Pancreatic Duct Patterns in Acute Pancreatitis: A MRI Study

Objectives

To study the MRI findings of the pancreatic duct in patients with acute pancreatitis.

Materials and Methods

A total of 239 patients with acute pancreatitis and 125 controls were analyzed in this study. The severity of acute pancreatitis was graded using the MR severity index (MRSI) and the Acute Physiology And Chronic Healthy Evaluation II(APACHE II) scoring systems. The number of main pancreatic duct (MPD) segments visualized, and both MPD diameter and pancreatic duct disruption were noted and compared with the severity of acute pancreatitis.

Results

The frequency of MPD segment visualization in the control group was higher than that in the acute pancreatitis group (p<0.05). The number of MPD segments visualized was negatively correlated with the MRSI score (p<0.05) and the APACHE II score (p<0.05). There was no difference in the MPD diameter between the acute pancreatitis and control groups or among the patients with different severities of acute pancreatitis (p>0.05). The prevalence of pancreatic duct disruption was 7.9% in the acute pancreatitis group. The prevalences of pancreatic duct disruption were 4.8% and 15.3% in the mild and severe acute pancreatitis groups based on the APACHE II score, respectively, and were 0%, 5.7% and 43.5% in the mild, moderate and severe acute pancreatitis groups according the MRSI score, respectively. The prevalence of pancreatic duct disruption was correlated with the severity of acute pancreatitis based on the APACHE II score (p<0.05) and MRSI score (p<0.05).

Conclusion

The pancreatic duct in acute pancreatitis patients was of normal diameter. The number of MPD segments visualized and visible pancreatic duct disruption on MRI may be supplementary indicators for determining the severity of acute pancreatitis.     

Pancreatic Duct Obstruction in the Pig: Light Microscopy of Chronic Pancreatitis

Morphological changes of pancreatic tissue in young pigs caused by surgical ligation of the main pancreatic duct are described. Nineteen animals from 6 to 7 weeks in age were operated on and necropsied 3 or 6 to 8 weeks later. Twelve pigs developed a pronounced chronic pancreatitis with complete exocrine insufficiency. Of the 7 animals failing to develop ectasia of pancreatic ducts, 2 died due to surgical complications. In addition, 3 pigs were sham-operated and served as controls. In macroscopical studies it was observed that in the pronounced pancreatitis cases the ligated duct was greatly dilated by a clear watery fluid. Only remnants of pale and firm grandular tissues were seen around the ectatic ducts. Microscopically, typical changes of chronic pancreatitis were noted. Complete disappearance of acini was followed by ductular cell proliferations. Glandular tissues were divided into lobuli by fibrotic tissues and fat cells. The wall of the main pancreatic duct was greatly thickened and fibrotic, presenting intensely proliferating ductular cells and round cell infiltrates. Furthermore, enlarged endocrine islets surrounded by connective tissue fibres were seen.     

Glyceryl Trinitrate for Prevention of Post-ERCP Pancreatitis and Improve the Rate of Cannulation: A Meta-Analysis of Prospective,Randomized, Controlled Trials

Background

Acute pancreatitis is the most common complication of diagnostic and therapeutic endoscopic retrograde cholangiopancreatography (ERCP). Several clinical trials used glyceryl trinitrate (GTN) to prevent the incidence of post-ERCP pancreatitis (PEP). However, the results were still controversial.

Objective

To conduct a meta-analysis of published, full-length, randomized controlled trials evaluating the effect of prophylactic GTN on the prevention of PEP, improve the rate of cannulation and the prevention of hyperamylasemia.

Methods

Literature searches were conducted using PubMed, EMBASE, The Cochrane Library and Web of Knowledge databases, using keywords "post-ERCP" and "pancreatitis" and limited in randomized controlled trials.

Results

Twelve RCTs involving 2649 patients were included. Eleven RCTs compared GTN with placebo for PEP prevention. Meta-analysis showed the overall incidence of PEP was significantly reduced by GTN treatment (RR 0.67; 95% CI, 0.52-0.87). Nevertheless, GTN administration did not decrease the incidence of moderate to severe PEP (RR 0.70; 95% CI, 0.42-1.15). Subgroup analyses revealed that GTN administered by sublingual was more effective than transdermal and topical in reducing the incidence of PEP. Besides, the prophylactic effect of GTN was far more obvious in the group of high PEP incidence than in the group of low PEP incidence. Additionally, the incidence of hyperamylasemia was significantly reduced by GTN treatment (RR 0.69; 95% CI, 0.54-0.90). No differences of the successful cannulation rate of bile ducts (RR 1.03; 95% CI, 0.99-1.06) attributable to GTN were observed.

