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| 1 | Ellagic acid induces apoptosis through inhibition of nuclear factor κB in pancreatic cancer cells显示文摘AIM:To determine the effect of ellagic acid on apop-tosis and proliferation in pancreatic cancer cells and to determine the mechanism of the pro-survival effects of ellagic acid. METHODS:The effect of ellagic acid on apoptosis was assessed by measuring Phosphatidylserine externalization,caspase activity,mitochondrial membrane potential and DNA fragmentation;and proliferation by measuring DNA thymidine incorporation. Mitochondrial membrane potential was measured in permeabilized cells,and in isolated mitochondria. Nuclear factor kB(NF-kB) activity was measured by electromobility shift assay(EMSA) . RESULTS:We show that ellagic acid,a polyphenolic compound in fruits and berries,at concentrations 10 to 50 mmol/L stimulates apoptosis in human pancreatic adenocarcinoma cells. Further,ellagic acid decreases proliferation by up to 20-fold at 50 mmol/L. Ellagic acid stimulates the mitochondrial pathway of apoptosis associated with mitochondrial depolarization,cytochrome C release,and the downstream caspaseactivation. Ellagic acid does not directly affect mitochondria. Ellagic acid dose-dependently decreased NF-kB binding activity. Furthermore,inhibition of NF-kB activity using IkB wild type plasmid prevented the effect of ellagic acid on apoptosis. CONCLUSION:Our data indicate that ellagic acid stimulates apoptosis through inhibition of the prosu-rvival transcription factor NF-kB. | Mouad Edderkaoui Irina Odinokova Izumi Ohno Ilya Gukovsky Vay Liang W Go Stephen J Pandol Anna S Gukovskaya | 2008 | World Journal of Gastroenterology2008，14，23： | 30 |
| 2 | XIAP抑制剂Embelin体外对人胰腺癌细胞株的抑制效应与机制研究显示文摘目的探讨XIAP小分子抑制剂Embelin体外对人胰腺癌细胞株MIAPaCa-2的抑制效应与机制。方法将生长至第4-12代之间的MIAPaca-2细胞分为DMSO对照组与Embelin实验组,在实验组细胞中加入不同浓度的Embelin共孵育72h,收集细胞并裂解后取上清液用细胞凋亡试剂盒检测组蛋白(凋亡指标)的OD值水平。MIAPaca-2细胞加入不同浓度的Embelin共孵育60h后再加入3H胸腺嘧啶继续孵育12h,取细胞裂解液用同位素γ闪烁计数仪检测3H-CPM数值以判断细胞增殖程度。对DMSO对照组与Embelin实验组的组蛋白OD值与3H-CPM数值分别进行比较分析。结果Embelin实验组的MIAPaCa-2细胞株组蛋白OD值显著高于DMSO对照组而3H-CPM数值明显低于DMSO对照组(P<0.01),且实验组Embe-lin的作用浓度与组蛋白OD值呈正相关(r=0.996,P<0.01),而与3H-CPM数值呈负相关(r=-0.993,P<0.01)。结论Embelin呈剂量依赖性地诱导人胰腺癌细胞株MIAPaCa-2凋亡并抑制其增殖,有肿瘤抑制效应。 | 郑玲 吕寒静 Mouad Edderkaoui Stephen J Pandol | 2009 | 山西医科大学学报2009，40，1： | 4 |
| 3 | Alcoholic hepatitis: The pivotal role of Kupffer cells显示文摘Kupffer cells play a central role in the pathogenesis of alcoholic hepatitis(AH). It is believed that alcohol increases the gut permeability that results in raised levels of serum endotoxins containing lipopolysaccharides(LPS). LPS binds to LPS-binding proteins and presents it to a membrane glycoprotein called CD14, which then activates Kupffer cells via a receptor called tolllike receptor 4. This endotoxin mediated activation of Kupffer cells plays an important role in the inflammatory process resulting in alcoholic hepatitis. There is no effective treatment for AH, although notable progress has been made over the last decade in understanding the underlying mechanism of alcoholic hepatitis. We specifically review the current research on the role of Kupffer cells in the pathogenesis of AH and the treatment strategies. We suggest that the imbalance between the pro-inflammatory and the anti-inflammatory process as well as the increased production of reactive oxygen species eventually lead to hepatocyte injury, the final event of alcoholic hepatitis. | Duminda B Suraweera Ashley N Weeratunga Robert W Hu Stephen J Pandol Richard Hu | 2015 | World Journal of Gastrointestinal Pathophysiology2015，6，4： | 3 |
| 4 | Impaired autophagic flux mediates acinar cell vacuole formation and trypsinogen activation in rodent models of acute pancreatitis显示文摘 | Mareninova Olga A Hermann Kip French Samuel W O’Konski Mark S Pandol Stephen J Webster Paul Erickson Ann H Katunuma Nobuhiko Gorelick Fred S Gukovsky Ilya Gukovskaya Anna S | 2009 | Journal of Clinical Investigation2009，，11： | 1 |
