重症胰腺炎二十碳烯酸类的异常代谢与大黄素、生长抑素的作用

重症胰腺炎(AHNP)胰组织出血、坏死被认为与二十碳烯酸类的异常代谢有关。在牛磺胆酸钠诱发大鼠AHNP模型,测定前列腺素E_1(PGE_2)、6-酮-前列腺素F_2(6-keto-PGF_2),血栓烷B_2(TXB_2)等变化,并以大黄素、生长抑素进行药物干预,以了解AHNP时二十碳烯酸类的异常代谢和上述药物的作用,结果显示,重症胰腺炎时血浆TXB_2显著增高,发病6小时达假手术组的4.5倍,而6-keto-PGF或PGE的测定值则呈降低趋势。应用大黄素或生长抑素后,TXB_2测定值显著降低,生长抑素组TXB_2测定值较之于大黄素组降低更为显著:6-keto-PGF_1和PGE_2则呈上升趋势。给药两组12小时生存率显著高于非治疗组:病理组织学评分及电镜超微结构观察示给药两组腺细胞坏死等病理损害减轻。作者认为,大黄素和生长抑素对AHNP时TXB_2等异常代谢有明显调整作用,与此相关的改善微循环和细胞保护机制可能是两药治疗AHNP的重要药理基础:联合应用大黄素与生长抑素可能会有协同作用。     

重症胰腺炎二十碳烯酸的异常代谢与大黄素,施他宁的作用

目的：探讨重症胰腺炎（AHNP）胰组织出血、坏死与二十碳烯酸类的异常代谢关系。方法：以牛黄胆酸钠诱发大鼠AHNP模型，测定前列腺素E2（PGE2）、6-酮-前列腺素F1a（6－keto－PGE1a）、血栓烷B2（TXB2）等变化，并以大黄素、施他宁药物干预，以了解AHNP时二十碳烯酸类的异常代谢和上述药物的作用。结果：重症胰腺炎时血浆TXB2显著增高．发病6小时达假手术组的4．5倍，而6－keto－PGF1a或PGE2的测定值则呈降低趋势．应用大黄素或施他宁后，TXB2测定值显著降低，施他宁组TXB2测定值较之于大黄素组降低更为显著；6－keto－PGE1a和PGE2则呈上升趋势．给药两组12小时生存率高于非治疗组；给药两组胰腺细胞坏死等病理损害减轻．结论：大黄素和施他宁对AHNP时TXB2等异常代谢有明显调整作用，与此相关的改善微循环和细胞保护机制可能是两药治疗AHNP的重要药理基础；联合应用大黄素与施他宁可能会有协同作用．     

大黄素诱导急性胰腺炎胰腺细胞凋亡机制的实验研究

目的从凋亡信号传导的角度探讨中药大黄素治疗大鼠急性胰腺炎的分子生物学机制.方法将44只雄性Wistar大鼠随机分为正常组、非治疗组、大黄素组.以腹腔注射雨蛙肽的方法诱导大鼠急性胰腺炎模型,并于大黄素治疗后6、24、48、72、96小时处死大鼠.应用HE染色比较胰腺组织病理学改变,应用Tunel法检测胰腺细胞凋亡指数,应用RT-PCR技术检测治疗前后凋亡调控基因Bak 和Bax mRNA表达.结果大黄素干预治疗急性胰腺炎后96小时淀粉酶值显著低于未治疗组,胰腺细胞凋亡指数显著高于未治疗组,凋亡调控基因Bak mRNA 的表达与未治疗组之间无显著性差异,而Bax mRNA的表达显著高于未治疗组.结论大黄素治疗实验性急性胰腺炎的机制可能与干预凋亡调控基因有关,诱导凋亡调控基因Bax表达增强可能是干预凋亡信号传导的重要机制,而与Bak 基因表达无关.     