Conclusion

Prophylactic use of GTN reduced the overall incidence of PEP and hyperamylasemia. However, GTN was not helpful for the severity of PEP and the rate of cannulation.     

Clinical Investigation of Fasudil for the Prevention of Cerebral Vasospasm in Extracranial Carotid Artery Stenting

To evaluate fasudil hydrochloride for the prevention of cerebral vasospasm (CVS) in extra-cranial carotid angioplasty and stenting (CAS). We retrospectively analyzed 178 patients with unilateral CAS who were given intravenous fasudil hydrochloride during the perioperative period. CVS, hypotension, stroke, and mortality incidence rates were recorded. Of the cohort studied, 80.9 % patients exhibited no local CVS, asymptomatic vasospasm was observed in 17.4 % patients and symptomatic vasospasm in 1.7 % patients via DSA imaging. All CVS was relieved and symptoms disappeared after intra-arterial infusion of papaverine hydrochloride. Intracerebral hemorrhage occurred in two cases during the perioperative period, one of which resulted in death. CVS is a severe complication of CAS. Fasudil hydrochloride can rapidly relieve cerebral vasospasm, has no selective effect on cerebral vasculature, and little influence on blood pressure. It is suitable for the prevention of CVS during interventional treatment of ischemic cerebrovascular disease.     

胰腺发育相关maf基因在胰腺导管和胰岛的表达

为探讨胰岛功能和发育相关maf基因在胰腺导管上皮中的表达情况,对新鲜小鼠胰腺组织切片进行显微切割,分离纯化胰腺组织中的导管和胰岛,以及外分泌腺组织细胞作为对照,利用荧光实时定量PCR的方法完成对目的基因的相对定量.结果显示,mafa mRNA,mafb mRNA水平在胰岛及导管中非常接近,无统计学差异.而c-maf在导管的表达高于胰岛(P<0.05),外分泌腺则无上述基因的表达.胰腺导管中mafa,mafb,cmaf均有表达,肯定了导管上皮细胞向内分泌细胞分化的潜能,而c-maf在导管中的表达高于胰岛,提示导管上皮c-maf的下调可能有助于导管上皮细胞向内分泌细胞的分化成熟.     

重症急性胰腺炎并发胰性脑病的临床特点及相关影响因素分析

目的:探究重症急性胰腺炎并发胰性脑病(PE)的临床特点及相关影响因素分析。方法:本研究于2008年3月~2015年3月期间,选择我院收治的重症急性胰腺炎患者93例为研究对象,根据患者是否并发PE临床症状将其分为PE组和非PE组。收集所有患者基本资料、实验室检查指标及病原学培养检查资料,采用logistics回归对PE发病的影响因素进行分析。结果:93例重症急性胰腺炎中23例被诊断为PE,发病率为24.73%,临床主要表现为兴奋性、烦躁不安、谵妄等症状;PE组患者APACHEⅡ评分、MODS发生率、肌酐、甘油三脂水平及真菌感染率均高于非PE组,差异有统计学意义(P0.05);多因素logistics回归显示,高APACHEⅡ评分和高甘油三脂是PE发生的危险因素(OR=3.221,2.973;均P0.05)。结论:重症急性胰腺炎并发PE的发病率较高,临床有较高的APACHEⅡ评分、MODS发生率、肌酐、甘油三脂水平及真菌感染率,其中高APACHEⅡ评分和高甘油三脂是PE发生的危险因素。     

Bile Acids Induce Pancreatic Acinar Cell Injury and Pancreatitis by Activating Calcineurin

