复合益生菌制剂对急性坏死性胰腺炎大鼠的保护作用

背景:肠道细菌易位是重症急性胰腺炎(SAP)时胰腺坏死感染的主要来源,因此保护肠黏膜屏障对SAP的治疗具有重要意义。目的:探讨复合益生菌制剂对急性坏死性胰腺炎(ANP)大鼠肠黏膜屏障和胰腺损伤的保护作用。方法:50只SPF级大鼠随机分为假手术组(n=10)、ANP模型组(n=20)和益生菌干预组(n=20)。采用胰腺被膜下均匀注射牛磺胆酸钠制备ANP模型,干预组术前30 min以双歧杆菌四联活菌片溶液灌胃。术后6 h采集标本,检测血淀粉酶、二胺氧化酶(DAO)、TNF-α水平,观察胰腺组织病理学表现和末端回肠组织超微结构。结果:ANP模型组血淀粉酶、DAO、TNF-α水平和胰腺组织学评分均显著高于假手术组(P<0.05),益生菌干预组各项指标均较ANP模型组有所改善(P<0.05)。假手术组末端回肠黏膜结构完整;ANP模型组回肠黏膜上皮细胞微绒毛萎缩、排列稀疏,细胞间连接松弛;益生菌干预组微绒毛稍稀疏,细胞间连接紧密度较ANP模型组增高。结论:复合益生菌制剂对ANP大鼠具有保护作用,不仅能减轻肠黏膜损伤,保护肠黏膜屏障功能,还能减轻胰腺局部损伤和全身性炎症反应。     

TGF-β1对大鼠肠黏膜缺血再灌注损伤的保护作用

选择30只SD大鼠,随机分成三组,假手术组(A组)、对照组(B组)和实验组(C组)各10只.B组夹闭肠系膜上动脉(SMA)60 min,再灌注120 min,缺血前10 min经SMA注入生理盐水0.5 ml.C组以TGF-β1代替生理盐水.A组单纯分离肠SMA,不做阻断.采用HE染色及chiu评分法判断小肠黏膜形态学损伤程度,检测门静脉血浆中D-乳酸水平及大肠杆菌易位情况.发现B组与A组相比,肠黏膜组织损伤严重,chiu评分显著升高,门静脉血D-乳酸水平和大肠杆菌易位率显著升高;C组与B组相比,肠黏膜组织损伤较轻,chiu评分显著降低,门静脉血D-乳酸水平和大肠杆菌易位率显著降低;门静脉血浆D-乳酸水平与肠黏膜损伤病理评分有明显的正相关性.认为肠缺血再灌注可引起肠黏膜屏障形态和功能的损伤,使细菌及其代谢产物易位增加;TGF-β1可以显著减轻损伤程度;血D-乳酸水平可以间接反映肠黏膜屏障的通透性,进而评价肠黏膜屏障的损伤程度.     

急性肝衰竭大鼠血浆D-乳酸、二胺氧化酶和内毒素的变化及其意义

目的探讨血浆D-乳酸、二胺氧化酶（DAO）和内毒素水平在急性肝衰竭大鼠的变化及其意义。方法选取健康雌性SD大鼠40只,随机分为对照组（15只）和实验组（25只）,采用分光光度法检测血浆中D-乳酸、DAO和内毒素水平,分别用HE染色及电镜观察大鼠回肠的组织形态和超微结构。结果 实验组大鼠血浆D-乳酸、DAO和内毒素水平均明显高于对照组（P〈0.05）;实验组大鼠回肠黏膜明显萎缩,部分绒毛断裂、脱落。结论急性肝衰竭大鼠肠黏膜屏障出现明显障碍。     

