Cholecystokinin antagonist L364,718 induces alterations in acinar cells that prevent improvement of acute pancreatitis induced by obstruction

The aim of this study was to examine the effect of the most potent CCK receptor antagonist, L364,718, on two major factors involved in pancreatitis development: enzyme load and cytosolic calcium (Ca²⁺) levels in acinar cells. L364,718 (0.1 mg/kg/12 hr) was administered from 30 min before inducing acute pancreatitis (AP) by pancreatic duct obstruction (PDO) for 48 hr. The results obtained at different AP stages in PDO rats treated and not treated with the CCK antagonist were compared. Similar increases in the intracellular enzyme content were found at earlier stages of pancreatitis in all PDO rats treated or not treated with L364,718. The CCK antagonist increased cytosolic Ca²⁺ levels up to 6 hr after administration, inducing a higher cytosolic Ca²⁺ overload at the earliest stages of pancreatitis in L364,718-treated PDO rats than in those not treated. This event might justify the higher increases in ascites volume and haematocrit found in PDO rats treated with L364,718 and the exacerbation in pancreatic morphological alterations induced by PDO. The CCK receptor antagonist L364,718 produces alterations in the acinar calcium homeostasis that prevent to reduction in the severity of pancreatitis induced by obstruction.     

吡咯烷二硫代氨基甲酸盐对大鼠急性坏死性胰腺炎肝损伤的保护作用

目的:探讨核因子KB(NF-κB)抑制剂吡咯烷二硫代氨基甲酸盐(PDTC)对大鼠急性坏死性胰腺炎(ANP)的预防治疗作用。方法:大鼠80只随机分为正常对照组(Z)、胰腺炎组(Y)和干预纽.干预组又分为建模前1h PDTC干预组(A)、建模后1h PDTC干预组(B)和建模后6h干预组(C).干预组按不同时间ip PDTC.建模后6,12,24 h分批处死,临床全自动生化仪检测血清谷丙转氨酶(ALT)和淀粉酶(AMY),用凝胶迁移率改变分析法(EMSA)测定胰腺和肝脏中NF-κB的活性.同时观察胰腺和肝脏的病理改变.结果:正常大鼠组织中几乎测不到NF-κB的活性,与Z组比较,Y组胰腺和肝脏组织中6,12,24 h NF-κB活性分别明显增加(P<0.001).建模前1h,1h后使用PDTC,胰腺和肝脏组织中NF-κB活性均受到抑制(18.14±3.30,23.79±3.62 vs 24.82±4.57:10.68±2.51,13.83±2.70 vs 16.38±2.50;P<0.05),Y组血清ALT,AMY均高于对照组.病理学检查可以见到Y组和A,B,C组的胰腺和肝脏均有炎性改变,但A组较Y组明显为轻.结论:NF-κB的异常活化与SAP以及肝损伤有明显关系:PDTC对SAP时肝损伤的发生有一定的预防作用.     

Decreased survival rate of pancreatic acinar cells isolated from rats with acute pancreatitis

Viable acinar cells were isolated from normal rat pancreas as well as from pancreata pretreatedin situ by a short-term ischemia without and with reperfusion, induction of a pancreatic juice edema, and acute pancreatitis (AP), respectively. The isolated cells were incubated at 37 °C in an oxygenated Krebs-Henseleit bicarbonate buffer lacking any nutrient. As an analogto in vivo acinar cell necrosis, the decline of the isolated cells was followed up in vitro. During the first 5–6 h of incubation, the percentage of damaged cells increased only slightly. A second phase of about 30 min followed, during which nearly all residual cells died. The mean half-life (t₅₀) of the cells in all experimental groups ran to about 330 min, with the exception of the AP group (t₅₀= 132 min). The importance of an intact energy metabolism to prevent premature cell killing was underlined indirectly by the diminished t₅₀ (about 120 min in all groups) of the cells exposed to excess 2,4-dinitrophenol, an uncoupler of oxidative phosphorylation. The results suggest that experimental AP induced by a combination of biliary-pancreatic duct obstruction, stimulation of pancreatic secretion, and short-term pancreatic ischemia with subsequent reperfusion finds a reflection within the acinar cells themselves and that these effects are not clouded by the isolation procedure. Thus, the application of acinar cells isolated from pancreatic glands pretreatedin situ may offer a new tool for pathophysiological research into AP at the cellular level.     