Biliary pancreatitis is the leading cause of acute pancreatitis in both children and adults. A proposed mechanism is the reflux of bile into the pancreatic duct. Bile acid exposure causes pancreatic acinar cell injury through a sustained rise in cytosolic Ca²⁺. Thus, it would be clinically relevant to know the targets of this aberrant Ca²⁺ signal. We hypothesized that the Ca²⁺-activated phosphatase calcineurin is such a Ca²⁺ target. To examine calcineurin activation, we infected primary acinar cells from mice with an adenovirus expressing the promoter for a downstream calcineurin effector, nuclear factor of activated T-cells (NFAT). The bile acid taurolithocholic acid-3-sulfate (TLCS) was primarily used to examine bile acid responses. TLCS caused calcineurin activation only at concentrations that cause acinar cell injury. The activation of calcineurin by TLCS was abolished by chelating intracellular Ca²⁺. Pretreatment with 1,2-bis(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (acetoxymethyl ester) (BAPTA-AM) or the three specific calcineurin inhibitors FK506, cyclosporine A, or calcineurin inhibitory peptide prevented bile acid-induced acinar cell injury as measured by lactate dehydrogenase leakage and propidium iodide uptake. The calcineurin inhibitors reduced the intra-acinar activation of chymotrypsinogen within 30 min of TLCS administration, and they also prevented NF-κB activation. In vivo, mice that received FK506 or were deficient in the calcineurin isoform Aβ (CnAβ) subunit had reduced pancreatitis severity after infusion of TLCS or taurocholic acid into the pancreatic duct. In summary, we demonstrate that acinar cell calcineurin is activated in response to Ca²⁺ generated by bile acid exposure, bile acid-induced pancreatic injury is dependent on calcineurin activation, and calcineurin inhibitors may provide an adjunctive therapy for biliary pancreatitis.     

Pancreatic Degenerative Atrophy and Chronic Pancreatitis in Dogs a Comparative Study of 60 Cases

During the years 1977–1980 60 cases of non-neoplastic chronic exocrine pancreatic disease in dogs were investigated clinically and pathologically. The disorders were clinically divided into pancreatic degenerative atrophy (PDA) and chronic pancreatitis. Fifty dogs had PDA and 45 of them were German shepherd dogs. The PDA cases formed both clinically and pathologically a homogeneous group except for 1 case. All the dogs had maldigestion and protease activity was absent from the faeces. General inanition and highly atrophic pancreas were the most typical macroscopic findings. Histologically the exocrine pancreas contained atypical acinar tissue and mononuclear cell infiltrations. Five of the dogs died spontaneously, 4 of them had intestinal torsion and 1 had paralytic ileus. There were 10 dogs with chronic pancreatitis. This group was rather heterogeneous both clinically and pathologically. The pancreas was slightly enlarged and the consistency was firm. The histologic picture was one of fibrous tissue proliferation and inflammatory cell infiltrations in the interstitium. The dogs nutritional state as well as faecal protease activity were normal.     

儿童急性胰腺炎病因、临床特征及诊治的回顾性研究

目的：探讨儿童急性胰腺炎的病因、临床特征及诊治的临床特点,为其临床诊断和治疗提供参考依据。方法：回顾性分析2009年1月～2012年6月我院诊治的107例儿童急性胰腺炎患者的临床资料（病因、临床特点、症状体征、实验室检查、影像学特征、诊断证据、治疗及预后等）,综合比较儿童急性胰腺炎与成人急性胰腺炎的不同。结果：107例儿童急性胰腺炎,主要以腹痛为首发症状（81.3%）,10例出现腹胀（9.3%）,7例出现恶心或呕吐（6.5%）,其他或主诉不明确者3例（2.8%）。季节性不明显,四季可发病。PAP的原因中特发性占近40%,其次是外伤和先天性畸形,胆道结石致使的胰腺炎多发于年龄偏大儿童,药物、系统性疾病也均可导致PAP。单纯靠症状诊断PAP有困难,需结合血尿淀粉酶的变化及胰腺影像学检查的结果共同诊断。PAP的治疗强调个体化,科学,合理,及时的补液,及时的生长抑素、抗生素的使用至关重要（不同于成人急性胰腺炎）,手术也是必需的备选手段,但需注意手术适应症和时机的选择。结论：儿童急性胰腺炎的发病率呈上升趋势,其诊断和治疗均有其自身的特点,与成人急性胰腺炎并不完全相同,在临床诊断和治疗中应引起足够的重视。     

Survivin和MMP14在胰腺癌中的表达及临床病理意义

目的:研究胰腺癌组织中Survivin和MMP14的表达及其临床病理意义,为筛选胰腺癌分子诊断新靶标提供理论依据。方法:采用免疫组织化学技术(S-P)法检测44例胰腺癌、13例胰腺炎及21例正常胰腺组织中Survivin和MMP14表达情况,并分析其与胰腺癌临床病理参数的相关性。结果:胰腺癌组织中Survivin和MMP14蛋白均呈明显高表达,其表达与胰腺癌患者的性别、年龄、肿瘤部位、临床分期、分级及有无淋巴结转移均显著相关性(P0.05)。胰腺炎与正常胰腺组织中Survivin和MMP14蛋白表达的差异无统计学意义(P0.05),但均显著低于胰腺癌组织(P=0.000/P=0.001)。结论:Survivin和MMP14蛋白在胰腺癌组织中均呈异常高表达,但与胰腺癌的临床病理特点均无关,可能成为新的胰腺癌诊断标志物。     

