Effect of Chaiqinchengqi decoction on sarco/endoplasmic reticulum Ca~（2＋）-ATPase mRNA expression of pancreatic tissues in acute pancreatitis rats

AIM： To investigate the effect of Chaiqinchengqi decoction （CQCQD） on sarco/endoplasmic reticulum Ca2＋-ATPase （SERCA） mRNA expression of pancreatic tissues in acute pancreatitis （AP） rats. METHODS： Thirty Sprague-Dawley （SD） rats were randomized into control group, AP group and CQCQD group （n = 3 × 10）. The rats in the CQCQD group were intragastrically administered with CQCQD （10 mL/kg every 2 h） after induction of AP by intraperitoneal injection of caerulein （50 μg/kg.h × 5） within 4 h. At 6 h after the induction of AP model, pancreatic tissues were collected for the pathological observation, mRNA extraction for determination of SERCA1 and SERCA2 mRNA expression or pancreatic acinar cell isolation for measurement of fluorescence intensity （FI） of intracellular calcium ion concentration [Ca2＋ i. RESULTS： There was no expression of pancreatic SERCA1 mRNA in the control group and the AP group. The expression of pancreatic SERCA2 mRNA in the AP group was down-regulated （expression ratio = 0.536; P = 0.001） compared with the control group, while that in the CQCQD group was up-regulated （expression ratio= 2.00; P = 0.012） compared with AP group. The FI of intracellular [Ca2＋ of pancreatic acinar cells in the AP group （138.2 ± 23.1） was higher than the C group （111.0 ± 18.4） and the CQCQD group （118.7 ± 15.2 ） （P 〈 0.05） and the pancreatic pathological score in the CQCQD group was lower than that in the AP group （5.7 ± 1.9 vs 9.2 ± 2.7, P 〈 0.05）.CONCLUSION： CQCQD can up-regulate the expression of SERCA2 mRNA of pancreatic tissues, reduce intracellular calcium overload and relieve pancreatic tissue lesions.     

The Expression of β3-adrenoceptor of Left Ventricle and the Effect on Heart Function by Stimulating β3-AR in Rats With Experimental Heart Failure

Objectives To observe the expression of β3-adrenoceptor （β3-AR） of left ventricle and the effect on heart function by stimulating β3-AR in rats with experimental heart failure. Methods Rats were randomly divided into heart failure group and control group. Heart failure models were built up by ligating coronary artery in rats. The expression of β3-AR mRNA were detected with RT-PCR; The change of heart function were observed after administration of BRL37344 （β3-AR agonist） by measuring left ventricular end-systolic pressure （LVESP）, left ventricular end-diastolic pressure （LVEDP）, the maximum pressure ascending rate of left ventricle （＋dp/ dtmax） and the maximum pressure descending rate of left ventricle（-dp/dtmax）. Results The expression of β3-AR mRNA （β3/β-actin） was 0.028±0.005 and the proportion of β3-AR （β3/β1＋β2＋β3） was 5.4%±0.06% in failure rats while the expression of β3-AR mRNA was 0.011 ±0.004 and the proportion was 1.2%±0.04% in control rats; The descending percentage of LVESP, ＋ dp/dtmax and -dp/dtmax were 16.1%, 21.7% and 13.2% respectively with administration of BRL37344 in failure rats, while 12.2%, 15.8% and 11.5% in control rats. Conclusions Compared with control group the expression of β3-AR mRNA of left ventricle was obviously increased and the negative inotropic function with exciting β3-AR was obviously enhanced in failure groups.     