不同部位及性质胆石症患者肠黏膜通透性改变的临床分析

目的研究不同部位及性质胆石症患者肠黏膜通透性的改变,并探讨肠屏障功能在胆石形成中的作用。方法选择2011年3月-2013年3月收治的108例胆结石患者,健康对照者20例,按结石部位不同分为4组:健康对照组(A1组)、胆囊结石组(B1组)、胆管结石组(C1组)、胆囊结石合并胆管结石组(D1组);所有入选患者全部行手术治疗,收集胆石进行化学分析,根据结石不同性质分为健康对照组(A2组)、胆固醇结石(B2组)、胆色素结石(C2组)、混合性结石组(D2组)。分别用分光光度法测定各组血浆及回肠末端黏膜组织中D-乳酸浓度、二胺氧化酶(DAO)活性,组间比较采用方差分析和LSD-t检验。结果 (1)不同部位结石患者(A1、B1、C1、D1 4组)之间血浆及肠黏膜组织D-乳酸及DAO活性水平相比较差异无统计学意义(P0.05);(2)术后对胆石进行化学分析,胆固醇结石40例(37.04%)、胆色素结石52例(48.15%),混合性结石16例(14.81%);与A2组及B2组比较,C2组血浆及肠黏膜组织D-乳酸及DAO活性差异有统计学意义(P0.05),与D2组比较,差异无统计学意义(P0.05);B2组与A2、D2组比较,差异无统计学意义(P0.05)。结论胆色素结石患者存在肠黏膜通透性的改变,胆色素结石形成与肠屏障功能损伤有一定的关系,肠屏障功能损伤可能在促进胆色素结石的形成中发挥一定的作用。     

清胰Ⅱ号对重症急性胰腺炎大鼠胰腺及肠组织中MCP-1表达的影响

目的探究清胰Ⅱ号对重症急性胰腺炎(SAP)大鼠胰腺及肠组织中单核细胞趋化蛋白(MCP)-1表达及细胞凋亡的影响。方法将36只大鼠随机分为对照组、模型组、模型+清胰Ⅱ号组,每组12只,对照组正常饲养,其余各组采用胆胰管逆行注射牛磺胆酸钠0.1 ml/100 g的方法建立SAP模型,模型+清胰Ⅱ号组造模后给予清胰Ⅱ号10 ml/kg。造模后12、24 h随机选取7只大鼠采样,比较各组腹水量、胰腺和回肠病理学变化,判断造模是否成功。酶联免疫吸附测定法(ELISA)检测血清MCP-1、白细胞介素(IL)-10、二胺氧化酶(DAO)、血清淀粉酶(AMY)活力。实时定量PCR(qRT-PCR)检测胰腺及肠组织中MCP-1 mRNA表达情况。流式细胞术检测胰腺细胞的凋亡率。结果模型组大鼠腹内血性腹水及胰腺坏死显著高于对照组,表明造模成功。造模后12、24 h,模型+清胰Ⅱ号组大鼠血性腹水、血清MCP-1、IL-10、DAO、AMY活力及胰腺、回肠组织中MCP-1mRNA的表达显著低于模型组(P<0.05);与对照组相比,模型组及模型+清胰Ⅱ号组胰腺细胞的凋亡率显著增加,且模型+清胰Ⅱ号组SAP显著高于模型组(P<0.05)。结论清胰Ⅱ号可下调炎症因子MCP-1、IL-10表达,降低DAO、AMY活力,促进胰腺细胞凋亡,对重症急性胰腺炎大鼠胰腺及肠组织具有良好的修复和保护作用。     

谷氨酰胺对急性胰腺炎大鼠肠黏膜胰岛素样生长因子表达及肠黏膜屏障的影响

目的 观察急性坏死性胰腺炎（ANP）时肠黏膜屏障的损伤情况,以及谷氨酰胺（Gln）和胰岛素样生长因子（IGF）对肠黏膜屏障的保护作用.方法 成功诱导ANP模型雄性Wistar大鼠48只,随机分为ANP组和Gln组各24只,另取假手术组24只作为对照.Gln组每日以Gln灌胃2次,剂量为1.5g/（kg·d）;ANP组和假手术组以同等量的生理盐水灌胃.分别在模型制作术后3、6、24、48 h时间点杀死大鼠,取胰头和末端回肠3～5 cm放入液氮中保存.观察胰腺和肠黏膜组织形态学改变,测定肠黏膜中IGF-1的表达、血清中二氨氧化酶（DAO）活性和内毒素浓度.结果 ANP组大鼠肠黏膜屏障功能严重破坏,肠道通透性明显增加,肠黏膜损伤评分明显增加;血清内毒素浓度、DAO活性明显升高（P均＜0.01）.与ANP组比较,Gln组动物肠黏膜损伤减轻,损伤评分有所下降,血清内毒素水平、DAO活性下降（P均＜0.05）.ANP组IGF-1表达水平明显下降（P ＜0.05）;Gln组明显升高（P＜0.05）,同时肠黏膜屏障功能得到一定的改善.结论 ANP时肠黏膜屏障结构和功能存在严重破坏;Gln能一定程度上减轻肠黏膜屏障损伤并能维护其功能;IGF-1参与Gln对ANP肠黏膜屏障损伤的修复和维持.     