生长抑素联合泮托拉唑钠治疗重症急性胰腺炎的临床研究

目的:探讨生长抑素联合泮托拉唑钠治疗重症急性胰腺炎(SAP)的临床效果。方法:选取我院2011年1月至2014年1月收治的83例SAP患者,按随机数字表法分为两组,研究组42例,对照组41例。对照组患者在常规治疗基础上给予生长抑素治疗,研究组患者给予生长抑素联合泮托拉唑钠治疗。比较两组患者治疗疗效,并记录患者腹痛缓解时间、脱离呼吸机时间、肠道功能恢复时间、血淀粉酶恢复正常时间。结果:研究组总有效率为90.5%(38/42),明显高于对照组的75.6%(31/41),差异有统计学意义(P0.05);研究组患者腹痛缓解时间、脱离呼吸机时间、肠道功能恢复时间及血淀粉酶恢复正常时间均明显短于对照组(P0.05)。结论:生长抑素与泮托拉唑钠联合治疗SAP疗效显著,可有效改善患者临床症状,值得临床推广应用。     

乌司他丁治疗急性胰腺炎的临床疗效及机制研究

目的:探讨乌司他丁对急性胰腺炎患者的临床疗效及可能机制。方法:收集我院收治的重症急性胰腺炎患者66例,随机分为实验组和对照组。所有患者均给予禁食水、充分补液、纠正电解质紊乱等常规支持对症治疗。对照组予奥曲肽,实验组予乌司他丁,共治疗7天。测定两组患者治疗前、后各血清白介素-6(IL-6)、白介素-8(IL-8)及肿瘤坏死因子-α(TNF-α)水平;治疗前、治疗第1、3天及治疗后进行血常规检测,观察白细胞计数(WBC),并进行血淀粉酶(AMS)、尿淀粉酶(UAMY)测定;分别记录两组患者临床症状及体征恢复时间,判定临床疗效。结果:1治疗后,两组患者血清IL-6、IL-8及TNF-α水平均较治疗前显著下降,且实验组较对照组下降更明显(P0.05);2治疗后,两组患者白细胞计数及血、尿淀粉酶水平均较治疗前明显下降,且实验组较对照组下降更明显(P0.05);3治疗后,实验组各项临床症状及体征消失时间均明显短于对照组(P0.05)。结论:乌司他丁可有效改善急性胰腺胰腺炎患者的各项临床症状,这可能与其显著降低其血清IL-6、IL-8、TNF-α、淀粉酶水平、白细胞计数及尿淀粉酶水平有关。     

3.0T磁共振多序列成像对鉴别胰头癌与胰头肿块型慢性胰腺炎的应用价值

目的：探讨磁共振多序列成像对鉴别胰头癌与胰头肿块型慢性胰腺炎的临床价值及意义。方法：对已确诊的16例胰头癌患者和5例胰头肿块型慢性胰腺炎患者的磁共振多序列成像MR进行回顾性分析。主要征象包括：①肿块信号及形态学特点;②胰管及胆管扩张情况;③动态增强的特征;④胰周及大血管受累情况;⑤邻近器官受累与淋巴结肿大情况。检查方法包括：平扫T1WI＋FST2WI＋FS,MRCP,3D—VIBE动态增强扫描。结果：1）肿块形态信号异常：胰头癌与胰头肿块型胰头慢性胰腺炎的信号有较多重叠,在TlwI上均表现为相对低信号,T2WI表现为不均匀稍高、相等或低信号。2）胰管与胆管的异常：胰头癌表现为胰管扩张至肿块处突然截断12例,胆总管突然截断10例,“双管征”10例。胰头肿块型慢性胰腺炎胰管扩张3例,2例为串珠样扩张,扩张的胰管可贯通病灶区,胆总管5例均扩张,远端呈短锥形狭窄3例,鼠尾样狭窄2例。3）3D—VIBE强化特征分析结果：随着时间的延长胰头癌强化程度和强化百分率较胰头肿块型慢性胰腺炎明显减低。4）胰周大血管受累情况：胰头癌肿块与血管分界不清者8例,部分包绕血管6例完全包绕血管6例;胰头肿块型慢性胰腺炎1例与血管分界不清,1例部分被包绕。5）邻近器官受累与淋巴结肿大情况：胰头癌有7例淋巴结肿大主要分布在胰周及腹主动脉旁,胰头肿块型慢性胰腺炎,未见明显肿大淋巴结,有四例肾周筋膜增厚,两例肾前筋膜增厚。结论：磁共振多序列成像的联合使用及征象分析,有助于鉴别胰头癌与胰头肿块型慢性胰腺炎。     