A20 inhibits lipopolysaccharide-induced inflammation in enterocytes

AIM To examine the role of A20 in the regulation of intestinal epithelial cells(IECs) inflammation.METHODS Using gene transfection,both stable overexpression and knockdown A20-expressed HT-29 cell lines were established.Accordingly,the cells were divided into the following groups:The control group,the A20 overexpression group,the A20 knockdown group and the respective controls.A20 was stimulated with lipo-polysaccharide(LPS) in a dose- and time-dependent manner and was detected using western blotting and real-time polymerase chain reaction(PCR) analyses.Immunofluorescence and western blotting analyses were performed to investigate the role of A20 in the regulation of nuclear factor(NF)-κB activation and translocation into the nucleus.ELISA and real-time PCR were performed to examine A20 in regulating the release of the following inflammatory cytokines:Tumor necrosis factor(TNF)-a,interleukin(IL)-1b,IL-6 and IL-8.RESULTS The expression of A20 in IECs was inducible.When intestinal epithelial cells were subjected to the stimulation of LPS,the expression of A20 was increased,and the expression of A20 was induced in a dose-and timedependent manner.The expression of A20 was very low in HT-29 cells without LPS stimulation but rapidly increased and was maintained at a high level 2-4 h after stimulationwith LPS.These levels gradually declined with a change in time-course,and the expression of A20 increased with increasing LPS stimulation.Western blotting and immunofluorescence revealed that overexpression of A20 can inhibit NF-κB activation and its translocation to the nucleus.The overexpression of A20 can reduce the levels of proinflammatory cytokines involved in the pathophysiology of inflammatory bowel disease.There was no significant difference in the expression of IL-8 mR NA in the control group,A20 overexpression group or A20 knockdown group without LPS stimulation(P 0.05);however,while after 2 h,4 h and 8 h stimulation with LPS,the expression of IL-8 in the A20 overexpression group was lower than the control group and the A20 knockdown group(P 0.05 or P 0.01).The expression of TNF-a was different at different time points after 8 h of LPS stimulation(F = 31.33,DF = 5,P 0.001),and the expression of TNF-a increased as the LPS stimulation time increased.Upon LPS stimulation,lower levels of TNF-a were detected in the A20 overexpression cell lines(P 0.05).There were no significant differences in the induction of IL-6 and IL-1b among the control group,A20 overexpression group and A20 knockdown group(P 0.05).CONCLUSION A20 plays an important role in limiting inflammation by inhibiting LPS-induced NF-κB responses in the gut luminal.A20 may be a potential therapeutic tool for inflammatory diseases.     

Effect of SecinH3 on lung injury induced by sepsis of rats

Objective:To study effect of SecinH3 on lung injury induced by the sepsis of rats.Methods:A total of 30 SPF Wistar rats were randomly divided into two groups,including 5 rats in the control group and 25 in the model group.The intraperitoneal injection of endotoxinlipopolysaccharide(LPS) was performed to build the animal model of sepsis.The blood gas analysis was carried out.Afterwards,change in the expression of pro-inflammatory factors of IL-1,IL-6 and TNF- a in the serum were detected.To study the mechanism of SecinH3 in the process of lung injury induced by the sepsis,the rats with the successful modeling of sepsis were randomly divided into two groups.Rats in the SecinH3 group were given the intraperitoneal injection of 100 μg/12 h SecinH3 for 24 h;while rats in the control group were given the injection of same solvent by the same dosage.The blood was drawn from the heart by 500 μL for the blood gas analysis to detect the change in the expression of proinflammatory factors of IL-1,IL-6 and TNF-α in the treatment group and control group.After separating the lung tissue,the Real-time PCR and western blotting were performed to analyze the effect of SecinH3 on the expression of cytohesins and also discuss the change of epidermal growth factor receptor(EGFR) and p-EGFR related to the signaling pathway of EGFR-p38mitogen-activated protein kinase that is regulated by cytohesins.Results:Three rats died within 4 h after the injection of LPS,while other 22 ones had the successful modeling,with the success rate of 88%.After being stimulated by LPS,compared with the control group,the arterial partial pressure of oxygen of rats in the treatment group was significantly reduced(P0.05),while the partial pressure of CO_2 was significantly increased(P0.01).After being treated by SecinH3,Pa/O_2 was increased with the sepsis,while Pa/CO_2 was decreased with the action of SecinH3,which indicated that SecinH3 had the certain 'repairing' ability for the lung injury.SecinH3 might inhibit the cytohesins and then inhibit the phosphorylation of EGFR.Conclusions:SecinH3 can significantly inhibit the cytohesins and then relieve the lung injury induced by the sepsis of rats.     