益活清胰汤与葡激酶在大鼠重症急性胰腺炎治疗中的协同作用

[目的]研究葡激酶(r-Sak)和益活清胰汤对大鼠重症急性胰腺炎(SAP)的治疗作用及2药合用的协同作用.[方法]162只SD大鼠随机分为假手术(A)组(n=18)、造模(B)组、益活清胰汤治疗(C)组、r-Sak治疗(D)组及益活清胰汤合用r-Sak治疗(E)组(均n=36).每组随机选9只用于测定18 h存活情况,SAP造模术后6、12、18h各取9只测定胰腺血流量,计算腹水量,测定血清淀粉酶(AMY)、脂肪酶(LPO),并在光镜下观察胰腺病理变化.[结果]A、B、C、D和E组大鼠18 h存活数分别为9、2、6、7、8只.A、C、D、E 4组SAP术后6、12、18 h AMY、LPO、腹水均较B组明显降低,C组较D组低,E组较C、D组低(均P＜0.05).术后各时点B组胰组织血流量呈逐渐下降趋势,B、C、D、E组较A组显著下降(P＜0.05).C、D、E 3组各时点胰组织血流量降低值＜B组,D组＜C组,E组＜C、D组(均P＜0.05).C、D、E组胰腺的病理损伤程度较B组减轻.[结论]r-Sak及益活清胰汤均对大鼠SAP具有治疗作用,且2药具有协同作用.     

前列地尔联合胰激肽原酶治疗早期糖尿病足的疗效观察

目的 探究前列地尔联合注射用胰激肽原酶治疗早期糖尿病足的临床疗效.方法 120例早期糖尿病足患者按照随机数字表法分成3组,每组40例.A组给予前列地尔10 μg+生理盐水20 ml静脉推注,B组给予注射用水1.5 ml+注射用胰激肽原酶40 IU肌肉注射,C组予前列地尔10 μg和胰激肽原酶40 IU联合应用,3组治疗均为1次/d,连续给药4周后比较3组的临床疗效并记录3组患者治疗前、后踝肱指数及足背动脉流速数据.结果 治疗后C组总有效率(95％)显著高于A组(77.5％)和B组(75％)(x2=6.580,P＜0.05),且踝肱指数和足背动脉流速亦高于A组和B组(x2=24.59,95.99,P均＜0.05).结论 前列地尔联合胰激肽原酶是治疗早期糖尿病足较为理想的配伍方案.     

丙谷胺对急性胰腺炎大鼠的治疗作用

观察CCK受体拮抗剂丙谷胺对急性胰腺炎(AP)大鼠治疗作用。应用胰胆管内注射5％牛磺胆酸钠溶液诱发大鼠急性胰腺炎模型,术后腹腔内注射丙谷胺溶液(剂量400mg/kg);观察术后6h各组腹水量、胰重、血清脂肪酶活性和病理变化,计算大鼠24h内死亡率。丙谷胺治疗组鼠腹水量、胰重、脂肪酶活性分别为2.04±0.39(g)、1.57±0.38(g)、577.97±8.38(U),均显著低于非治疗组(9.34±2.04、2.04±0.39、715.38±44.76),P<0.05;鼠死亡率由非治疗组的100％降至40％;病理损害程度减轻。丙谷胺对牛磺胆酸钠诱发的大鼠急性胰腺炎有一定治疗作用。     

大黄素诱导急性胰腺炎胰腺细胞凋亡机制的实验研究

目的 从凋亡信号传导的角度探讨中药大黄素治疗大鼠急性胰腺炎的分子生物学机制。方法 将44只雄性Wistar大鼠随机分为正常组，非治疗组，大黄素组，以腹腔注射雨蛙肽物方法诱导大鼠急性胰腺炎模型。并于大黄素治疗后6，24，48，72，96小时处死大鼠。应用HE染色比较胰腺组织病理学改变，应用Tunel法检测胰腺细胞凋亡指数，应用RT-PCR技术检测治疗前后凋亡调控基因Bak和BaxmRNA表达。结果 大黄素干预治疗急性胰腺炎后96小时淀粉酶值显低于未治疗组，胰腺细胞凋亡指数显高于未治疗组，凋亡调控基因BakmRNA的表达与未治疗组之间无显性差异。而BaxmRNA的表达显高于未治疗组。结论 大黄素治疗实验性急性胰腺炎的机制可能与干预凋亡调控基因有关。诱导凋亡调控基因Bax表达增强可能是干预凋亡信号传导的重要机制，而与Bak基因表达无关。     