实验性肝损伤大鼠肠道屏障功能障碍研究

目的 观察不同程度肝损伤大鼠血浆及肠道组织内毒素、D-乳酸、二胺氧化酶的动态变化,探讨肝损伤时肠道机械屏障功能的损伤情况.方法 15只大鼠作为正常对照组(A组),15只大鼠作为急性肝损伤组(B组),25只大鼠作为急性肝功能衰竭组(C组),采用分光光度法测定血浆内毒素、D-乳酸、二胺氧化酶,回肠组织内毒素及二胺氧化酶水平的动态变化,HE染色及电镜观察肝组织细胞形态和亚细胞的结构变化.组间比较采用单因素方差分析.结果 B、C组大鼠血浆D-乳酸活性均明显高于A组,分别为(4.32±1.13)mg/L和(11.62±5.44)mg/L对比(0.77±0.25)mg/L,P＜0.05;血浆二胺氧化酶活性先升高后降低,但均明显高于A组,分别为(0.81±0.26)U/ml和(0.62±0.22)U/ml对比(0.47±0.11)U/ml,P＜0.05;回肠二胺氧化酶活性逐渐降低,B、C两组与A组比较,差异均有统计学意义(P＜0.05);B组血浆及肠组织内毒素活性与A组相比差异不明显(P＞0.05);c组则明显高于A、B两组(P＜0.05).HE染色发现C组存在大片肝细胞坏死,回肠黏膜明显萎缩,部分绒毛断裂、脱落或相互融合,上皮细胞变性、坏死、脱落.电镜观察可见肠黏膜微绒毛稀疏脱落,细胞内线粒体肿胀.结论 D-乳酸和二胺氧化酶在肝损伤早期即可以明显升高,是检测肠黏膜屏障功能的敏感指标,内毒素血症是肝损伤加重的重要因素.     

NF-κB、HMGB1在重症急性胰腺炎肠黏膜损伤中的时点表达及其意义

目的:探讨NF-κB、HMGB1在SAP大鼠肠黏膜损伤发生发展过程中的时点表达规律及其意义.方法:将70只SD大鼠随机分为A组(n=40)和S组(n=30),再分别按3、6、12、24、36h时点随机均等分成5个亚组.A组大鼠行逆行胰胆管匀速泵入5%牛磺胆酸钠建立SAP模型,S组大鼠开腹仅翻动十二指肠.两组大鼠均在建模后按时点开腹,门静脉取血检测AMY、DAO浓度,ELISA法和免疫组化法检测小肠黏膜NF-κB和HMGB1的表达.结果:(1)A组大鼠血DAO浓度随时点延迟逐渐增加;(2)肠黏膜NF-κB表达在3h最高,随时点延迟逐渐下降,24h、36h降至正常水平;(3)肠黏膜HMGB1表达6h开始明显升高,且随时点延迟逐渐增高,在24h最高,一直持续到36h仍然保持在较高水平.结论:(1)SAP大鼠早期即出现肠黏膜损伤;(2)SAP肠黏膜早期的损伤可能与小肠组织NF-κB的表达增加有关;(3)HMGB1作为晚期炎症介质可能介导了SAP肠黏膜损伤的发生发展;(4)HMGB1的调控可能受到了NF-κB的调节.     

乌司他丁对急性坏死性胰腺炎大鼠肠黏膜屏障的保护作用

目的 观察乌司他丁干预急性坏死性胰腺炎(ANP)大鼠后血TNF-α、二胺氧化酶(DAO)及肠黏膜组织紧密连接蛋白-1( zonula occludens-1,ZO-1)表达水平的变化,探讨其可能机制.方法 按完全随机法将SD雄性大鼠随机分为假手术组、ANP组及乌司他丁组.采用5％牛磺胆酸钠逆行注入胆胰管的方法制模.制模后6、24h取血检测TNF-α、DAO活性,胰腺及回肠组织常规病理检查,RT-PCR及免疫组化法检测回肠组织ZO-1 mRNA及蛋白的表达.结果 术后6h,ANP组胰腺大片坏死,大量炎细胞浸润;回肠黏膜绒毛上皮坏死、血管出血、炎细胞浸润.乌司他丁组的胰腺及回肠组织损伤较ANP组减轻.假手术组、ANP组、乌司他丁组术后6h的血TNF-α水平分别为(10.83±0.96)、( 181.89±4.93)、(128.23±2.40) ng/L;DAO活性分别为(354.79±3.67)、(117.21±5.58)、(282.98±9.12) U/L;回肠组织ZO-1蛋白表达量分别为(10.00±1.87)、(1.20±0.84)、(5.80±2.86)分;Z(O)-1 mRNA表达量为0.878±0.015、0.466±0.023、0.778±0.033.ANP组血TNF-α水平较假手术组明显升高,DAO活性、回肠组织ZO-1 mRNA及蛋白表达较对照组明显降低(P值均＜0.05);乌司他丁组的血TNF-α水平较ANP组降低,DAO活性、回肠组织ZO-1 mRNA及蛋白表达较ANP组明显升高(P值均＜0.05).结论 乌司他丁可能通过抑制TNF-α的过度释放、提高血浆中DAO活性,从而上调回肠组织中ZO-1 mRNA和蛋白表达,进而保护肠黏膜屏障.     