高脂血症性胰腺炎26例临床治疗分析

目的:分析26例高脂血症性胰腺炎的治疗及预后,探讨高脂血症性胰腺炎的治疗特点。方法:总结我科03．8-06．10间收治的高脂血症性胰腺炎病人26例的治疗及预后。结果:在高脂血症性胰腺炎26例,其中重症病例11例,重症病例中死亡二例,手术三例,合并糖尿病4例、合并高血压、冠心病5例,在所有高脂血症性胰腺炎中除重症中2例死亡外,其余根据胰腺炎的严重程度不同采用相应的治疗办法而全部治愈。结论:高脂血症性胰腺炎的发病率相对较高,其并发病多、死亡率高,治疗以降血脂为主的多方位的综合治疗,血液净化是重症高脂血症性胰腺炎早期治疗一种较有用的方式。     

Loss of Ifnar1 in Pancreatic Acinar Cells Ameliorates the Disease Course of Acute Pancreatitis

Type I interferon constitutes an essential component of the combinational therapy against viral disease. Acute pancreatitis is one side effect of type I interferon-based therapy, implying that activation of type I interferon signaling affects the homeostasis and integrity of pancreatic acinar cells. Here, we investigated the role of type I interferon signaling in pancreatic acinar cells using a caerulein-induced murine model of acute pancreatitis. Pancreas-specific ablation of interferon (alpha and beta) receptor 1 (Ifnar1) partially protected animals from caerulein-induced pancreatitis, as demonstrated by reduced tissue damage. Profiling of infiltrating immune cells revealed that this dampened tissue damage response correlated with the number of macrophages in the pancreas. Pharmacologic depletion of macrophages reversed the protective effect of Ifnar1 deficiency. Furthermore, expression of chemokine (C-C motif) ligand 2 (Ccl2), a potent factor for macrophage recruitment, was significantly increased in the Ifnar1-deficient pancreas. Thus, type I interferon signaling in pancreatic acinar cells controls pancreatic homeostasis by affecting the macrophage-mediated inflammatory response in the pancreas.     

SIRT-1和Ku70在胰腺癌中的表达及其临床病理意义

目的:研究胰腺癌中S IRT-1和Ku70的表达及其临床病理意义,为胰腺癌患者的预后及生物治疗提供理论依据.方法:采用免疫组织化学技术(S-P)法检测46例胰腺癌及20例非肿瘤性胰腺组织中SIRT-1和Ku70表达情况,并分析其与胰腺癌临床病理参数的关系.结果:胰腺癌组织中SIRT-1的表达明显升高,其表达强度与临床分期、淋巴结有无转移、年龄和肿瘤大小呈正相关(P＜0.05),与组织学分级呈负相关(P＜0.05),与患者的性别和肿瘤部位均无关.胰腺癌组织中Ku70表达明显升高,其表达强度与临床分期、淋巴结有无转移及呈正相关(P＜0.05),与组织学分级呈负相关(P＜0.05),与患者的性别、年龄、肿瘤部位和大小均无关.结论:SIRT-1和Ku70在胰腺癌组织中的表达显著高于非肿瘤胰腺组织,且与胰腺癌的临床病理及预后相关,在胰腺癌的发展中也起一定作用,存在协同关系.     

