaO2, reduce the W/D value and the contents of TNF-α and IL-6 in BALF. Conclusion Propofol effectively suppressed the pro-duction and release of inflammatory cytokine, therefore it can protect the lung from isehemia/reperfusion injury.     

降钙素对大白兔糖尿病骨质疏松模型假体骨密度及生物力学的影响

Objective To investigate the influence of calcitonin on bone mineral density and biomechanics around the artificial pros-thesis in ovariectomized diabetic rabbit model. Methods Fourteen femina New Zealand white rabbits at the age of 5 months old were select-ed, which weight 2.24 -2.65kg, averaging 2.26kg. First, the model of rabbit with diabetic osteoporosis was successfully established by the compound method of ovariectomy plus streptozotocin. Osteotomy in the middle part of femur was performed in both groups, fixation of artifi-cial prosthesis was done with 3.0 kirschner wire. After that, Rabbit models with diabetic osteoporosis were randomly divided into experimen-tal group and control group. Rabbits in the experimental group were treated with calcitonin 6U intramuscular injection once every other day. In control group, intramuscular injection of normal saline solution 1.5ml once every three days. Rabbit models of two groups were sacrificed in the 24th week. The BMD of the region of interest (ROI) around the prosthesis were detected before experiment and 8, 16 and 24 weeks after injection. After rabbits were killed, experimental femurs in both groups were complete removal and soft tissues were rejected. Determi-nation of the pull-out and torsion bone biomechanics experiments of prosthesis was done in both groups respectively. Results The BMD of ROI in the experimental group before operation was (0.1863±0.004)g/cm2 and (0.1753±0.005)g/cm2 in 24 weeks after operation, in control group before operation was (0.1865±0.002)g/cm2 and (0.1638±0.005)g/cm2 in 24 weeks after operation. There were significant difference between the two groups(P < 0.05). Biomechanical show that the pull-out strength in the experimental group was (312.68±8.73 )N/cm2 and (205.43±12.45 ) N/cm2 in control group. There were significant difference between the two groups(P < 0.05). The tor-sion strength in experimental group was (80.47±2.51) N/cm2 and (38.52±0.64) N/cm2 in control group. There were significant differ-ence between the two groups(P < 0.05). Conclusion Salmon calcitonin can reduce the bone turnover rate around prosthesis and decrease bone absorption in the rabbit of diabetic osteoporosis models, accelerate the bone formation around prosthesis, and increase the BMD. It can ameliorate the quality of bone around prosthesis, improve its biomechanics property, and increase the holding power between prosthesis and body mass. It is of clinical significance for the prevention and treatment of aseptic loosening artificial prosthesis.     

强直性脊柱炎合并骨质疏松的临床研究

Objective To investigate the incidence of osteoporosis (OP) in patients with ankylosing spondylitis and the relationship between OP and the clinical data. Methods Serum levels of bone alkaline phosphatase (BALP) and tartrate resistant acid phosphatase 5b (TRACP5b) were detected by enzyme linked immunosorbent assay ( ELISA ) in 60 cases with ankylosing spondylitis, and it was compared with normal controls. Bone mineral density (BMD) was measured through dual-energy X-ray absorptiometry ( DXA), including lumbar ( L2 - L4), bilateral femoral neck and greater trochanter. Some clinical data was collected and analyzed at the same time. Results The incidence of OP in AS patients was 35%, and the incidence of OP in the femoral proximal end was higher than that in lumbar. Compared with normal controls[ ( 1.06 ±0. 18 )U/L ], the levels of serum TRACP5b in AS[ (1.31 ± 0. 82 )U/L] patients was significantly higher ( P <0. 05 ). The levels of serum BLAP in OP combined AS group[ ( 21.65 ± 5.41 ) U/L]were significantly lower than non-OP group[ (32. 37 ± 16. 5 ) U/L] ( P <0. 05 ). The disease duration was negatively correlated with the BMD of femoral neck ( P < 0. 01 ). Conclusions There was higher incidence of OP in AS patients, which were related with the abnormality of bone metabolism and the disease duration.Multiple factors participated in the regulation of bone metabolism of AS.     

蝶鞍结构与垂体瘤生长方式关系的影像学研究

目的 从影像学角度探讨蝶鞍相关解剖对垂体腺瘤生长方式的潜在影响.方法 按照常用蝶窦分类方法,共收集83例蝶窦气化类型为全鞍型和20例鞍前型正常头颅的影像学资料;同时收集45例影像学提示为侵入蝶窦生长的垂体腺瘤临床资料进行分析.结果 （1）正常鞍底形态与蝶窦气化程度的关系：全鞍型蝶窦更易导致凹陷型鞍底（98.8%）.（2）正常鞍底形态与垂体上缘形态的关系：凹陷型垂体上缘更易伴随凹陷型鞍底（93.8%）.（3）根据正常头颅正中矢状位鞍窝骨性上口前后径与鞍窝前后最大径之间的关系,对蝶鞍形态提出初步分型：囊袋型、炒锅型、直筒型及筛型.（4）所有向蝶窦生长的垂体腺瘤患者蝶窦均为全鞍型.结论 鞍底形态、蝶窦气化程度及蝶鞍形态等综合因素能够解释垂体腺瘤向鞍底蝶窦生长的现象;结合文献,蝶鞍的相关形态学基础应该是影响垂体腺瘤生长方式的主要因素.     