Magnolol attenuates sepsis-induced gastrointestinal dysmotility in rats by modulating inflammatory mediators

AIM： To investigate the protective effects of magnolol on sepsis-induced inflammation and intestinal dysmotility. METHODS： Sepsis was induced by a single intraperitoneal injection of lipopolysaccharide （LPS）. Male Wistar rats were randomly assigned to one of three treatment groups： magnolol prior to LPS injection （LPS/Mag group）; vehicle prior to LPS injection （LPS/Veh group）; vehicle prior to injection of saline （Control/Veh）. Intestinal transit and circular muscle mechanical activity were assessed 12 h after LPS injection. Tumor necrosis factor-α （TNF-α）, interleukin-10 （IL-10）, monocyte chemoattractant protein-1 （MCP-1） and inducible nitric oxide synthase （iNOS） mRNA in rat ileum were studied by RT-PCR 2 h after LPS injection. Nuclear factor-κB （NF-κB） activity in the intestine was also investigated at this time using electrophoretic mobility shift assay. In addition, antioxidant activity was determined by measuring malondialdehyde （MDA） concentration and superoxide dismutase （SOD） activity in the intestine 2 h after LPS iniection.RESULTS： Magnolol significantly increased intestinal transit and circular muscle mechanical activity in LPS- treated animals. TNF-α, MCP-1 and iNOS mRNA expression in the small intestine were significantly reduced after magnolol treatment in LPS-induced septic animals, compared with untreated septic animals. Additionally,magnolol significantly increased IL-10 mRNA expression in septic rat ileum. Magnolol also significantly suppressed NF-κB activity in septic rat intestine. In addition, magnolol significantly decreased MDA concentration and increased SOD activity in rat ileum. CONCLUSION： Magnolol prevents sepsis-induced suppression of intestinal motility in rats. The potential mechanism of this benefit of magnolol appears to be modulation of self-amplified inflammatory events and block of oxidative stress in the intestine.     

CO liberated from CORM-2 modulates the inflammatory response in the liver of thermally injured mice

AIM： To explore the effects of CO-releasing molecules [tricarbonyldichlororuthenium （Ⅱ） dimer, CORM-2]- liberated CO on attenuation of inflammatory responses in liver of an experimental animal model of thermal injury and to investigate the associated potential mechanisms. METHODS： Thirty-six mice were assigned to three groups in three respective experiments. In each experiment, mice in sham group （n = 4） received sham thermal injury, whereas mice in burn group （n = 4） received a 15% of total body surface area （TBSA） fullthickness thermal injury, and mice in burn ＋ CORM-2 group （n = 4） received the same thermal injury with immediate administration of CORM-2 （8 mg/kg, iv）. Hepatic tissue sections were stained with hematoxylin and eosin and examined under a light microscope. Levels of aminotransferases （ALT and AST） and nitric oxide （NO） were measured by biochemical methods. Tumor necrosis factor-α （TNF-α） and interleukin （IL-1β） activity, and the protein expression of iNOS and HO-1 in serum and tissue homogenates were assessed. In in vitro experiments, Kupffer cells were stimulated with LPS （10 μg/mL） for 4 h in the presence or absence of CORM-2 （10-100 μmol/L）. Subsequently, the expression levels of TNF-α and NO production were assessed. RESULTS： Pro-inflammatory mediators （TNF-α, IL- 1β, NO） in serum and liver homogenates of thermally injured mice were significantly reduced by CORM-2 administration. This was accompanied by a decrease in the expression of iNOS while an increase in the expression of HO-1 in the liver tissue. In parallel, the concentrations of TNF-α and NO in supernatants of LPS-stimulated Kupffer cells co-incubated with CORM-2 （10-100 μmol/L） were also markedly decreased.Histological examination demonstrated that CORM-2 could attenuate the leukocytes infiltration to the liver tissue. CONCLUSION： CORM-released CO modulates liver inflammation and significantly protects liver injury in burn mice by inhibiting the expression     