Survival and morphology of isolated pancreatic acinar cells from rats with induced acute pancreatitis are not improved with anti-inflammatory drugs

Summary The influence from anti-inflammatory drugs on cellular damage of pancreatic acinar cells after induction of an acute pancreatitis (AP) in a rat model was investigated. Necrotizing pancreatitis was induced by retrograde instillation of trypsin solution in the pancreatic duct (group I). The severity of inflammation was determined using morphological and histological parameters 6, 24, and 48h after induction of the necrotizing pancreatitis. After isolation of acinar cells, the degree of damage was measured by trypan blue exclusion—a parameter of membrane permeability—as well as accumulation of rhodamine 6G—a parameter of the mitochondrial membrane potential. In groups II–V, rats were treated with the anti-inflammatory drugs indomethacine, hydrocortisone, cimetidine, and acetylsalicylic acid (ASS) before induction of AP. There was no significant benefit from therapy in either group regarding cell membrane damage, cellular energy metabolism, or histology.     

Mitochondrial dysfunction and apoptosis of acinar cells in chronic pancreatitis

BACKGROUND: The mechanism of acinar cell death in human chronic pancreatitis (CP) remains largely unexplored. Previous studies have demonstrated the role played by apoptosis and necrosis in experimental pancreatitis; however, their relationship with the progression of CP remains unknown. The present study was carried out to elucidate the role and extent of apoptosis in CP tissues with different histopathological scores and to examine the possible apoptotic pathway involved. METHODS: Pancreatic tissues (25 CP patients) that had been histopathologically graded (I-III) and ten normal pancreatic tissue samples were evaluated for apoptosis by DNA fragmentation and an in situ TUNEL assay. The expression of various apoptotic and antiapoptotic markers in the tissues were studied by immunohistochemistry and Western blotting. To elucidate the role of the mitochondria in acinar cell death, the mitochondrial membrane potential (DeltaPsim) and ATP levels were determined by flow cytometry and a luminometer. RESULTS: The presence of DNA fragmentation and apoptotic nuclei in all CP tissues confirmed the presence of apoptosis. The apoptotic index in CP tissue ranged from 0.09% to 0.86% +/- 0.02% and was highest in grade II (0.7 +/- 0.04%) tissues. Differential upregulation of the apoptotic mediators p53, Bax, cytochrome c, and caspase-3 and -9, and downregulation of antiapoptotic Bcl-2, was observed in CP. DeltaPsim on the order of 1.2-to 2.2-fold and ATP depletion in the range of 23%-84% in CP tissues was observed. CONCLUSIONS: Apoptosis plays an important role both in the initial stages and during the progression of CP, as evident in all tissue grades. Increased DeltaPsim, loss of ATP, and activation of caspases suggests the involvement of intrinsic pathways.     

Effects and mechanisms of somatostatin analogs on apoptosis of pancreatic acinar cells in acute pancreatitis in mice