尿淀粉酶检测对急性胰腺炎临床诊断的意义

目的:探讨尿淀粉酶检测结果对急性胰腺炎临床诊断的意义。方法:选取2011年6月至2012年7月在我院接受治疗的急性胰腺炎患者50例定义为AP组,选取非胰腺炎急腹症患者50例定义为NP组,选取健康人群50例定义为HS组。分别检测三组患者的血淀粉酶(SAMY),尿淀粉酶(UAMY),尿肌酐(UCR)及尿淀粉酶与尿肌酐的比值(UACR),整理并分析检测结果。结果:急性胰腺炎组和非胰腺炎急腹症组的患者的血淀粉酶、尿淀粉酶、尿淀粉酶与尿肌酐的比值均高于健康对照组,组间比较差异显著(P0.05);非胰腺炎急腹症组与健康对照组的尿淀粉酶和尿肌酐比值相比差异不明显(P0.05)。急性胰腺炎组的淀粉酶和尿肌酐比值的敏感性为93.41%,特异性为93%;血清淀粉酶的敏感性为86.7%,特异性为92.2%,均高于临床诊断指标的常用值。结论:急性胰腺炎尿液与尿肌酐比值的测定是早前急性胰腺炎诊断和治疗的重要检测指标。     

早期肠内营养辅助治疗重症胰腺炎的临床疗效分析

目的：探讨早期肠内营养辅助治疗重症胰腺炎的临床效果。方法：选择2009年4月-2012年2月我院收治的重症胰腺炎患者共46例,随机分为实验组和对照组各23例,实验组在综合治疗的基础采用早期肠内营养治疗（EN）,而对照组在综合治疗的基础上采用全胃肠外营养治疗（TPN）,比较两组患者的血清总蛋白、白蛋白、尿素氮水平及血淋巴细胞百分比变化、血淀粉酶和尿淀粉酶恢复正常时间、住院时间及病死率,并比较两组治疗前及治疗后24、48及72小时的APACHEII评分。结果：治疗后,实验组患者的血清总蛋白、白蛋白、尿素氮水平及血淋巴细胞百分比变化均较对照组明显增高,差异有统计学意义（P〈0．05）,而血淀粉酶、尿淀粉酶恢复时间、病死率及住院时间分别均明显较对照组降低或缩短,差异有统计学意义（P〈0．05）。治疗24、48及72小时后,实验组APACHEII评分均较治疗前显著减低（P〈o．05）,而对照组治疗24、48h后APACHEⅡ评分与治疗前比较差异无统计学意义（P〉0．05）,治疗72h后APACHEII评分较治疗前显著减低（P〈O．05）。结论：采用早期肠内营养辅助治疗重症胰腺炎患者能有效保护肠黏膜屏障功能,改善患者的营养状况,增强患者的免疫力,并改善患者的预后。     

Rhein,a Natural Anthraquinone Derivative,Attenuates the Activation of Pancreatic Stellate Cells and Ameliorates Pancreatic Fibrosis in Mice with Experimental Chronic Pancreatitis

Pancreatic fibrosis, a prominent histopathological feature of chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma, is essentially a dynamic process that leads to irreversible scarring of parenchymal tissues of the pancreas. Though the exact mechanisms of its initiation and development are poorly understood, recent studies suggested that the activation of pancreatic stellate cells (PSCs) plays a critical role in eliciting such active course of fibrogenesis. Anthraquinone compounds possess anti-inflammatory bioactivities whereas its natural derivative rhein has been shown to effectively reduce tissue edema and free-radical production in rat models of inflammatory conditions. Apart from its anti-inflammatory properties, rhein actually exerts strong anti-fibrotic effects in our current in-vivo and in-vitro experiments. In the mouse model of cerulein-induced CP, prolonged administration of rhein at 50 mg/kg/day significantly decreased immunoreactivities of the principal fibrotic activators alpha-smooth muscle actin (α-SMA) and transforming growth factor-beta (TGF-β) on pancreatic sections implicating the activation of PSCs, which is the central tread to fibrogenesis, was attenuated. Consequently, the overwhelmed deposition of extracellular matrix proteins fibronectin 1 (FN1) and type I collagen (COL I-α1) in exocrine parenchyma was found accordingly reduced. In addition, the expression levels of sonic hedgehog (SHH), which plays important roles in molecular modulation of various fibrotic processes, and its immediate effector GLI1 in pancreatic tissues were positively correlated to the degree of cerulein-induced fibrosis. Such up-regulation of SHH signaling was restrained in rhein-treated CP mice. In cultured PSCs, we demonstrated that the expression levels of TGF-β-stimulated fibrogenic markers including α-SMA, FN1 and COL I-α1 as well as SHH were all notably suppressed by the application of rhein at 10 μM. The present study firstly reported that rhein attenuates PSC activation and suppresses SHH/GLI1 signaling in pancreatic fibrosis. With strong anti-fibrotic effects provided, rhein can be a potential remedy for fibrotic and/or PSC-related pathologies in the pancreas.