血管内皮生长因子基因转染骨髓间充质干细胞移植对肺气肿大鼠的疗效

目的：观察血管内皮生长因子（VEGF）基因转染大鼠骨髓间充质干细胞（MSCs）移植对肺气肿大鼠肺泡壁细胞的修复作用。方法：pcDNA3．1-hVEGF转染雄性Lewis大鼠MSCs。雌性Lewis大鼠随机分为4组：正常对照组、肺气肿组、单纯MSCs移植组,hVEGF移植组。观察MSCs移植28d后肺组织形态学变化,支气管肺泡灌洗液细胞分类计数,ELISA法检测VEGF含量。Y染色体荧光原位杂交（Y-FISH）示踪雄性大鼠MSCs在雌性肺气肿大鼠肺组织内的植入情况;采用TUNEL法检测肺泡壁细胞凋亡,免疫组化法检测Bcl-2蛋白的表达。结果：hVEGF移植组肺气肿改变较肺气肿组、单纯MSCs移植组减轻;支气管肺泡灌洗液炎性细胞数较后2组减少;肺组织VEGF含量较后2组增多;肺泡壁细胞凋亡指数明显低于后2组;Bcl-2染色阳性细胞百分比高于后2组;Y-FISH显示hVEGF移植组、单纯MSCs移植组的雌性大鼠肺组织中有Y染色体阳性的细胞。结论：真核表达载体pcDNA3．1hVEGF可以成功地在MSCs中表达,pcDNA3．1hVEGF转染MSCs移植能够减轻大鼠肺气肿样改变,其疗效优于单纯MSCs移植治疗。

Abstract：

Objective： To evaluate the effect of mesenchymal stem cells （MSCs） transfected with human vascular endothelial growth factor （VEGF） gene for rats with pulmonary emphysema. Methods： MSCs from male lewis rats were transfected with the pcDNA3. 1-hVEGF control vector. Female Lewis rats were randomly divided into four groups： normal control group, emphysema group, emphysema ＋ MSCs transplantation group, emphysema ＋ hVEGF-transfected MSCs transplantation group. Morphologie changes of the lung tissue were observed 28 Jays after treatment. The total cell number of bronchoalveolar lavage fluid were counted, and the content of VEGF was de tected by ELISA. The engraftment of male bone marrow MSCs in female recipient lung was determined by Y chromosome fluorescent in situ hybridization （Y-FISH）. The apoptosis of the lung cells was assessed by TUNEL stai ning. The expression of Bcl-2 were determined by immunohistochemical staining. Results： Emphysematous change in the emphysema ＋ hVEGF transfeeted MSCs transplantation group was improved compared with those in emphysema group and the emphysema ＋ MSCs transplantation group. The total cell number of bronchoalveolar lavage fluid was decreased in the emphysema ＋ hVEGF transfected MSCs transplantation group compared to the emphysema group and the emphysema ＋ MSCs transplantation group. The level of VEGF was higher in emphysema ＋ hVEGF transfected MSCs transplantation group compared with those of the emphysema group and the emphysema ＋ MSCs transplantation group. The apoptotic index of the alveolar wall cells in the emphysema ＋ hVEGF transfeeted MSCs transplantation group was less than that of the emphysema group and the emphysema ＋ MSCs transplantation group. The percentage of Bcl-2 positive cells in the emphysema ＋ hVEGF transfected MSCs transplantation group was significantly higher than that of the emphysema group and the emphysema ＋ MSCs transplantation group. Y chromo some positive cells were observed in the lungs of rats from the emphysema ＋ hVEGF transfected MSCs transplantation group and the emphysema ＋ MSCs transplantation group, Conclusions： The hVEGF gene could expressed in MSCs. Trans plantation of MSCs transfected with hVEGF gene can improve emphysematous changes than single cellular therapy.     

大鼠Kupffer细胞分泌的促炎因子在实验性急性胰腺炎肝损伤中的作用

背景：促炎因子在急性胰腺炎（AP）胰腺局部损伤以及全身炎症反应过程中起重要促进作用。目的：探讨大鼠Kupffer细胞分泌的促炎因子在实验性AP肝损伤中的作用。方法：提取24只Sprague-Dawley大鼠肝脏Kupffer细胞,并分为正常对照组、脂多糖（LPS）组、LPS＋胰弹性蛋白酶（PE）组和AG490预处理组。采用酶联免疫吸附测定（ELISA）法检测Kupffer细胞上清液中肿瘤坏死因子（TNF）-α、白细胞介素（IL）-6和IL-18含量;以细胞免疫荧光双重染色法观察细胞形态和JAK2荧光表达;以蛋白质印迹法检测JAK2蛋白表达。结果：与正常对照组相比,LPS组TNF．仅、IL-6和IL-18含量以及JAK2表达均显著增高（P〈0．01）;LPS＋PE组TNF—α、IL-6和IL-18含量以及JAK2表达显著高于LPS组（R0．01）：AG490预处理组TNF-仅、IL-6和IL—18含量以及JAK2表达显著低于LPS＋PE组（P〈0．01）,但与LPS组相比无明显差异。Kupffer细胞形态改变与JAK2表达一致,Kupffer细胞胞质中JAK2荧光量、荧光强度以及蛋白表达的动态变化与TNF-α、IL-6和IL-18含量基本一致。结论：Kupffer细胞过度活化在炎症放大和AP时胰外器官损伤中起重要作用,抑制Kupffer细胞内JAK2活化可减少促炎因子的分泌．从而有效减轻AP合并的肝损伤。     

