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| 1 | Pathogenic mechanisms of pancreatitis显示文摘Pancreatitis is inflammation of pancreas and caused by a number of factors including pancreatic duct obstruction, alcoholism, and mutation in the cationic trypsinogen gene. Pancreatitis is represented as acute pancreatitis with acute inflammatory responses and; chronic pan-creatitis characterized by marked stroma formation with a high number of infiltrating granulocytes(such as neutrophils, eosinophils), monocytes, macrophages and pancreatic stellate cells(PSCs). These inflammatory cells are known to play a central role in initiating and promoting inflammation including pancreatic fibrosis, i.e., a major risk factor for pancreatic cancer. A number of inflammatory cytokines are known to involve in pro-moting pancreatic pathogenesis that lead pancreatic fibrosis. Pancreatic fibrosis is a dynamic phenomenon that requires an intricate network of several autocrine and paracrine signaling pathways. In this review, we have provided the details of various cytokines and molecular mechanistic pathways(i.e., Transforming growth factor-β/SMAD, mitogen--activated protein kinases, Rho kinase, Janus kinase/signal transducers and activators, and phosphatidylinositol 3 kinase) that have a critical role in the activation of PSCs to promote chronic pancreatitis and trigger the phenomenon of pancreatic fibrogenesis. In this review of literature, we discuss the involvement of several pro-inflammatory and anti-inflammatory cytokines, such as in interleukin(IL)-1, IL-1β, IL-6, IL--8 IL-10, IL-18, IL--33 and tumor necrosis factor-α, in the pathogenesis of disease. Our review also highlights the significance of several experimental animal models that have an important role in dissecting the mechanistic pathways operating in the development of chronic pancreatitis, including pancreatic fibrosis. Additionally, we provided several intermediary molecules that are involved in major signaling pathways that might provide target molecules for future therapeutic treatment strategies for pancreatic pathogenesis. | Murli Manohar Alok Kumar Verma Sathisha Upparahalli Venkateshaiah Nathan L Sanders Anil Mishra | 2017 | World Journal of Gastrointestinal Pharmacology and Therapeutics2017，8，1： | 21 |
| 2 | 急性胰腺炎肝损伤的发病机制和治疗显示文摘急性胰腺炎(acute pancreatitis,AP)是临床常见的急腹症,常常引起胰外器官损伤,肝脏是主要受损器官之一,其损害的不断加重可导致胰腺炎病情恶化,目前认为肝脏损伤的机制主要有细胞因子、胰酶、氧化应激、微循环障碍、细胞凋亡和胰腺炎相关性腹水等.目前AP肝损伤的治疗也主要从上述各方面着手,但更多的方法仍仅仅局限于动物实验,临床应用还需进一步研究. | 于洪海 冯志杰 | 2008 | 世界华人消化杂志2008，16，4： | 14 |
| 3 | Clinical Observation on the Effect of Dexamethasone and Chinese Herbal Decoction for Purgation in Severe Acute Pancreatitis Patients显示文摘Objective:To investigate the effect of dexamethasone(Dx) combined with modified Dachengqi Decoction(大承气汤,DCQD),a Chinese herbal decoction for purgation,on patients with severe acute pancreatitis(SAP) accompanied with systematic inflammatory response syndrome(SIRS).Methods:A total of 81 patients diagnosed as SAP were randomly