急性胰腺炎时胰腺诱生型一氧化氮合酶及瘦素与肠壁通透性的关系及大黄素对其的影响

目的探讨大黄素在急性胰腺炎（AP）时对胰腺诱生型一氧化氮合酶（iNOS）和血清瘦素表达,以及对肠壁通透性的影响及作用机制。方法60只成年SD大鼠随机分为AP组（n=20）,假手术组（n=20）,和大黄素组（n=20）。检测血清淀粉酶活性、血清瘦素含量、胰腺组织中iNOS及NO含量、肠黏膜通透性（以血液与肠内125I-清蛋白累积指数表示）,并对胰腺和回肠进行病理学检查。结果AP组和大黄素组血清淀粉酶活性、瘦素含量、胰腺组织内的NO和iNOS水平及125I-清蛋白累积指数均显著高于假手术组（P〈0．05）;与AP组比较,大黄素组血清淀粉酶活性、胰腺组织内的NO、iNOS水平及125I-清蛋白累积指数均显著下降（P〈0．05）,血中瘦素含量明显升高（P〈0．05）,同时胰腺及回肠病理损害明显减轻。结论AP肠壁通透性增加的原因之一可能与AP时胰腺iNOS的过度表达产生过多NO有关,大黄素可降低胰腺iNOS的表达,该作用可能与升高血清瘦素水平有关,大黄素对降低AP时肠壁通透性的增加有一定预防和治疗作用。     

急性出血坏死性胰腺炎64例

目的观察近8a间治疗急性出血坏死性胰腺炎（AHNP）64例（其中非手术综合治疗9例，先行非手术治疗后再手术24例，早期手术治疗31例）的治疗效果．方法非手术综合治疗为尽早行快速扩容，应用血管活性药物，抑制胰腺分泌（善得定效果较好），有效的抗生素，营养支持和防治并发症的发生．根据有无感染确定手术时机．手术方式根据病情和术中所见，分别采用胰床灌洗引流，坏死组织清除，规则性胰腺切除和肢肿切开引流．结果非手术综合治疗9例，死亡率11．1％，先行非手术综合治疗后再手术24例，死亡率为12．5％，早期手术治疗31例，死亡率为25．8％．结论对AHNP先行非手术治疗可明显降低死亡率，晚期手术较早期手术可提高其治愈率．积极防治并发症是提高治疗效果的重要一环．     

急性出血坏死性胰腺炎治疗进展

急性出血坏死性胰腺炎 (AHNP)行早期手术治疗往往不能终止胰腺炎的病理进程 ,常促使全身循环及代谢紊乱 ,且增加了术后胰腺感染、腹腔内出血、急性呼吸窘迫综合征(ARDS)、多脏器功能障碍 (MODS)等并发症的发生率及病死率。近年来文献报导 AHNP早期手术治疗者的病死率为5 0 %～ 5 6 %。后期中转手术者病死率为 11.3%～ 5 .6 % ,故目前主张早期 AHNP应以积极、有效、综合的非手术治疗为主。1　非手术治疗　适用于诊断明确 ,无胰腺及胰周感染 ,无明显胆道梗阻的患者。1.1　早期 (3～ 5日 )1.1.1　抗休克、补充血容量、纠正水电解质紊乱…     

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.     

Experimental research on production and uptake sites of TNFalpha in rats with acute hemorrhagic necrotic pancreatitis

AIM:To determine the site of production and uptake of tumor necrotic factor alpha (TNFalpha),and evaluate the relationship between serum TNFalphaand pla-sma endotoxin (ET) in rats with acute hemorrhagic necrotic pancreatitis (AHNP).METHODS:Sprague Dawley rats were divided into AHNP group and control group (n = 12). AHNP model was induced by retrograde injection of 5% sodium taurocholate via pancreatic bile duct. The blood samples were obtained through portal vein 2 and 6 hours after the operation.RESULTS:The contents of TNFalphain portal vein were increased rapidly in the development of AHNP. They were lower in hepatic vein (280.59 plus minus 20.02) and femoral artery (310.82 plus minus 7.97) than in portal vein (354.91 plus minus 25.50) (P < 0.05), and higher in femoral artery than in hepatic vein 6 hours after the operation (P <0.05). TNFalphalevel in plasma was increased significantly when ET level in portal vein showed no increase. CONCLUSION: Pancreas, spleen, liver, intestinal tract and lung are the main organs to produce TNFalpha, and liver is also an important site for TNFalphauptake in the development of AHNP. Plasma endotoxin is not a trigger for TNFalpharelease in rats with AHNP.     