唐古特大黄多糖组分1对大鼠急性放射性肠损伤的保护作用

目的探讨唐古特大黄多糖组分1(Rheum tanguticum polysaccharides,RTP1)对辐射所致大鼠急性肠黏膜损伤的保护作用。方法 RTP1灌胃给药(剂量200、400、800 mg/kg)7 d后,除正常组大鼠外,其余各组均接受10.0 Gy/只一次性全腹均匀X射线照射1次,3 d后处死动物,观察小肠黏膜病理形态改变,测定肠黏膜屏障功能、小肠组织氧化还原酶活性及血浆内毒素水平。结果RTP1预处理后可以改善肠黏膜损伤,升高SOD活性及GSH含量,降低MDA水平,抑制血浆中DAO、D-乳酸及内毒素水平,与IC组比较,差异具有统计学意义(P0.05)。结论 RTP1通过减轻肠黏膜屏障功能损害,增强抗氧化能力保护辐射所致肠黏膜损伤。     

An experimental study of emodin assisted early enteral nutrition for the treatment of severe acute pancreatitis

BACKGROUND/AIMS: Both emodin and early enteral nutrition (EEN) have been affirmed as effective means to restore the intestinal mucosal function and abate the severity of severe acute pancreatitis (SAP). However, whether a combined strategy applying both is more effective than either one alone is still undetermined. In this study, we investigated the feasibility and efficacy of emodin assisted early enteral nutrition (EAEEN) for the treatment of SAP. METHODOLOGY: Sixty male Wistar rats were randomly divided into four groups (n=15). SAP was induced in all the rats by a retrograde infusion of 5.0% sodium taurocholate into the pancreatic main duct. Rats in group A received no further intervention, group B with emodin alone, group C with early enteral nutrition (EEN) alone, and group D with emodin assisted early enteral nutrition (EAEEN), respectively, all through an enteral nutrition tube incubated after the induction of SAP. 72 hours after SAP induction, all surviving animals were sacrificed to collect blood and tissue samples for the following measurements: serum amylase, tumor necrosis factor-alpha (TNF-alpha), angiotensin II (AngII) and maleic dialdehyde (MDA), intestinal mucosal secretory IgA (SIgA), pancreatic myeloper oxidase (MPO) activity, and the wet-dry weight ratio of pancreatic tissue (pww/dw). The severity of pancreatic destruction was analyzed by pathological grading and scoring. The severity of intestinal mucosal damage was assessed by the wet-dry weight ratio of ileum (iww/dw), plasma D-lactate and plasma endotoxin. RESULTS: The results of every index in group B, C and D were significantly better than those in group A (P<0.05). Compared with group B and C, group D had significantly reduced levels of serum amylase, TNF-alpha, Ang-II and MDA (P<0.05). Group D also had significantly lowered plasma D-lactate and endotoxin, and decreased pancreatic MPO activity (P<0.05). The pww/dw and iww/dw ratios were decreased, while the SIgA level increased in this group, both with statistical significance (P<0.05). Furthermore, group D had significantly better pancreatic pathologic scores over group B and group C (P<0.05). CONCLUSIONS: Our results suggested that EAEEN could obviously abate the severity of experimental SAP in rats. This combined strategy was rational, safe and more effective than either EEN or emodin used alone, and has a broad potential for future clinical application.     