| 5 | Extracellular matrix proteins protect pancreatic cancer cells from death via mitochondrial and nonmitochondrial pathways显示文摘 | Eva C Vaquero Mouad Edderkaoui Kyung J Nam Ilya Gukovsky Stephen J Pandol Anna S Gukovskaya | 2003 | Gastroenterology2003，，4： | 1 |
| 6 | Idiopathic chronic pancreatitis:Beyond antioxidants显示文摘Chronic pancreatitis(CP)is a complex disease associated with gene-gene or geneenvironment interactions.The incidence of idiopathic CP has shown an increasing trend,withits phenotypeshaving changed considerably in the last two decades.The diseaseitself can be regulated before it reaches the stage of established CP;however,the etiopathogenesis underlying idiopathic CP remains to be established,making the condition difficult to cure.Unfortunately,there also remains a lack of consensus regarding the beneficial effects of antioxidant therapiesfor CP.It is known that antioxidant therapy does not reduce inflammatory and fibrotic cytokines,making it unlikely that they could modulate the disease process.Although antioxidants are safe,very few studies to date have reported the long-term beneficial effects in patients with CP.Thus,studies are being performed to identify drugs that can improve symptoms and alter the natural history of CP.Statins,with their numerous pleiotropic effects,may play a role in the treatment of CP,butin 2006,their use was found to be associated with the undesirable side effect of promoting pancreatitis.Latter studies showed favourable effects of statins in CP,highlighting the particular benefits of lipophilic statins,such as lovastatin and simvastatin,over the hydrophilic statins,such as rosuvastatin.Ultimately,studies to repurpose N-acetylcysteine as a CP therapy areyielding very promising results. | Rajiv M Mehta Stephen J Pandol Prachi R Joshi | 2021 | World Journal of Gastroenterology2021，27，43： | 0 |
| 7 | Epidemiologic risk factors for patients admitted with chronic pancreatitis and pancreatic ductal adenocarcinoma in the United States显示文摘BACKGROUND Epidemiological studies of chronic pancreatitis(CP)and its association with pancreatic ductal adenocarcinoma(PDAC)are limited.Understanding demographic and ethno-racial factors may help identify patients at the highest risk for CP and PDAC.AIM To evaluate the ethno-racial risk factors for CP and its association with PDAC.The secondary aim was to evaluate hospitalization outcomes in patients admitted with CP and PDAC.METHODS This retrospective cohort study used the 2016 and 2017 National Inpatient Sample databases.Patients included in the study had ICD-10 codes for CP and PDAC.The ethnic,socioeconomic,and racial backgrounds of patients with CP and PDAC were analyzed.RESULTS Hospital admissions for CP was 29 per 100000,and 2890(0.78%)had PDAC.Blacks[adjusted odds ratio(aOR)1.13],men(aOR 1.35),age 40 to 59(aOR 2.60),and being overweight(aOR 1.34)were significantly associated with CP(all with P<0.01).In patients with CP,Whites(aOR 1.23),higher income,older age(aOR 1.05),and being overweight(aOR 2.40)were all significantly associated with PDAC(all with P<0.01).Men(aOR 1.81)and Asians(aOR 15.19)had significantly increased mortality(P<0.05).Hispanics had significantly increased hospital length of stay(aOR 5.24)(P<0.05).CONCLUSION Based on this large,nationwide analysis,black men between 40-59 years old and overweight are at significantly increased risk for admission with CP.White men older than 40 years old and overweight with higher income were found to have significant associations with CP and PDAC.This discrepancy may reflect underlying differences in healthcare access and utilization among different socioeconomic and ethno-racial groups. | Daniel Lew Fatima Kamal Khiem Phan Karamvir Randhawa Sam Cornwell Ayrton I Bangolo Simcha Weissman Stephen J Pandol | 2022 | World Journal of Clinical Oncology2022，13，11： | 0 |
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