Role of nitric oxide in Toil-like receptor 2 and 4 mRNA expression in liver of acute hemorrhagic necrotizing pancreatitis rats

AIM: To investigate the role of nitric oxide (NO) in Tolllike receptor 2 (TLR2)/4mRNA expression in livers of acute hemorrhagic necrotizing pancreatitis (AHNP) rats.METHODS: One hundred and ten SD male rats were randomly divided into sham-operated group (n= 10),AHNP group (n = 30), chloroquine (CQ)-treated group(n= 30) and L-Arg-treated group (n =40). TLR2/4mRNA expression in the liver of AHNP rats was measured by RT-PCR.RESULTS: Expression of TLR2/4mRNA could be detected in the liver of AHNP rats in sham-operated group (0.155E-5±0.230E-6 and 0.115E-2±0.545E-4),but was markedly increased at 3 h in AHNP group(0.197E-2±0.114E-3 and 0.175±0.349E-2) peaking at 12 h (0.294E-2±0.998E-4 and 2.673±2.795E-2,P＜0.01). Hepatic injuries were aggravated, TNF-αconcentration in the liver was increased and NO concentration was decreased (P＜ 0.05 or P＜ 0.01).When TLR2/4mRNA expression was inhibited by CQ(3 h: 1.037E-4±3.299E-6 and 0.026±3.462E-3;6 h: 1.884E-4±4.679E-6 and 0.108±6.115E-3; 12 h:2.443E-4±7.714E-6 and 0.348±6.807E-3; P＜ 0.01),hepatic injuries were relieved, NO concentration in the liver was increased and TNF-α concentration was decreased (P＜0.05 or P＜0.01). When rats with AHNP were treated with L-Arg, TLR2/4mRNA expression in the liver could be effectively inhibited (50 mg-T:0.232E-2 ± 0.532E-4 and 0.230 ± 6.883E-3; 100 mg-T:0.210E-2±1.691E-4 and 0.187±0.849E-2; 200 mg-T:0.163E-2±0.404E-4 and 0.107±0.195E-2; 400 mg-T:0.100E-2±0.317E-4 and 0.084±0.552E-2; P＜0.01)and hepatic injuries were relieved. At the same time,NO concentration in the liver was markedly increased and TNF-α concentration was decreased (P＜0.05 or P＜0.01).CONCLUSION: The expression of TLR2/4mRNA is increased and hepatic injuries are aggravated in the liver of AHNP rats. TLR2/4mRNA gene expression in the liver of AHNP rats can be markedly inhibited by NO, leading to the relief of hepatic injuries.     

Role of nitric oxide in Toll-like receptor 2 and 4 mRNA expression in liver of acute hemorrhagic necrotizing pancreatitis rats

AIM:To investigate the role of nitric oxide(NO)in Toll-like receptor 2(TLR2)/4mRNA expression in livers ofacute hemorrhagic necrotizing pancreatitis(AHNP)rats.METHODS:One hundred and ten SD male rats wererandomly divided into sham-operated group(n=10),AHNP group(n=30),chloroquine(CQ)-treated group(n=30)and L-Arg-treated group(n=40).TLR2/4mRNAexpression in the liver of AHNP rats was measured byRT-PCR.RESULTS:Expression of TLR2/4mRNA could bedetected in the liver of AHNP rats in sham-operatedgroup(0.155E-5 0.230E-6 and 0.115E-2±0.545E-4),but was markedly increased at 3 h in AHNP group(0.197E-2±0.114E-3 and 0.175±0.349E-2)peakingat 12 h(0.294E-2±0.998E-4 and 2.673±2.795E-2,P<0.01).Hepatic injuries were aggravated,TNF-αconcentration in the liver was increased and NOconcentration was decreased(P<0.05 or P<0.01).When TLR2/4mRNA expression was inhibited by CQ(3h:1.037E-4±3.299E-6 and 0.026±3.462E-3;6 h:1.884E-4±4.679E-6 and 0.108±6.115E-3;12 h:2.443E-4±7.714E-6 and 0.348±6.807E-3;P<0.01),hepatic injuries were relieved,NO concentration inthe liver was increased and TNF-α concentration wasdecreased(P<0.05 or P<0.01).When rats with AHNP were treated with L-Arg,TLR2/4mRNA expressionin the liver could be effectively inhibited(50 mg-T:0.232E-2±0.532E-4 and 0.230±6.883E-3;100 mg-T:0.210E-2±1.691E-4 and 0.187±0.849E-2;200 mg-T:0.163E-2±0.404E-4 and 0.107±0.195E-2;400 mg-T:0.100E-2±0.317E-4 and 0.084±0.552E-2;P<0.01)and hepatic injuries were relieved.At the same time,NO concentration in the liver was markedly increasedand TNF-α concentration was decreased(P<0.05 orP<0.01).CONCLUSION:The expression of TLR2/4mRNA isincreased and hepatic injuries are aggravated in the liverof AHNP rats.TLR2/4mRNA gene expression in the liverof AHNP rats can be markedly inhibited by NO,leadingto the relief of hepatic injuries.     