assigned to a control group or treatment group according to a random number table generated from an SPSS software.The patients in the control group(38 cases) received standard treatment and Chinese herbal decoction for purgation;those in the treatment group(43 cases) received additional 1 mg/(kg·d) dexamethasone(Dx) treatment for three days based on the above treatment.The mortality rate,acute respiratory distress syndrome(ARDS),renal failure,hemorrhage,sepsis,pancreatic pseudocyst, pancreatic abscess,operability,and days of hospitalization were compared between the two groups.Results: Three patients in the control group and eight patients in the treatment group dropped out from the study with a drop-out rate of 7.8%and 18.6%,respectively,and no statistics difference was shown between the two groups (P>0.05).Dx treatment significantly reduced ARDS rate and shortened the length of hospitalization compared to those in the control group(7/35,20.0%versus 15/35,42.9%,P=0.0394;32.5±13.2 days versus 40.2±17.5 days,P=0.0344).Other parameters including the mortality rate were not significant different between the two groups.Conclusion:Dx combined with DCQD could decrease the risk of developing ARDS in SAP patients with SIRS and shorten their length of hospitalization. | 万美华 李娟 龚翰林 薛平 朱林 陈光远 夏庆 唐文富 | 2011 | Chinese Journal of Integrative Medicine2011，17，3： | 10 |
| 4 | 糖皮质激素受体在大鼠重症胰腺炎中的表达变化及甲强龙冲击治疗后的影响显示文摘目的了解糖皮质激素受体在大鼠重症胰腺炎中的表达变化情况,观察早期大剂量甲基强的松龙冲击治疗后对大鼠重症胰腺炎的治疗作用。方法 72只SD大鼠[(300±50)g]随机分成生理盐水组(NS组)、重症胰腺炎组(SAP组)、重症胰腺炎甲强龙治疗组(MES组),每组24只,三组再各分为6h、12h、24h三个时间点,每个时间点8只,通过腹腔内注射L-精氨酸(320mg/100g)制作大鼠重症胰腺炎模型,观察各时间点血清淀粉酶、胰腺湿\干值、胰腺病理变化及糖皮质激素受体变化。结果 SAP组较NS组在6h、12h、24h三个时间点的血清淀粉酶、胰腺湿干比率、胰腺病理评分均显著升高(P(0.01),糖皮质激素受体水平明显下降(P(0.01);而MES组较SAP组在6h、12h、24h三个时间点的血清淀粉酶、胰腺湿干比率、胰腺病理评分均显著降低,糖皮质激素受体水平明显升高。结论重症胰腺炎早期糖皮质激素受体水平下降,早期大剂量的使用甲强龙能有效的减轻炎症反应,改善病理损伤,有效的提高糖皮质激素受体水平。 | 李树生 熊建平 曾永明 王维刚 陈少锋 | 2010 | 海南医学2010，21，13： | 2 |
| 5 | 早期大剂量甲强龙冲击治疗对大鼠重症急性胰腺炎的影响显示文摘目的观察早期大剂量甲强龙冲击治疗对大鼠重症急性胰腺炎(SAP)炎症变化以及胰腺组织内T淋巴细胞浸润情况的影响。方法通过腹腔内注射L-精氨酸(320mg/100g)制作大鼠重症胰腺炎模型,96只雄性SD大鼠随机分成正常对照组(NS组,n=32),重症急性胰腺炎组(SAP组,n=32),重症胰腺炎甲基强地松龙治疗组(MES组,n=32),观察SAP模型后6h、12h、24h、72h胰腺湿干比重、血清淀粉酶以及胰腺CD3+、CIM+、CD8+T淋巴细胞及CD4+/CD8+比值变化水平。另外3组各取15只SD大鼠观察72h病死率。结果SAP组较NS组各时段72h病死率、血清淀粉酶、胰腺湿干比,而胰腺CD3+、CD4+、CD8+T淋巴细胞百分数及CD4/CD8比值明显降低,MES组较SAP组各时段胰腺湿干比、血清淀粉酶明显降低,CD3+、CD4+、CD8+T淋巴细胞百分数及CD4/CD8比值有所降低,但差异无统计学意义。结论早期大剂量甲强龙冲击治疗重症急性胰腺炎对降低病死率,改善胰腺炎炎性介质反应具有明显作用,对内毒素水平、胰腺免疫功能影响无统计学意义。 | 李树生 熊建平 曾永明 王维刚 陈少锋 | 2010 | 国际外科学杂志2010，37，4： | 1 |
| 6 | 早期小剂量甲强龙治疗重症急性胰腺炎应用价值显示文摘目的探讨早期小剂量使用甲强龙治疗重症急性胰腺炎(SAP)应用价值。方法回顾性分析桂林市人民医院2002年1月至2010年6月在治疗的重症急性胰腺炎患者115例,分为研究组和对照组,两组患者在入院后均予采用重症急性胰腺炎常规综合治疗方案基础上予研究组早期注射甲强龙80mg/d,连续给药2~7d后停药,观察两组多个衡量SAP治疗效果的主要指标的差异。结果研究组在腹痛腹胀缓解时间、血淀粉酶恢复正常时间、血常规白细胞恢复正常时间、腹腔积液消退时间、出现急性肺损伤(ALI)及急性呼吸窘迫综合征(ARDS)等并发症比例、死亡率及平均住院日等衡量SAP治疗效果的主要指标均有明显改善。结论早期小剂量使用甲强龙治疗重症急性胰腺炎效果确定,值得推广。 | 廖日斌 唐建光 潘旻 苏燕波 刘晓敏 | 2011 | 医药论坛杂志2011，32，14： | 0 |
| 7 | 白细胞黏附分子与急性胰腺炎研究进展显示文摘 | 杨国溜 王立 | 2010 | 重庆医学2010，39，21： | 0 |
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