重症急性胰腺炎中性粒细胞凋亡延迟机制研究进展

中性粒细胞凋亡延迟在重症急性胰腺炎发病中具有重要作用。许多细胞外因子可以抑制中性粒细胞,但其具体机制尚不清楚。线粒体参与了中性粒细胞凋亡的调控。survivin在成熟的中性粒细胞中低或不表达,但是在活体外粒细胞/巨噬细胞集落刺激因子(CSF)或粒细胞集落刺激因子的刺激下高表达,在炎症状态下的活体内也高表达,因此survivin可能在中性粒细胞凋亡延迟的调控中有重要作用。     

中性粒细胞活化和上皮细胞凋亡在急性肺损伤发生中的作用

致病因子一方面诱导肺泡巨噬细胞和上皮细胞产生多种细胞因子和趋化因子,激活中性粒细胞并使其向损伤部位聚集,从而产生炎症因子的瀑布式反应;另一方面激活死亡受体通路Fas-FasL等诱发肺上二皮细胞凋亡,从而引起肺组织损伤.另外,Fas活化后可通过介导肺内炎症介质释放和中性粒细胞聚集进一步加重肺损伤.中性粒细胞活化和上皮细胞凋亡在急性肺损伤的发生过程中起重要作用.     

中性粒细胞趋化因子在重症急性胰腺炎中的表达及临床意义

目的:探讨中性粒细胞趋化因子(CINC)在重症急性胰腺炎 (SAP)发病机制中的作用．方法:采用向胆胰管逆行注射50 g／L牛磺胆酸钠建立大鼠 SAP模型,48只♂SD大鼠随机分为手术对照组和SAP组,分别检测各组不同时间点血清淀粉酶和胰腺组织病理学改变, 用免疫组织化学法和半定量逆转录聚合酶链反应(RT-PCR) 法检测胰腺组织中CINC蛋白和CINCmRNA表达的变化情况．结果:牛磺胆酸钠组与手术对照组相比,大鼠的血清淀粉酶明显增高、胰腺组织学改变明显;术后1 h胰腺腺泡细胞 CINC蛋白和胰腺组织中CINC mRNA的表达高于手术对照组,随着时间的延长表达逐渐增强,牛磺胆酸钠组术后1 h胰腺腺泡细胞CINC mRNA表达较手术对照组明显增高分别为 (0.37±0．10 vs 0．29±0．10,P<0．05),并且随着时间的延长差别更加明显;免疫组化显示CINC蛋白表达也高于手术对照组．结论:CINC可能在SAP发病过程中起了重要的作用.     

中性粒细胞趋化因子在急性胰腺炎相关急性肺损害中的作用

目的:探讨中性粒细胞趋化因子(CINC)在急性胰腺炎相关的急性肺损害(ALI)中的作用.方法:分别采用ip雨蛙肽和胰胆管逆行注射50g/L牛磺胆酸钠建立大鼠轻症、重症急性胰腺炎模型.84只SD大鼠随机分为雨蛙肽组、生理盐水组、牛磺胆酸钠组和手术对照组.分别检测各组不同时间点血清淀粉酶、肺干湿重比和肺组织病理学改变,用免疫组织化学法和半定量逆转录聚合酶链反应(RT-PCR)法检测肺组织中CINC蛋白和CINCmRNA表达的变化情况.结果:雨蛙肽组各时间点CINC蛋白和CINCmRNA的表达与生理盐水组无明显差异(P>0.05);牛磺胆酸钠组与手术对照组相比,血清淀粉酶、肺干湿重比显著升高(P<0.05),术后1h肺组织CINCmRNA的表达开始升高(1h:0.23±0.07vs0.07±0.04,P<0.05;3h:0.36±0.07vs0.06±0.04,P<0.05;6h:0.56±0.07vs0.09±0.05,P<0.01;12h:0.49±0.09vs0.11±0.03,P<0.01),术后3h开始有CINC蛋白的表达,随着时间的延长表达逐渐增强,且与肺组织的病理改变呈正相关.结论:CINC可能在胰腺炎相关的急性肺损害中起了重要的作用.     