环氧合酶-2在小肠缺血再灌注损伤中对免疫状态的影响

背景：小肠缺血再灌注（I／R）是危重症过程中常见的病理改变,研究其损伤发生机制对多器官功能障碍综合征的防治具有重要意义。目的：探讨COX-2在小肠I／R损伤中对免疫状态的影响。方法：48只大鼠随机分为假手术组（n=8）、I／R模型组（n=20）和COX-2选择性抑制剂尼美舒利干预组（n=20）,干预组于造模前1h予尼美舒利80mg／kg灌胃。各组分别于再灌注3、6、12、24h后采集标本,行小肠组织COX-2mRNA、血清D-乳酸、血清促炎（IL-6、TNF-a）和抗炎（IL-10）细胞因子以及全血T细胞亚群检测。结果：I／R模型组小肠组织COX-2mRNA表达、血清D-乳酸水平在再灌注后3h即明显增高,6h时达峰值,各时点均显著高于假手术组（P〈0．05）,同时血清IL-6、TNF-a、IL-10水平显著增高（P〈0．05）,全血CD4＋／CD8＋比值持续降低（P〈0．05）。与同时点I／R模型组相比,尼美舒利干预组COX-2mRNA表达、D哥L酸水平显著降低（P〈0．05）,IL-10水平、CD4＋／CD8＋比值显著增高（P〈0．05）,IL-6、TNF-a水平略有降低。结论：COX-2在小肠I／R损伤中发挥重要作用,其机制可能为改变促炎／抗炎细胞因子之间以及CD4＋／CD8＋细胞之间的动态平衡,即同时作用于非特异性和特异性免疫系统,导致严重的机体免疫状态紊乱。COX-2选择性抑制剂可能系通过抗炎和免疫调节作用改善小肠I／R损伤。     

人脐带间充质干细胞对ALI治疗作用的研究

目的探讨输入人脐带间充质干细胞（human umbilical cord mesenchymal stem cells,HUMscs）对脂多糖（LPS）诱导的大鼠ALI的治疗作用。方法将30只Wistar大鼠随机分为3组：正常对照组、ALI模型组和HUMSCs移植组,每组10只。健康大鼠LPS气管滴入方法建立ALI模型,尾静脉输入HUMSCs。输入7h后,处死各组大鼠,取肺组织行病理学观察,测定肺湿／干重比（W／D）,ELISA法测定肺组织匀浆中肿瘤坏死因子α（TNF-α）和IL-1β的含量。结果肺组织病理学显示：ALI模型组大鼠肺组织呈现典型的炎症病理变化,包括肺泡充血、水肿、出血,肺泡腔和血管壁中性粒细胞浸润,肺泡壁增厚等肺损伤性病变;HUMSCs移植组大鼠肺组织损伤程度明显减轻。与正常对照组比较,ALI模型组W／D、TNF-α和IL-1β含量明显升高（P〈0．05）。与Au模型组比较,HUMSCs移植组W／D、TNF-α和IL-1β含量明显降低（P〈0．05）。结论输入HUMSCs能减轻ALI,并能降低肺W／D和肺组织TNF-α及IL-1β含量。     

骨髓间充质干细胞条件培养液对急性百草枯中毒肺损伤的影响

目的通过将骨髓间充质干细胞(BMSCs)条件培养液注入到急性百草枯中毒大鼠体内,观察其对急性百草枯中毒肺损伤的影响。方法选4周龄SPF级雄性SD大鼠,原代培养BMSCs,传至第3代的BMSCs无血清培养24 h,收集的培养基即为BMSCs条件培养液。将30只SPF级雄性大鼠随机分为3组:百草枯组、BMSCs条件培养液治疗组(治疗组)、正常对照组。将BMSCs条件培养液通过尾静脉注入各组大鼠体内,观察各组大鼠肺组织肺泡炎评分、肺组织α-SMA表达水平和各组大鼠血浆中TNF-α、IL-1β的水平变化。结果与百草枯组相比,治疗组肺泡炎症反应较轻,肺组织α-SMA表达水平较低(P0.05),血浆中TNF-α、IL-1β的含量较低(P0.05)。结论 BMSCs条件培养液可减缓急性百草枯中毒引起的肺损伤。     