AIM: To investigate the effects of somatostatin analogs (SSa) on apoptosis of pancreatic acinar cells and apoptosis-regulated gene bax, and p53 in treating acute pancreatitis in mice. METHODS: In cerulein-induced pancreatitis, with or without treatment of somatostatin, analogs (Octreotide) in CD-1 (BALB/c x DBetaAlpha/1) mice, apoptosis of pancreatic acinar cells was detected by using the TdT-mediated dUTP nick-end labeling (TUNEL) method, and the expression of apoptosis-regulated gene bax and p53 was determined by using the streptavidin-peroxidase immunohistochemical technique and the RT-PCR method, respectively. RESULTS: On HE staining, acinar cells in the pancreas showed pyknotic nuclei and the formation of apoptotic bodies, which are the typical morphological features of apoptosis. Regarding TUNEL use, the apoptotic index of pancreatic acinar cells in the non-treated group at 5 and 14 h after induction of acute pancreatitis was significantly lower than those of the SSa-treated group, respectively (P < 0.01). On immunohistochemistry and RT-PCR, there was an expression of neither bax nor p53 in normal pancreatic tissues. The expression of bax in the SSa-treated group at 5 and 14 h after treatment of SSa was markedly higher than those of the non-treated group, respectively (P < 0.01), but there was no significant difference in the expression of p53 between the SSa-treated group and the non-treated group. CONCLUSIONS: The induction of apoptosis in pancreatic acinar cells injury to reduce inflammatory reaction might be one of the mechanisms of SSa in treating acute pancreatitis in mice, and the mechanisms of apoptosis probably correlated with the expression of apoptosis-regulated gene bax, but have no relationship with the expression of p53.     

长期乙醇摄入导致胰腺腺泡细胞退行性改变

目的探讨长期摄入乙醇对胰腺腺泡细胞结构和外分泌功能的影响。方法将12只Wistar大鼠平均分为乙醇组和对照组,乙醇组饲以25%乙醇6个月,在光镜和电镜下观察胰腺腺泡细胞结构变化,用比色法检测胰腺组织匀浆淀粉酶和脂肪酶,用TUNEL法检测细胞凋亡,用免疫组化检测COX2的变化。结果与对照组相比,乙醇组腺泡细胞中出现较多空泡,腺泡细胞内脂滴增加,酶原颗粒减少,髓样结构形成。乙醇组胰腺组织匀浆淀粉酶、脂肪酶分别为(2807.26±50.10)U/G组织、(3650.00±80.18)U/G组织,与对照组相比有显著降低(P<0.05)。乙醇组胰腺组织细胞凋亡指数、COX2的表达与对照组比较差异无统计学意义。结论长期乙醇摄入可导致大鼠胰腺腺泡细胞退行性改变及外分泌功能减低。     

Emodin and baicalein inhibit sodium taurocholate-induced vacuole formation in pancreatic acinar cells

AIM To investigate the effects of combined use of emodin and baicalein(CEB) at the cellular and organism levelsin severe acute pancreatitis(SAP) and explore the underlying mechanism.METHODS SAP was induced by retrograde infusion of 5% sodium taurocholate into the pancreatic duct in 48 male SD rats. Pancreatic histopathology score, serum amylase activity, and levels of tumour necrosis factor alpha(TNf-α), interleukin 6(IL-6), and IL-10 were determined to assess the effects of CEB at 12 h after the surgery. The rat pancreatic acinar cells were isolated from healthy male SD rats using collagenase. The cell viability, cell ultrastructure, intracellular free Ca2+ concentration, and inositol(1,4,5)-trisphosphate receptor(IP3 R) expression were investigated to assess the mechanism of CEB.RESULTS Pancreatic histopathology score(2.07 ± 1.20 vs 6.84 ± 1.13, P 0.05) and serum amylase activity(2866.2 ± 617.7 vs 5241.3 ± 1410.0, P 0.05) were significantly decreased in the CEB(three doses) treatment group compared with the SAP group(2.07 ± 1.20 vs 6.84 ± 1.13, P 0.05). CEB dose-dependently reduced the levels of the pro-inflammatory cytokines IL-6(466.82 ± 48.55 vs 603.50 ± 75.53, P 0.05) and TNF-α(108.04 ± 16.10 vs 215.56 ± 74.67, P 0.05) and increased the level of the anti-inflammatory cytokine IL-10(200.96 ± 50.76 vs 54.18 ± 6.07, P 0.05) compared with those in the SAP group. CEB increased cell viability, inhibited cytosolic Ca2+ concentration, and significantly ameliorated intracellular vacuoles and IP3 m RNA expression compared with those in the SAP group(P 0.05). There was a trend towards decreased IP3 R protein in the CEB treatment group; however, it did not reach statistical significance(P 0.05).CONCLUSION These results at the cellular and organism levels reflect a preliminary mechanism of CEB in SAP and indicate that CEB is a suitable approach for SAP treatment.     