重症急性胰腺炎外周血中性粒细胞凋亡及其调控机制的研究

目的初步探讨重症急性胰腺炎（SAP）外周血中性粒细胞的凋亡及凋亡抑制蛋白survivin在SAP中性粒细胞凋亡延迟调控中的作用。方法48只SD大鼠随机分为急性坏死性胰腺炎（ANP）组和假手术（SO）组。采用胰胆管逆行注射4％牛磺胆酸钠（1ml／kg体重）制模，制模后24、48、72h分别处死动物。取胰腺组织评估病理变化；TUNEL荧光标记法检测外周血中性粒细胞的凋亡；RTPCR检测外周血中性粒细胞survivin mRNA的表达。结果ANP组胰腺病理评分较（SO）组明显升高（P〈0．05）。ANP组中性粒细胞凋亡率较SO组明显降低，随时间延长更明显（P〈0．05）。ANP组中性粒细胞survivin mRNA水平均较SO组明显升高，且随时间延长更明显（P〈0．05）。ANP组中性粒细胞凋亡率分别与胰腺病理评分和survivin mRNA水平呈负相关（r=0．97，r=0．99，P〈0．05）。结论ANP时外周血中性粒细胞凋亡明显延迟，survivin mRNA高表达．表明survivin在调控SAP外周血中性粒细胞凋亡延迟机制中可能具有重要作用。     

雷米芬太尼复合丙泊酚对老年手术患者中性粒细胞凋亡及白介素-10水平的影响

目的 探讨雷米芬太尼复合丙泊酚对老年患者术中中性粒细胞(PMN)凋亡及白介素(IL)-10水平的影响.方法 选择2011年6月至2012年12月来我院手术治疗的老年患者64例,随机分为雷米芬太尼联合丙泊酚组(雷-酚)32例,雷米芬太尼联合七氟醚组(雷-醚)32例,分别于手术开始时(T1)、手术开始后2 h(T2)、手术开始后12 h(T3)、手术开始后24 h(T4)及手术开始后48 h(T5)抽取所有患者肘正中静脉血,检测PMN凋亡及IL-10水平.结果 两组老年患者手术开始后(T1～T4) PMN凋亡率均比术前(T0)低,差异有统计学意义(P＜0.05),雷-酚组老年患者在T2～T5时点PMN凋亡率高于雷-醚组,差异有统计学意义(P＜0.05)；手术开始后(T1～ T4) IL-10水平呈升高趋势,雷-酚组老年患者在T2 ～T5时点IL-10水平高于雷-醚组,差异有统计学意义(P＜0.05).结论 雷米芬太尼联合丙泊酚能够抑制老年患者术中及术后PMN凋亡和提高IL-10水平.     

急性胰腺炎血浆白介素-18水平与急性时相蛋白的关系

目的探索急性胰腺炎病人血浆白介素-18(IL-18)水平变化情况,及其与急性时相蛋白变化的关系,了解急性胰腺炎病人血浆IL-18水平的变化及其意义。方法将病人分为3组:急性水肿型胰腺炎组、急性坏死型胰腺炎组和对照组。分别检测血浆C反应蛋白(CRP)、前白蛋白(PA)、转铁蛋白(TRA)和IL-18水平。结果急性胰腺炎病人血浆IL-18和CRP明显升高,TRA和PA明显降低。IL-18水平与CRP呈正相关,与TRA和PA呈负相关。结论IL-18可能作为一种新的应激指标,反映机体的炎症情况,对急性胰腺炎的严重程度和预后评估有一定的临床应用价值。     