关节腔内注射洛伐他汀预防骨关节炎软骨退变

目的 研究洛伐他汀关节腔内注射对骨关节炎(OA)模型关节软骨退变及对基质金属蛋白酶(matrix metalloprotein-ase-1,3)mRNA表达的影响.方法 30只6个月龄新西兰大白兔行右膝关节前交叉韧带切断术.手术后将动物随机分为实验组和对照组,实验组术后立即给予关节腔内注射0.5 mg/ml洛伐他汀0.2 ml/kg,每周1次,连续6周;对照组则关节腔内注射等容量的生理盐水.术后6周处死动物.在解剖镜下观察股骨内髁关节软骨的大体形态学改变并评分.用反转录-聚合酶链式反应检测软骨及滑膜中MMP-1,3 mRNA的表达.结果 解剖镜下实验组软骨退变程度较对照组明显减轻;实验组关节液中IL-1水平较对照组明显降低;实验组滑膜中MMP-1,3 mRNA的表达水平显著低于对照组(P<0.05),而软骨中的MMP-1,3 mRNA的表达较对照组差异无统计学意义(P>0.05).结论 在OA早期关节腔内注射L洛伐他汀能够明显降低MMP-1,3 mRNA的表达,减轻骨关节炎软骨的退变.     

利尿剂在三聚氰胺及三聚氰酸致大鼠急性肾损伤中的治疗作用

Objective To investigate the effect of diuretic (furosemide) therapy on kidney injury induced by melamine and cyanuric acid in rats. Methods 36 male Spragne Dawley rats were random disided into 3 groups. Group A was treated with 2mL of water daily, group B was treated with melamine and cyanuric acid ( each 100 mg/kg) daily for 4 days and then 2ml of water daily, group C was treated with the same as group B at the first 4 days and then treatment with furosemide (20mg/kg) daily. Samples of blood and 24h urine were collected to detective biochemical indexes, and kidney sections were performed on days 4 and 11 ( each end point, n = 6). The kidneys were observed with histopathology and renal crystal deposition scores were determined. Results On the 4th day, group B and group C were resulted in acute kidney injury such as oliguria [ ( 3. 39 ± 1.02 ) ml, ( 3. 20 ± 0. 86 ) ml ] and high serum creatinine [ ( 153.54 ±27. 08)μmol/L, (160. 11 ± 19. 55)μmol/L] and renal melamine cyanurate crystal were found in the renal tissues. On the 11th day, the renal crystal deposition score in the rats was reduced by 9. 52% ( P >0. 05). Compared with those of the 4th day in group B, it reduced by 63.63%( P <0.05) in group C. Urine volume were increased significantly compared with those of the 4th day( P < 0. 05 ) in group C [ from (3.20±0. 86)ml to (25.96 ±5.97)ml] and group B [ from(3. 39 ± 1.02)ml to (8. 57 ± 1.66)ml] , and Urine volume in group C was increased significantly more than that in group B ( P < 0. 05 ). The serum creatinine was obviously reduced as compared with those of the 4th day in group B and C( P <0.05), from[ (153. 54±27.08) μmol/L] to [ ( 106. 10 ±5.53) μmol/L] in group B and from [ ( 160. 11 ± 19. 55) μmol/L] to [ (67. 17 ± 12. 80 ) μmol/L] in group C, but the serum creatinine in group B was still higher than that in group A and C ( P < 0. 05). Conclusions Furosemide can attenuate the damage of acute kidney injury induced by melamine and cyanuric acid.     

脓毒症血清对大鼠小肠微血管内皮细胞ICAM-1的影响及肾上腺髓质素的干预作用

Objective To observe the levels of intercellar adhesion molecule-1(ICAM-1)of rat intestinal mucosa microvascular endothelial cells in sepsis rat,and to investigate the possible protective effect of adrenomedullin on the expression of intercellar adhesion molecule-1(ICAM-1)of rat intestinal mucosa microvascular endothelial cells,and to confirm whether adrenomedullin can decrease released inflammatory factors to slow down or inhibit the occurrence and development of sepsis.Methods The rat intestinal mucosa microvascular endothelial cells were isolated and cultured in vitro,and it was divided into sham operated(sham operated serum),sepsis serum(with addition of sepsis serum)and ADM serum(with 0.lng/kg adrenomedullin 6h after sepsis treatment)groups.The soluble ICAM-1(sICAM-1)content in RIMMVECs culture supernatant was measured by ELISA at the 24th hour after serum stimulation.Results The ICAM-1 content in the supernatant of sepsis group [(0.33 ±0.04)ng/L] was obviously higher than that in sham operated [(0.15 ± 0.02)ng/L] and ADM [(0.17 ± 0.04)ng/L] group(P ＜ 0.05),but ADM group was no significantly different compared with sham operated group(P ＞ 0.05).Conclusions ADM could decrease the expression of ICAM-I in RIMMVECs,and the low level of ICAM-1 could suppress its downstream inflammation factors and inhibit the occurrence and development of sepsis.