Effect of urinary trypsin inhibitor on pancreatic cellular and lysosomal fragility in cerulein-induced acute pancreatitis in rats

We evaluated the protective effect and the mechanism of action of the trypsin inhibitor, urinastatin, extracted from human urine, in experimental acute pancreatitis induced by a supramaximal dose of cerulein (5 g/kg/hr for 3.5 hr). Urinastatin in a dose of 10,000 units/kg/hr was given by three different methods of continuous infusion: (1) 2 hr before and during cerulein infusion, (2) only during cerulein infusion, and (3) starting 1 hr after the beginning of cerulein infusion and continued for 3.5 hr. In protocol 1 and 2 urinastatin was significantly more protective than in 3. In protocol 1 urinastatin was very protective in all parameters tested (serum amylase level, pancreatic water and amylase content, distribution of lysosomal enzymes, cellular and lysosomal fragility). These results suggest that the administration of urinastatin before and during cerulein infusion may suppress the pathogenesis and evolution of pancreatitis by inhibiting the chain reaction of pancreatic enzyme activation closely related to redistribution of lysosomal enzyme and lysosomal fragility.     

牛胆酸钠诱导大鼠急性胰腺炎系列模型的研究

目的 用牛胆酸钠纯化学制剂诱导大鼠实验性急性胰腺炎系列模型。 方法 用0.25％(n=4),1.0％(n=7),2.0％(n=7)或3.5％(n=7)牛胆酸钠溶液0.1 ml/100g逆行注入Wistar大鼠胰管内诱导急性胰腺炎。诱导急性胰腺炎前,及诱导后6,12 h分别取血分离血清,测定淀粉酶值。同时,观察各实验组胰腺病理组织光镜和电镜变化。 结果 随牛胆酸钠诱导浓度提高,血清淀粉酶逐渐升高,组织病理改变依次加重。1.0％和2.0％牛胆酸钠分别诱导轻度及重度水肿型胰腺炎;3.5％牛胆酸钠则诱导坏死型胰腺炎。 结论 胰腺病变程度与牛胆酸钠诱导浓度呈正相关,本系列模型适合评价药物的防治效应。     

Role of bone marrow-derived mesenchymal stem cells in a rat model of severe acute pancreatitis

AIM: To investigate the role and potential mechanisms of bone marrow mesenchymal stem cells (MSCs) in severe acute peritonitis (SAP).METHODS: Pancreatic acinar cells from Sprague Dawley rats were randomly divided into three groups: non-sodium deoxycholate (SDOC) group (non-SODC group), SDOC group, and a MSCs intervention group (i.e., a co-culture system of MSCs and pancreatic acinar cells + SDOC). The cell survival rate, the concentration of malonaldehyde (MDA), the density of superoxide dismutase (SOD), serum amylase (AMS) secretion rate and lactate dehydrogenase (LDH) leakage rate were detected at various time points. In a separate study, Sprague Dawley rats were randomly divided into either an SAP group or an SAP + MSCs group. Serum AMS, MDA and SOD, interleukin (IL)-6, IL-10, and tumor necrosis factor (TNF)-α levels, intestinal mucosa injury scores and proliferating cells of small intestinal mucosa were measured at various time points after injecting either MSCs or saline into rats. In both studies, the protective effect of MSCs was evaluated.RESULTS: In vitro, The cell survival rate of pancreatic acinar cells and the density of SOD were significantly reduced, and the concentration of MDA, AMS secretion rate and LDH leakage rate were significantly increased in the SDOC group compared with the MSCs intervention group and the Non-SDOC group at each time point. In vivo, Serum AMS, IL-6, TNF-α and MAD level in the SAP + MSCs group were lower than the SAP group; however serum IL-10 level was higher than the SAP group. Serum SOD level was higher than the SAP group at each time point, whereas a significant between-group difference in SOD level was only noted after 24 h. Intestinal mucosa injury scores was significantly reduced and the proliferating cells of small intestinal mucosa became obvious after injecting MSCs.CONCLUSION: MSCs can effectively relieve injury to pancreatic acinar cells and small intestinal epithelium, promote the proliferation of enteric epithelium and repair of the mucosa, attenuate systemic inflammation in rats with SAP.     