纳屈酮治疗大鼠急性出血坏死性胰腺炎内毒素血 症的效果

目的探讨纳屈酮治疗大鼠急性出血坏死性胰腺炎内毒素血症的效果．方法应用５０ｇ／Ｌ牛磺胆酸钠逆行胰胆管注射诱发大鼠急性出血坏死性胰腺炎（ＡＨＮＰ）模型,观察对照组、ＡＨＮＰ组及纳屈酮（ＮＴＸ）治疗组６,１２,２４ｈ大鼠血浆淀粉酶、内毒素（ＥＴ）及胰腺组织光镜和电镜下病理改变,并统计３组大鼠４８ｈ存活率结果ＡＨＮＰ组较对照组：于６,１２,２４ｈ时点血浆淀粉酶（２４０７±５１２,２８７２±４１３,３４１５±５９４,ｎｍｏｌ／ｓ）、ＥＴ（４５±２３,９３±１２,１６０±３５,ＥＵ／Ｌ）升高;ＮＴＸ组较ＡＨＮＰ组：血浆淀粉酶（１５３２±５６７,１８９５±５９４,２４８３±８１８,ｎｍｏｌ／ｓ）、ＥＴ（２８±３,２１±８,６９±９,ＥＵ／Ｌ）下降;而且光镜及电镜下,ＮＴＸ组胰腺腺胞及间质病理损害减轻．结论ＮＴＸ可通过降低ＡＨＮＰ大鼠血浆ＥＴ,而改善胰腺病理损害,降低其死亡率     

Experimental study of therapeutic efficacy of Baicalin in rats with severe acute pancreatitis

AIM： To observe the therapeutic efficacy of Baicalin in rats with severe acute pancreatitis （SAP） and explore its therapeutic mechanisms. METHODS： The SAP rat models were randomly divided into the model control group, Baicalin treatment group, octreotide treatment group and sham operation group. All groups were randomly subdivided into 3 h, 6 h and 12 h groups with 15 rats in each group. The survival, ascites volume and pathological changes of pancreas in all rats were observed at different time points after operation. The plasma amylase content and serum TNF-α, IL-6, malonaldehyde （MDA） and PLA2 contents were also determined. RESULTS： The survival was not obviously different between the treated groups, and was significantly higher in treated groups at 12 h compared to the model control group （P 〈 0.05, 15 vs 10）. The ascites/body weight ratio at 3 h and 6 h was significantly lower in Baicalin treatment group compared to the model control group and octreotide treatment group （P 〈 0.05, 1.00 vs 2.02 and 1.43 and P 〈 0.001, 2.29 （1.21） vs 2.70 （0.80） and 2.08 （2.21）, respectively）. The contents of amylase, TNF-α, IL-6, MDA and PLA2 were significantly lower in the treated groups than in the model control group （P 〈 0.05, 4342 vs 5303, 5058 vs 6272 in amylase, P 〈 0.01, 21.90 vs 36.30, 23.80 vs 39.70, 36 vs 54.35 in MDA and 56.25 vs 76.10 in PIA2, or P 〈 0.001, 65.10 and 47.60 vs 92.15 in TNF-α, 3.03 vs 5.44, 2.88 vs 6.82, 2.83 vs 5.36 in IL-6, respectively）. The pathological scores of pancreas in the treated groups were significantly lower than that in the model control group （P 〈 0.05, 9.00 vs 10.05, 6.00 vs 9.00, 8.00 vs 10.05）, but no marked difference was found between the treated groups. CONCLUSION： The Baicalin injection has significant therapeutic effects on SAP rats, its effects are similar to those of octreotide. The Baicalin injection is also cheap and has a big application range, quite hopefully to be used in clinical treatment of SAP.     