西维来司钠对大鼠重症急性胰腺炎炎症反应的治疗作用

目的:检测重症急性胰腺炎(severe acute pancreatitis,SAP)大鼠血清中中性粒细胞弹性蛋白酶(neutrophil elastase,NE)、白介素-6(interfilon-6,IL-6)的含量及胰腺病理学改变,探讨西维来司钠对大鼠SAP的治疗作用.方法:采用经十二指肠乳头逆行胆胰管注射5%牛磺胆酸钠的方法制备大鼠SAP模型;药物治疗组静脉输入西维来司钠,切取胰腺组织行病理学评分,测定血清中NE、IL-6及淀粉酶的含量.结果:牛黄胆酸钠胰胆管注射可以制作典型的急性胰腺炎模型,其血清淀粉酶升高、胰腺病理损伤符合急性胰腺炎表现.西维来司钠治疗组血清淀粉酶值及NE、IL-6含量较模型组降低,有显著性差异(3h:5636.22±713.57 vs 5835.75±681.52,16.99±3.28 vs 22.93±4.74,181.86±36.56 vs 281.82±30.79;6h:5743.44±624.93 vs 6253.66±533.99,23.63±4.47 vs 31.81±4.69,184.15±28.56 vs 319.39±21.73;12h:7098.93±698....     

重症急性胰腺炎外周血中性粒细胞凋亡及其调控机制的研究

目的 初步探讨重症急性胰腺炎(SAP)外周血中性粒细胞的凋亡及凋亡抑制蛋白survivin在SAP中性粒细胞凋亡延迟调控中的作用.方法　48只SD大鼠随机分为急性坏死性胰腺炎(ANP)组和假手术(SO)组.采用胰胆管逆行注射4%牛磺胆酸钠(1 ml/kg体重)制模,制模后24、48、72 h分别处死动物.取胰腺组织评估病理变化;TUNEL荧光标记法检测外周血中性粒细胞的凋亡;RT-PCR检测外周血中性粒细胞survivin mRNA的表达.结果　ANP组胰腺病理评分较(SO)组明显升高(P ＜ 0.05).ANP组中性粒细胞凋亡率较SO组明显降低,随时间延长更明显(P ＜ 0.05).ANP组中性粒细胞survivin mRNA水平均较SO组明显升高,且随时间延长更明显(P ＜ 0.05).ANP组中性粒细胞凋亡率分别与胰腺病理评分和survivin mRNA水平呈负相关(r = 0.97,r = 0.99, P ＜ 0.05).结论 ANP时外周血中性粒细胞凋亡明显延迟,survivin mRNA高表达,表明survivin在调控SAP外周血中性粒细胞凋亡延迟机制中可能具有重要作用.     

白介素18在心血管系统疾病中的作用

白介素-18(IL-18)可与多种炎症因子相互作用,具有重要的生物学功能:可诱导辐助性T细胞(TH1)产生细胞因子(cytokine,CK),可诱导自然杀伤细胞(NK)的胞毒活性,促进 T细胞增生,可与IL-12产生协同作用等。研究发现IL-18广泛参与心血管系统疾病,并起重要作用。对IL-18进行深入研究有助于认识其在心血管系统疾病发生发展和转归中的作用, 为临床治疗提供新途径。     

Caspase-1 inhibition alleviates acute renal injury in rats with severe acute pancreatitis