Treg及IL-4对重症急性胰腺炎时枯否细胞M2极化状态的调节作用

目的探讨雨蛙肽联合脂多糖诱导小鼠重症急性胰腺炎(severe acute pancreatitis,SAP)的方法和Treg(CD4+CD25+FoxP3+T调节淋巴细胞)及IL-4(白介素-4)对SAP时枯否细胞(Kupffer cells)M2极化状态的调节作用的比较。方法 (1)正常组予腹腔注射生理盐水(NS);SAP组予腹腔注射雨蛙肽联合脂多糖。SAP组细分为3组:造模后9 h、12 h和24 h组,比较胰腺病理情况。(2)比较正常组与模型组(SAP 8 h+NS组)肝脏炎症因子的基因表达水平。(3)模型组分3组:SAP生理盐水对照组(SAP16 h+NS组)、SAP IL-4治疗组(SAP 16 h+IL-4组)、SAP Treg治疗组(SAP 16 h+Treg组)。RT-PCR检测肝脏炎症因子IL-1β、TNF-α和IL-10 mRNA表达水平;免疫荧光技术检测肝脏CD163、CCR7的表达。结果 (1)HE病理结果造模后24 h可见胰腺片状坏死。(2)模型组IL-1βmRNA的表达显著高于正常组(P0.05)。(3)SAP Treg治疗组IL-1β、TNF-αmRNA的表达显著低于SAP生理盐水对照组(P0.05);SAP Treg治疗组IL-1βmRNA的表达显著低于SAP IL-4治疗组(P0.05)。结论雨蛙肽联合脂多糖成功诱导小鼠SAP。IL-4和Treg对SAP具有一定的治疗作用。     

糖原合成酶激酶-3β对巨噬细胞系RAW264.7活化的影响

目的探讨糖原合成酶激酶-3β（GSK-3β）对巨噬细胞系RAW264.7活化的影响。方法将生长状态良好的RAW264.7细胞分为3组：实验对照组、脂多糖（LPS）组和GSK-3β特异抑制剂SB216763干预组,在12 h、24 h进行指标检测。采用Western印迹法检测细胞GSK-3β、p-GSK-3β^ser9蛋白的表达,ELISA试剂盒法检测细胞上清IL-10、TNF-α的变化,RT-PCR检测细胞中5-LO mRNA变化,免疫荧光法检测ED1表达,电镜下观察RAW264.7细胞形态变化。结果12 h和24 h LPS组与对照组相比,p-GSK-3β^ser9表达减少,GSK-3β表达不变,活性升高;TNF-α、IL-10及5-LO mRNA表达增多（P〈0.05）;ED1表达绿色荧光明显增多;透射电镜观察LPS组巨噬细胞形态不规则,吞噬坏死物质细胞变多。12 h和24 h SB216763干预组与LPS组进行比较,p-GSK-3β^ser9表达明显增多,GSK-3β表达不变,活性降低;TNF-α及5-LO mRNA表达减少（P〈0.05）,IL-10表达明显增多（P〈0.05）;ED1绿色荧光表达减少;透射电镜观察细胞形态较规则。结论 GSK-3β对于RAW264.7细胞活化发挥重要的作用。     

NADPH氧化酶2在AngⅡ促进高血压炎症因子IL-1β分泌中的意义

目的探讨NADPH氧化酶2（NOX2）在AngⅡ促进高血压炎症因子IL-1β分泌过程中的意义。方法分离雄性自发性高血压大鼠（SHR）外周血单个核细胞并进行培养,将细胞随机分为：空白对照组（A组）,AngⅡ组（B组）,AngⅡ＋NOX2抑制剂二苯基碘（DPI）组（C组）。分别检测单个核细胞NOX2蛋白、IL-1βmRNA及蛋白的表达。结果与A组比较,B组NOX2蛋白、IL-1βmRNA及蛋白的表达升高（P〈0.01或P〈0.05）;与B组比较,C组NOX2蛋白、IL-1β蛋白的表达降低（P〈0.01）,而IL-1βmRNA的表达无明显变化（P〉0.05）。结论 AngⅡ能通过上调单个核细胞NOX2的表达促进IL-1β蛋白的分泌。     