Protection effect of Emodin pretreatment on intestinal I-RI damage of intestinal mucosa in ratsa

Objective:To linvestigate the protective effect and mechanism of emodin pretreatment on intestinal mucosa of rats with intestinal ischemia-reperfusion injury.Methods:A total of 50SD rats were randomly divided into control group,model group,emodin groups of low,medium and high dose,with 10 in each group.Ischemia-reperfusion injury(I-RI)mode was established by using noninvasive clamp on superior mesentericartery(SMA).Control group and model group were pretreated with 0.5%sodium carboxymethyl cellulose solution lavage 2 h before operation,emodin groups of low,medium and high dose were given emodin lavage with 20,40,60 mg/kg pretreatment,femoral venous blood before the lavage pretreatment(TO)and 1 h ischemia(Tl),and inferior vena venous blood after 1 h of reperfusion(T2)were extracted from each group of rats for detection of serun level of intestinal fatty acid binding protein(I-FABP),tumor necrosis factor(TNF-α),endotoxin,interleukin 6(IL-6),and die content of diamine oxidase(DAO);Mter model establishment,the rats were sacrificed,intestine homogenate was prepared by using blind intestinal tissue to detect intestinal tissue myeloperoxidase(MPO],malondialdehyde(MDA)and superoxide dismutase(SOD)levels.And upper small intestine tissue was retrieved,followed by fixation and conventional HE staining to observe intestinal tissue morphology under light microscopy.Results:In emodin groups of low,medium and high dose at T1 and T2,I-FABP,TNF-α,endotoxin.IL,-6 and DAO level were significandy lower than that of model group(P0.05);in emodin group of low,medium and high dose,MPO and MDA content in intestinal tissue homogenate was significantly lower than that in model group(P0.05),SOD level was significantly higher than that of model group(P0.05).Intestinal damage of emodin low,medium and high dose groups were significandy lighter than model group.Conclusions:Emodin pretreatment has certain protective effect on intestinal mucosa in ischemia reperfusion injury.     

Role of Kupffer cells in acute hemorrhagic necrotizing pancreatitis-associated lung injury of rats

AIM:To investigate the role of Kupffer cells(KCs)inacute hemorrhagic necrotizing pancreatitis-associatedlung injury(AHNP-LI).METHODS:Forty-two rats were allocated to fourgroups[sham operation,AHNP model,gadoliniumchloride(GdCl_3)pretreatment,GdCl_3 control].In GdCl_3pretreatment group,GdCl_3 was administered by caudalvein injection 24 h before the AHNP model induction.Blood from the iliac artery,alveolar macrophages andtissues from the pancreas and lung,were collected insix animals per group 3 and 6 h after acute pancreatitisinduction.TNF-α,IL-1 of serum,myeloperoxidase(MPO)of lung tissue,NF-kB activation of alveolar macrophageswere detected.Serum AST and ALT in sham operationgroup and GdCl_3 control group were tested.In addition,histopathological changes of the pancreas and lung wereobserved under light microscope.RESULTS:MPO of lung tissue and TNF-α,IL-1 levelsof serum were all reduced significantly in GdCl_3pretreatment group compared to those in AHNP group(P<0.01).NF-kB activation of alveolar macrophageswas also attenuated significantly in GdCl_3 pretreatmentgroup compared to that in AHNP group(P<0.01).Thepathological injury of the lung was ameliorated obviouslyin GdCl_3 pretreatment group compared to that in AHNPgroup.Nevertheless,the serum amylase level did notreduce and injury of the pancreas was not prevented inGdCl_3 pretreatment group.CONCLUSION:Pulmonary injury induced by AHNPis mediated by KC activation and AHNP-LI can be significantly ameliorated by pretreatment with GdCl_3 andKCs play a vital role in AHNP-LI.