AIM:To assess the effect of inhibition of caspase-1 on acute renal injury in rats with severe acute pancreatitis(SAP).METHODS:Forty-two Sprague-Dawley rats were randomly divided into three groups:healthy controls(HC,n=6),SAP rats treated with saline(SAP-S,n=18),or SAP rats treated with a caspase-1/interleukin(IL)-1β-converting-enzyme(ICE)inhibitor(SAP-I-ICE,n=18).SAP was induced by retrograde infusion of 5%sodium taurocholate into the bile-pancreatic duct.HC rats were subjected to identical treatment and surgical procedures without sodium taurocholate.Rats received an intraperitoneal injection of isotonic saline(SAP-S)or the inhibitor(SAP-ICE-I)at 2 and 12 h after induction of acute pancreatitis.Surviving rats were sacrificed at different time points after SAP induction;all samples were obtained and stored for subsequent analyses.The levels of blood urea nitrogen(BUN)and creatinine(Cr)were measured using automatic methods,and serum IL-1βconcentrations were measured by an enzymelinked immunosorbent assay.Intrarenal expression of IL-1β,IL-18 and caspase-1 mRNAs was detected by RT-PCR.IL-1βprotein expression and the pathologic changes in kidney tissues were observed by microscopy after immunohistochemical or hematoxylin and eosin staining,respectively.RESULTS:The serum levels of BUN and Cr in the SAP-S group were 12.48±2.30 mmol/L and 82.83±13.89μmol/L at 6 h,23.53±2.58 mmol/L and 123.67±17.67μmol/L at 12 h,and 23.60±3.33 mmol/L and125.33±21.09μmol/L at 18 h,respectively.All were significantly increased compared to HC rats(P<0.01for all).Levels in SAP-ICE-I rats were significantly decreased compared to SAP-S rats both at 12 and 18 h(P<0.01 for all).Serum IL-1βlevels in the SAP-S group were 276.77±44.92 pg/mL at 6 h,308.99±34.95pg/mL at 12 h,and 311.60±46.51 pg/mL at 18 h;all significantly higher than those in the HC and SAP-ICE-I groups(P<0.01 for all).Intrarenal expression of IL-1βmRNA was weak in HC rats,but increased significantly in SAP-S rats(P<0.01).ICE inhibition significantly decreased the expression of IL-1βand IL-18 mRNAs(P<0.05 for all vs SAP-S),whereas caspase-1 mRNA expression was not significantly different.Weak IL-1βimmunostaining was observed in HC animals,and marked staining was found in the SAP-S group mainly in renal tubular epithelial cells.IL-1βimmunostaining was significantly descended in SAP-ICE-I rats compared to SAP-S rats(P<0.05).Caspase-1 inhibition had no effect on the severity of kidney tissue destruction.CONCLUSION:The expression of caspase-1-activated cytokines IL-1βand IL-18 plays a pivotal role in acute renal injury in rats with experimental SAP.Caspase-1inhibition improves renal function effectively.     

DDFA方案对重症急性胰腺炎大鼠心肌细胞凋亡及Bax,Bcl-2表达的影响

目的:探讨DDFA方案对重症急性胰腺炎(SAP)大鼠心肌细胞凋亡及Bax、Bcl-2基因表达的影响.方法:SD大鼠45只随机分为假手术组、SAP组和DDFA治疗组(DDFA:地塞米松、低分子右旋糖酐、5-氟脲嘧啶、抑肽酶)大鼠SAP模型采用0.05牛磺胆酸钠逆行胆胰管注射法建立,建模后6,12,18h时测定血心肌肌钙蛋白Ⅰ(cTnⅠ,μg/L)和肌酸激酶同功酶(CK-MB,nkat/L),光镜观察心肌组织病理变化,TUNEL法测定心肌细胞凋亡指数(AI),SABC免疫组化染色法测定心肌Bax和Bcl-2基因表达.结果:SAP组血cTnⅠ(6h:2.14±0.09vs0.18±0.07;12h:3.30±0.25vs0.20±0.08;18h:3.74±0.42vs0.19±0.08),CK-MB(6h:7681±252vs3389±204;12h:11576±251vs2553±205;18h:12972±458vs3522±218)和心肌细胞凋亡指数(6h:5.73±0.84vs0.99±0.13;12h:8.79±0.68vs1.00±0.44;18h:14.09±1.22vs1.02±0.32)、Bax(6h:4.42±1.05vs1.03±0.13;12h:7.39±0.38vs1.08±0.13;18h:8.51±1.07vs1.02±0.12)和Bcl-2(12h:1.83±0.18vs1.11±0.11;18h:3.31±0.75vs1.02±0.12)表达较假手术组升高(P<0.01),光镜下见心肌组织损害明显;经DDFA治疗后,血cTnⅠ(6h:0.87±0.06;12h:1.73±0.12;18h:2.48±0.34)、CK-MB(6h:5858±232;12h:8275±257;18h:8975±430)和心肌细胞凋亡指数(6h:2.44±0.27;12h:5.93±0.39;18h:8.75±0.66)、Bax表达(6h:3.05±0.87;12h:6.46±0.36;18h:6.97±1.04)下降(P<0.05),而Bcl-2表达(6h:3.05±0.87;12h:4.86±0.46;18h:4.53±1.04)增强(P<0.05),光镜下见心肌组织损害减轻.心肌细胞凋亡与血CK-MB、cTnⅠ呈正相关(r=0.812,P<0.05;r=0.807,P<0.05).结论:心肌细胞凋亡、Bax和Bcl-2表达参与SAP发病机制,在SAP早期给予DDFA治疗对减轻心脏损害程度、改善预后是有益的.     