Abdominal paracentesis drainage attenuates intestinal inflammation in rats with severe acute pancreatitis by inhibiting the HMGB1-mediated TLR4 signaling pathway

BACKGROUND Our previous studies confirmed that abdominal paracentesis drainage(APD)attenuates intestinal mucosal injury in rats with severe acute pancreatitis(SAP),and improves administration of enteral nutrition in patients with acute pancreatitis(AP).However,the underlying mechanisms of the beneficial effects of APD remain poorly understood.AIM To evaluate the effect of APD on intestinal inflammation and accompanying apoptosis induced by SAP in rats,and its potential mechanisms.METHODS SAP was induced in male adult Sprague-Dawley rats by 5%sodium taurocholate.Mild AP was induced by intraperitoneal injections of cerulein(20μg/kg body weight,six consecutive injections).Following SAP induction,a drainage tube connected to a vacuum ball was placed into the lower right abdomen of the rats to build APD.Morphological changes,serum inflammatory mediators,serum and ascites high mobility group box protein 1(HMGB1),intestinal barrier function indices,apoptosis and associated proteins,and toll-like receptor 4(TLR4)signaling molecules in intestinal tissue were assessed.RESULTS APD significantly alleviated intestinal mucosal injury induced by SAP,as demonstrated by decreased pathological scores,serum levels of D-lactate,diamine oxidase and endotoxin.APD reduced intestinal inflammation and accompanying apoptosis of mucosal cells,and normalized the expression of apoptosis-associated proteins in intestinal tissues.APD significantly suppressed activation of the intestinal TLR4 signaling pathway mediated by HMGB1,thus exerting protective effects against SAP-associated intestinal injury.CONCLUSION APD improved intestinal barrier function,intestinal inflammatory response and accompanying mucosal cell apoptosis in SAP rats.The beneficial effects are potentially due to inhibition of HMGB1-mediated TLR4 signaling.     

早期肠内营养对急性重症胰腺炎大鼠肠道粘膜屏障的保护作用

目的 探讨早期肠内营养对急性重症胰腺炎大鼠肠道粘膜屏障的保护作用。方法 SD大鼠48只，随机分成6组（n=8)；急性重症胰腺炎全肠外营养1天组（A组），模拟手术全肠外营养1天组（B组），急性重症胰腺炎全肠外营养5天组（C组）和肠内营养5天组（E组），模拟手术全肠外营养5天组（D组）和肠内营养5天组（F组）。采用逆行胰胆管注射3%牛磺胆酸钠溶液制成重症胰腺炎大鼠模型。E组和F组术后先予肠外营养，48h后开始肠内营养，观察大鼠的空肠组织形态学变化及空肠粘膜固有层CD4^ /CD8^ 比值。结果 急性重症胰腺炎大鼠均无死亡，E组和F组大鼠对肠内营养耐受良好，C组的CD4^ /CD8^ 比值明显低于D组。E组的空肠绒毛高度和CD4^ /CD8^ 比值明显高于C组。结论 重症胰腺炎大鼠肠道粘膜屏障功能受损。早期肠内营养可改善重症胰腺炎大鼠的肠道粘膜屏障功能。     

Early prediction of intestinal mucosal barrier function impairment by elevated serum procalcitonin in rats with severe acute pancreatitis

ObjectivesThe aim of this study was to evaluate serum procalcitonin (PCT) levels as a prognostic indicator of intestinal barrier function impairment in rats with severe acute pancreatitis (SAP).MethodsThirty-six male Sprague Dawley rats were randomly grouped into SAP group (injected sodium taurocholate via biliopancreatic duct), Gln group (gavaged with glutamine after modeling), and control group. Blood, pancreatic, and terminal ileum tissues were obtained from the rats after 6 h of modeling. Serum amylase (Amy) levels were determined using an automatic biochemical detector, while endotoxin (ET), diamine oxidase (DAO), and PCT levels were measured by ELISA test. The pathology of pancreatic and small intestine tissues were observed. PCT protein expression in intestinal tissues were detected by immunohistochemistry and western blot.ResultPancreatic and intestinal injuries in Gln group were significantly lower than SAP group. Serum amylase, DAO, and PCT levels in SAP and Gln groups differed greatly and were significantly higher than control group. Immuno-histochemistry and western blot results showed that PCT protein expression levels in small intestine tissues of SAP group were higher than Gln group and control group. Serum PCT levels had a significant correlation with serum endotoxin, DAO levels and intestinal mucosal injury scores.ConclusionPCT expression in serum and intestinal tissues in SAP rats increased significantly in the early stages of SAP, and was closely related to the onset and degree of intestinal barrier function impairment. Thus, our results showed that measuring serum PCT can be used to predict intestinal mucosal barrier function impairment in SAP rats.     