肺腺癌细胞系H114的建立

目的建立国人男性肺腺癌细胞系,为肺癌的防治研究提供理想的体外实验模型。方法以经组织学和／或细胞学确诊的标本进行原代培养,通过光镜观察、细胞苏木精．伊红（HE）染色、细胞生长曲线、异体移植实验及组织HE染色等对其进行分析鉴定,建立细胞系。结果细胞经液氮罐或-80℃低温冰箱反复冻存复苏后仍保持良好的增殖活性,复苏细胞经0．4％胎盘蓝染色,活细胞比率均保持在85％以上。在整个168h的观察时间里,肺腺癌H114细胞始终处于持续增殖状态,可见潜伏期和指数生长期,由于本细胞系传代次数较少,生长活跃,7d还没出现平顶期和退化衰亡期;体外培养细胞生长稳定,细胞形态学及浸润性生长结果表明该细胞系符合恶性细胞特性,裸鼠接种成功致瘤,瘤细胞形态与原患者的病理切片相似,命名为H114细胞系。结论该细胞系符合建系标准,是一株新建的人肺腺癌细胞系。     

生脉散对急性肝衰竭大鼠内毒素诱导细胞因子的影响

[目的]探讨生脉散对急性肝衰竭大鼠内毒素（LPS）诱导细胞因子水平的影响。[方法]采用胁氨基半乳糖腹腔注射法制作急性肝衰竭大鼠模型。予生脉散灌胃2h及8h后,检测血清LPS与细胞因子水平。[结果]D-氨基半乳糖能明显增加大鼠血清白细胞介素6（IL-6）、细胞间黏附分子1（ICAM-1）和IL-1β水平（P〈0．01）,随着D-氨基半乳糖作用时间延长的趋势明显减弱,但对血清LPS、肿瘤坏死因子α（TNF-α）水平无明显影响（P〉0．05）;生脉散能显著降低D氨基半乳糖肝衰竭大鼠血清IL-6、ICAM-1和IL-1β水平（P〈0．01,〈O．05）。LPS攻击2h和8h后,能明显诱导D-氨基半乳糖大鼠血清LPS、TNF-α、IL-6、ICAM-1和IL-1β水平增加（P〈0．01）;除在8h对TNF-α无影响外,生脉散能明显减轻LPS攻击D-氨基半乳糖大鼠后对血清LPS、TNF-α、IL-6、ICAM-1和IL-1β水平的影响（P〈0．01,〈O．05）。[结论]SD大鼠在急性肝衰竭状态下,存在严重LPS血症,并引起细胞因子水平变化的炎症级联反应,生脉散可通过调节细胞及炎症因子水平起到治疗作用。     

丹参酮ⅡA磺酸钠对急性坏死性胰腺炎大鼠肺损伤的抗炎作用及其机制研究

背景:急性肺损伤是重症急性胰腺炎(SAP)早期最主要的死亡原因,减轻肺损伤可能降低SAP的死亡率。目的:研究丹参酮ⅡA磺酸钠(STS)对SAP相关肺损伤的抗炎作用及其可能机制。方法:36只Sprague-Dawley大鼠随机分为假手术组、急性坏死性胰腺炎(ANP)组和STS组,后两组予5%牛磺胆酸钠胰管注射建立ANP模型,STS组于造模前30 min予腹腔注射STS预处理。造模后12 h和24 h分批处死动物,行胰腺、肺组织病理学检查和肺损伤评分,ELISA法检测肺组织肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)含量,蛋白质印迹法检测肺组织JNK、p-JNK蛋白表达。结果:ANP组肺组织实变明显,大量中性粒细胞浸润,肺损伤评分、肺组织TNF-α、IL-1β含量和JNK、p-JNK表达均显著高于同时间点假手术组(P0.05)。STS组肺损伤评分、肺组织TNF-α、IL-1β含量和p-JNK表达较同时间点ANP组显著降低(P0.05),JNK表达则无明显变化。结论:STS干预能下调ANP大鼠的肺组织炎症因子表达,降低肺损伤程度,其机制可能与抑制JNK信号通路激活有关。