Therapeutic effects of caspase-1 inhibitors on acute lung injury in experimental severe acute pancreatitis

AIM： To assess the therapeutic effect of Caspase-1 inhibitors （ICE-I） on acute lung injury （ALI） in experimental severe acute pancreatitis （SAP）.
METHODS： Forty-two SD rats were randomly divided into 3 groups： healthy controls （HC, n = 6）; SAP-S group （n = 18）; SAP-ICE-i group （n = 18）. SAP was induced by retrograde infusion of 5% sodium taurocholate into the bile-pancreatic duct. HC rats underwent the same surgical procedures and duct cannulation without sodium taurocholate infusion, in SAP-S group, rats received the first intraperitoneal injection of isotonic saline 2 h after induction of acute pancreatitis and a repeated injection after 12 h. In SAP-ICE-I group, the rats were firstly given ICE inhibitors intraperitoneally 2 h after induction of pancreatitis. As in SAP-S group, the injection was repeated at 12 h. Serum 1L-1β was measured by EUSA. Intrapulmonary expression of Caspase-1, IL-1β and IL-18 mRNA were detected by semi-quantitative RT-PCR. The wet/dry weight ratios and histopathological changes of the lungs were also evaluated.
RESULTS： Serum IL-1β levels in SAP-S group were 276.77 ± 44.92 pg/mL at 6 h, 308.99 ± 34.95 pg/mL at 12 h, and 311.60 ± 46.51 pg/mL at 18 h, which were increased significantly （P 〈 0.01, vs HC）. in SAP- ICE-I group, those values were decreased significantly （P 〈 0.01, vs SAP-S）. intrapulmonary expression of Caspase-1, IL-1β and IL-18 mRNA were observed in the HC group, while they were increased significantly in the SAP-S group （P 〈 0.01, vs HC）. The expression of IL-lβ and IL-18 mRNA were decreased significantly in the SAP- ICE-I group （P 〈 0.01, vs SAP-S）, whereas Caspase-1 mRNA expression had no significant difference （P 〉 0.05）. The wet/dry weight ratios of the lungs in the SAP-S group were increased significantly （P 〈 0.05 at 6 h, P 〈 0.01 at 12 h and 18 h, vs HC） and they were decreased significantly in the SAP-ICE-I group （P 〈 0.05, vs SAP-S）.Caspase-1 inhibitors ameliorated the severit     

实验性重症急性胰腺炎肺内IL—1β及IL—18mRNA的表达

目的：观察实验性重症急性胰腺炎（severe acute pancreatitis,SAP）肺内IL－1β及IL－18mRNA的表达，并探讨其与肺损伤的关系，方法：SD大鼠32只，随机分4组：正常对照组、SAP6h组、SAP12h组、SAP18h组。采用5％牛磺胆酸钠（0.1ml/100g）胆胰管内逆行注射诱导大鼠SAP模型。血清淀粉酶采用HITACHI－7150型自动生化分析仪测定；半定量RT－PCR检测肺组织内IL－1β及IL18mRNA的表达，结果：造模后各时间点血清淀粉酶水平显升高，12h达到高峰，与正常对照组相比，均具有显性差异（P＜0．01）。正常肺组织内可见IL－1β及IL－18mRNA表达；SAP各组肺组织内IL－1β及IL－18mRNA的表达明显增强，与正常对照组比较均有显性差异（P＜0．01），结论：除TNF-α外，肺内生成过多的IL－1β及IL－8在SAP并发急性肺损伤（acute lung injury,ALI）及急性呼吸窘迫综合征（acute respiratory distress sysdrome,ARDS)进程中可能发挥重要的作用。     

Effects of large dose of dexamethasone on inflammatory mediators and pancreatic cell apoptosis of rats with severe acute pancreatitis