氧化苦参碱诱导跨膜蛋白Claudin-1表达在重症急性胰腺炎大鼠肠黏膜损害中的作用

目的:探讨氧化苦参碱(OM)在重症急性胰腺炎(SAP)肠黏膜屏障损害中的作用及其机制.方法:采用L-精氨酸(1 750 mg/kg)腹腔注射制备SAP大鼠模型.将80只Wistar大鼠随机分为Control组、OM对照组、SAP对照组、OM治疗组1、12、24、36、48 h 5个亚组,每组10只.分时取材,测定血浆内...     

Alterations of intestinal immune function and regulatory effects of L-arginine in experimental severe acute pancreatitis rats

ABM: To discuss the changes of intestinal mucosal immune function in rats with experimental severe acute pancreatitis (SAP) and the regulatory effect of L-arginine. METHODS: Male adult Wistar rats were randomly divided into pancreatitis group, sham-operation group, and L-arginine treatment group. Animals were killed at 24, 48, and 72 h after SAP models were developed and specimens were harvested. Endotoxin concentration in portal vein was determined by limulus endotoxin analysis kit. CD3+, CD4+, CD8+ T lymphocytes in intestinal mucosal lamina propria were examined by immunohistochemistry. Secretory immunoglobulin A (SIgA) in cecum feces was examined by radioimmunoassay. RESULTS: Compared to the control group, plasma endotoxin concentration in the portal vein increased, percentage of CD3+ and CD4+ T lymphocyte subsets in the end of intestinal mucosal lamina propria reduced significantly, CD4+/CD8+ ratio decreased, and SIgA concentrations in cecum feces reduced at 24, 48, and 72 h after SAP developed. Compared to SAP group, the L-arginine treatment group had a lower level of plasma endotoxin concentration in the portal vein, a higher CD3+ and CD4+ T lymphocyte percentage in the end of intestinal mucosal lamina propria, an increased ratio of CD4+/CD8+ and a higher SIgA concentration in cecum feces. CONCLUSION: Intestinal immune suppression occurs in the early stage of SAP rats, which may be the main reason for bacterial and endotoxin translocation. L-arginine can improve the intestinal immunity and reduce bacterial and endotoxin translocation in SAP rats.     

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.     

重组肠三叶因子对急性坏死性胰腺炎大鼠肠黏膜保护作用的研究

目的 探讨重组肠三叶因子(rITF)对急性坏死性胰腺炎(ANP)大鼠肠黏膜的保护作用及其机制.方法 SD雄性大鼠60只,按随机数字表法分为对照组、ANP组、rITF组,每组20只.逆行胰胆管注射5%牛黄胆酸钠100μl/100 g体重制备ANP模型.rITF组制模前后尾静脉注射rITF 0.5mg/100 g体重,对照组及ANP组注射等量生理盐水,术后12、24 h分批处死大鼠.取血检测淀粉酶含量,取末端回肠组织观察病理学改变并予评分、免疫组化法检测肠黏膜NF-κB活性,RT-PCR法检测肠黏膜TNF-α mRNA、ICAM-1 mRNA的表达.结果 ANP组和rITF组血淀粉酶水平较同时点对照组均显著升高.ANP组肠黏膜损伤评分较同时点对照组高(P＜0.05);ANP 12 h组较rITF 12 h组高(P＜0.05),但24 h组间评分无明显差异.对照组、ANP组与rITF组12 h肠黏膜NF-κB阳性细胞数分别为(26±4)个、(55±8)个、(49±4)个;回肠组织TNF-α mRNA相对表达量分别为0.050±0.005、1.040±0.031和0.792±0.0256;回肠组织ICAM-1 mRNA相对表达量分别为0.045±0.010、0.795±0.037和0.400±0.031.ANP组上述各项指标值均较对照组显著增加(P＜0.05或P＜0.01),而rITF下组又较ANP组均显著减少(P＜0.05).结论 重组肠三叶因子对ANP大鼠肠黏膜具有保护作用,其机制可能通过抑制肠黏膜NF-κB活化,下调TNF-αmRNA、ICAM-1 mRNA表达.     

P-selectin、IVAM-1和ICAM-1在大鼠重症急性胰腺炎并发急性心肌损害中的作用机制

目的:研究大鼠重症急性胰腺炎(SAP)并发急性心肌损害(AMD)时心肌组织黏附分子(P-selectin、VCAM-1、ICAM-1)基因表达的变化以及丹红注射液对表达的影响.方法:90只S-D大鼠随机分为对照组(A组,n=30)、SAP模型组(B组,n=30)和治疗组(C组,n=30),采用腹腔注射L-Arg的制作S...