急性梗阻性胰腺炎大鼠胰腺腺泡细胞凋亡的变化

目的:结合胆管压力的变化来探讨胰腺炎轻重程度与胆胰管梗阻时间及腺泡细胞凋亡的关系．方法:采用结扎胆胰管的方法制成胰腺炎模型．分别于梗阻后4、8、12 h以及解除梗阻后1、3 d分别测定胆管压力．流式细胞分析法检测胰腺腺泡细胞Annexin V-FITC／PI和 Caspase-3的表达．结果:与正常对照组(16．42±1．03)相比,随着梗阻时间的延长,胆管压力明显增高(4,8, 12 h分别为49．98±3．05,90．20±8．66,589．00 ±60．10),而在解除梗阻后,压力迅速下降并在1 d即恢复正常(1,3 d分别为17．50±2．84, 16．37±0．46),变化显著(P<0．01)．AnnexinV- FITC／PI检测显示梗阻4 h时细胞凋亡较多, 至梗阻12 h时,腺泡细胞凋亡明显减少而坏死增加;在解除梗阻后,随着时间的延长凋亡明显增多,坏死逐渐减少,变化显著(P<0．01)． Caspase-3检测显示在梗阻4 h时凋亡表达最高,梗阻8 h已明显减少,12 h则以坏死为主要表达方式;解除梗阻后1 d仍以坏死为主,到第3天则表现出大量的凋亡,变化显著 (P<0．01)．结论:胆管压力升高引起的胆胰液返流是胰腺炎的发病机制之一,并可引起胰腺腺泡细胞的凋亡减少,而早期恢复正常胆胰管压力可使细胞凋亡增多,有效的阻止急性胰腺炎的病情发展．     

Decreased survival rate of pancreatic acinar cells isolated from rats with acute pancreatitis

Viable acinar cells were isolated from normal rat pancreas as well as from pancreata pretreated in situ by a short-term ischemia without and with reperfusion, induction of a pancreatic juice edema, and acute pancreatitis (AP), respectively. The isolated cells were incubated at 37 degrees C in an oxygenated Krebs-Henseleit bicarbonate buffer lacking any nutrient. As an analog to in vivo acinar cell necrosis, the decline of the isolated cells was followed up in vitro. During the first 5-6 h of incubation, the percentage of damaged cells increased only slightly. A second phase of about 30 min followed, during which nearly all residual cells died. The mean half-life (t50) of the cells in all experimental groups ran to about 330 min, with the exception of the AP group (t50 = 132 min). The importance of an intact energy metabolism to prevent premature cell killing was underlined indirectly by the diminished t50 (about 120 min in all groups) of the cells exposed to excess 2,4-dinitrophenol, an uncoupler of oxidative phosphorylation. The results suggest that experimental AP induced by a combination of biliary-pancreatic duct obstruction, stimulation of pancreatic secretion, and short-term pancreatic ischemia with subsequent reperfusion finds a reflection within the acinar cells themselves and that these effects are not clouded by the isolation procedure. Thus, the application of acinar cells isolated from pancreatic glands pretreated in situ may offer a new tool for pathophysiological research into AP at the cellular level.     

A mouse model of acute biliary pancreatitis induced by retrograde pancreatic duct infusion of Na-taurocholate

Objective

Most mechanistic studies of pancreatitis in mice employ the secretagogue‐induced model. The currently reported studies were designed to develop an alternative, and possibly more clinically relevant, mouse model of pancreatitis.