AIM： To investigate the influence of high dose of dexamethasone on inflammatory mediators and apoptosis of rats with severe acute pancreatitis （SAP）.
METHODS： SAP rats were randomly assigned to the model group and treatment group while the normal rats were assigned to the sham operation group. The mortality, ascite volumes, ascites/body weight ratio and pancreas pathological changes of all rats were observed at 3, 6 and 12 h after operation. Their contents of amylase and endotoxin in plasma and contents of tumor necrosis factor （TNF-α）, phospholipase A2 （PLA2） and IL-6 in serum were also determined. The microarray sections of their pancreatic tissues were prepared, terminal transferase dUTP nick end labeling （TUNEL） staining was performed and apoptotic indexes were calculated.
RESULTS： There was no marked difference between treatment group and model group in survival. The contents of amylase and endotoxin in plasma and contents of TNF-α, PLA2 and IL-6 in serum, ascite volumes, ascites/body weight ratio and pancreas pathological scores were all lower in treatment group than in model group to different extents at different time points [P 〈 0.05, 58.3 （26.4） ng/L vs 77.535 （42.157） ng/L in TNF-α content, 8.00 （2.00） points vs 9.00 （2.00） points in pathological score of pancreas respectively; P 〈 0.01, 0.042 （0.018） EU/mL vs 0.056 （0.0195） EU/mL in endotoxin content, 7791 （1863） U/L vs 9195 （1298） U/L in plasma amylase content, 1.53 （0.79） vs 2.38 （1.10） in ascites/body weight ratio, 8.00 （1.00） points vs 11.00 （1.50） points in pathological score of pancreas; P 〈 0.001, 3.36 （1.56） ng/L vs 5.65 （1.08） ng/L in IL-6 content, 4.50 （2.00） vs 7.20 （2.00）, 4.20 （1.60） vs 6.40 （2.30）, 3.40 （2.70） vs 7.90 （1.70） in ascite volumes, respectively]. The apoptotic indexes of pancreas head and pancreas tail were all higher in treatment group than in model group at 6 h [P 〈 0.01, 0.00 （2.00）% vs 0.00 （0.00）%,     

重症急性胰腺炎大鼠肺组织中LIF的表达变化及意义

目的:观察重症急性胰腺炎(SAP)大鼠白血病抑制因子(LIF)在肺组织中表达的时相变化, 探讨LIF在SAP病程及肺损伤中的意义．方法:36只♂SD大鼠随机分为正常对照组(N 组,n=6)、假手术组(Sham组,n=6)和重症急性胰腺炎组(SAP组,n=24)．采用胰管逆行灌注50 g/L牛磺胆酸钠的方法复制大鼠SAP模型．用RT-PCR法检测肺组织中LIF mRNA的表达水平,免疫组织化学方法检测NLIF在肺组织中的表达变化．结果:SAP组3 h后肺组织LIF mRNA的表达量明显高于对照组和假手术组(灰度值:1．018± 0．065 vs 1．451±0．067,1．322±0．072,P<0,05), 并且6,12,24 h持续升高(0．853±0．058,0．635 ±0．064,0．582±0．089)(P<0．01)．同样,SAP组 LIF蛋白表达在3和6 h后明显高于对照组和假手术(127．36±2．76,122．53±2．43 vs 159．46 ±2．78,156．35±3．12,P<0．05),并且12,24 h后也维持在很高的水平(109．37±2．87,102．42± 2．27)．结论:LIF作为促炎症因子参与了SAP肺组织的炎症反应．     

Effect of IL-4 on altered expression of complement activation regulators in rat pancreatic cells during severe acute pancreatitis

AIM: To investigate the effect of IL-4 on the altered expression of complement activation regulators in pancreas and pancreatic necrosis during experimental severe acute pancreatitis (SAP). METHODS: SAP model of rats was established by retrograde injection of 5% sodium taurocholate (1 mL/kg) into the pancreatic duct. We immunohistochemically assayed the expression of three complement activation regulators: decay accelerating factor (DAF; CD55), 20 ku homologous restriction factor (HRF20; CD59) and membrane cofactor protein (MCP; CD46), in the pancreatic acinar cells of rats at 0, 3, 6, 12, and 24 h after the induction of SAP model. Meanwhile the levels of amylase and lipase were determined, and morphological examination was performed. Then, 61 rats were randomly divided into three groups. Group A (n = 21) received no treatment after the SAP model was established; group B (n = 20) was given IL-4 (8 μg/animal) intraperitoneally 0,5 h before the SAP model was established; group C (n = 20) was given IL-4 (8 μg/animal) intraperitoneally 0.5 h after the SAP model was established. Plasma amylase and lipase, extent of pancreatic necrosis and expression of complement activation regulators were investigated 6 h after the induction of SAP model. RESULTS: Three complement activation regulators were all expressed in pancreatic acinar cells. MCP was not found on the basolateral surface as reported. Contrary to the gradually increasing plasma level of amylase and lipase, expression of complement activation regulators decreased after SAP model was set up. At the same time, the severity of pancreatic necrosis was enhanced. A strong negative correlation was found between the ex- pression of MCP, DAF, CD59 in pancreatic acinar cells and the severity of pancreatic necrosis (r=-0.748, -0.827, -0.723; P＜0.01). In the second series of experiments, no matter when the treatment of IL-4 was given (before or after the induction of SAP model), the serum level of amylase or lipase was decreased and the extent of pancreatic necrosis was ameliorated significantly. Compared to SAP control group, the expression of DAF and CD59 in pancreas was reinforced when IL-4 was given before the induction of SAP model (P＜0.01, P＜0.05), but the expression of MCP was not influenced (P＞0.05). The expression of DAF was enhanced, when IL-4 was given after the induction of SAP model (P＜0.05), but the expression of CD59 and MCP did not change (P＞0.05). CONCLUSION: Complement activation regulators may participate in the pathogenesis of pancreatic inflammation. Downregulation of complement activation regulators expression may be one of the causes of pancreatic necrosis. IL-4 treatment may control SAP aggravation by enhancing expression of DAF and CD59 in pancreas and decreasing pancreatic necrosis. Moreover, DAF and CD59 may play an important role in the regulation of complement activation regulators during SAP.     

Effects of emodin and baicalein on rats with severe acute pancreatitis

AIM: To investigate the therapeutic effects of emodin in combination with baicalein on severe acute pancreatitis (SAP) rats and to explore the mechanism of SAP. METHODS: A total of 112 SAP rats induced by retrograde injection of 5% sodium taurocholate into the biliary-pancreatic duct, randomly assigned to a untreated group and three treated groups emodin group, combined emodin and baicalein group, and sandostatin group. Meanwhile, another 28 other rats were selected as sham operation (SO) group. There were 28 rats in each group, 8 rats were in 3 and 6 h groups respectively, and 12 rats in 12 h group. At each time-points, survival rates,ascites volumes, pathological lesion scores of pancreas tissues,serum amylase, tumor necrosis factor-α and IL-6 levels were determined as the indexes of therapeutic effects. RESULTS: The survival rate at 12 h was significantly higher in three treated groups than in untreated group.The ascites volume at 12 h was remarkably less in combined and sandostatin groups than in emodin group,but there was no difference between combined group and sandostatin group (P>0.05). Serum amylase levels at all time-points were significantly lower in three treated groups than in untreated group. However, they had no difference among treated groups (P>0.05).Serum TNF-α were lower in three treated groups than in untreated group at all time points. Among the three treated groups, at 6 h, the TNF-α levels of combination and sandostatin groups were lower than those of emodin group. These was no difference between combined and sandostantin. Serum IL-6 concentration at 3 h were lower in combined and sandostatin groups than in untreated group, but at 6 and 12 h they were lower in all treated groups than in untreated group and the combined and sandostatin groups and in emodin group, no difference was found between combined and sandostatin groups at all time-points (P>0.05). The pathological scores of pancreas at all time points were significantly lower in three treated groups than in the untreated group, and at 6, 12 h, the scores of combined and sandostatin groups were lower than in emodin group. There was no difference between combined and sandostatin groups (P>0.05). CONCLUSION: Combination of emodin with baicalein has significant therapeutic effects on SAP rats.