Design

Na‐taurocholate (10–50 μl, 1–5%) in saline, or saline alone, was retrogradely infused into the mouse pancreatic duct. The animals were killed 6–24 hours later and the severity of pancreatitis in the pancreatic head and tail was examined by quantitating hyperamylasemia, pancreatic edema, acinar cell necrosis, and pancreatic inflammation. In addition, intrapancreatic activation of trypsinogen, generation of IL‐6, intrapulmonary sequestration of neutrophils, and alterations in lung compliance were evaluated. The effects of Na‐taurocholate on in‐vitro acinar cell calcium transients, viability, and trypsinogen activation were examined.

Results

Little or no evidence of pancreatitis was observed in mice infused with saline alone or in the tail of pancreata removed from animals infused with Na‐taurocholate. In the head of the pancreas, evidence of pancreatitis was observed 12–24 hours after infusion of 20–50 μl 2–5% Na‐taurocholate and the earliest morphological changes involved terminal duct and acinar cells. Intrapancreatic trypsin activity was transiently elevated within 5 minutes of Na‐taurocholate infusion and pancreatic IL‐6 levels were elevated 24 hours later. Under in‐vitro conditions, Na‐taurocholate triggered pathological acinar cell calcium transients, cell death, and calcium‐dependent trypsinogen activation.

Conclusion

This clinically relevant model of acute biliary pancreatitis yields reproducible results and its severity can be easily manipulated. It is ideally suited for use in mechanistic studies employing genetically modified mouse strains.     

Effect of resveratrol on pancreatic oxygen free radicals in rats with severe acute pancreatitis

AIM:To investigate the therapeutic effects of resveratrol(RESV) as a free radical scavenger on experimental se-vere acute pancreatitis (SAP).METHODS:Seventy-two male Sprague-Dawley ratswere divided randomly into sham operation group,SAPgroup,and resveratrol-treated group.Pancreatitis wasinduced by intraductal administration of 0.1 mL/kg 4%sodium taurocholate.RESV was given intravenouslyat a dose of 20 mg/kg body weight.All animals werekilled at 3,6,12 h after induction of the model.Serumamylase,pancreatic superoxide dismutase (SOD),malondialdehyde (MDA),and myeloperoxidase (MPO)were determined.Pathologic changes of the pancreaswere observed under optical microscope.RESULTS:The serum amylase,pancreatic MPO andthe score of pathologic damage increased after theinduction of pancreatitis,early (3,6 h)SAP sampleswere characterized by decreased pancreatic SODand increased pancreatic MDA.Resveratrol exhibiteda protective effect against lipid peroxidation in cellmembrane caused by oxygen free radicals in theearly stage of SAP.This attenuation of the redox stateimpairment reduced cellular oxidative damage,asreflected by lower serum amylase,less severe pancreaticlesions,normal pancreatic MDA levels,as well asdiminished neutrophil infiltration in pancreas.CONCLUSION:RESV may exert its therapeutic effecton SAP by lowering pancreatic oxidative free radicals andreducing pancreatic tissue infiltration of neutrophils.     

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.     

骨髓间充质干细胞移植对大鼠重症急性胰腺炎的治疗作用观察

目的探讨骨髓间充质干细胞（MSCs）移植对重症胰腺炎（SAP）的治疗作用及相关机制。方法将雄性SD大鼠120只随机分为假手术组、模型组及移植组各40只。模型组和移植组采用5%牛磺胆酸钠逆行胰胆管注射方法制作SAP模型,假手术组开腹后翻动肠壁即关腹。造模成功后移植组经门静脉植入MSCs;模型组及假手术组采用同样方法给予等量生理盐水。于24、48、72 h每组分别处死10只大鼠,对胰腺和肾脏损伤进行大体形态和光镜下观察,测定血清淀粉酶（AMY）、BUN、Cr、TNF-α和IL-6水平。结果模型组胰腺和肾脏组织损伤明显,各时间点血清AMY、BUN、Cr、TNF-α和IL-6水平均高于假手术组,P均〈0.05。移植组胰腺和肾脏组织损伤有所减轻;各时间点血清中AMY、BUN、Cr、TNF-α和IL-6水平均低于模型组及假手术组,P均〈0.05。结论经门静脉移植MSCs治疗SAP效果确切,可降低多器官功能障碍的发生率。