AIM:To evaluate the inhibitory effects of Scolopendra subspinipes mutilans(SSM) on cerulein-induced acute pancreatitis(AP) in a mouse model.METHODS:SSM water extract(0.1,0.5,or 1 g/kg) was administrated intraperitonea...AIM:To evaluate the inhibitory effects of Scolopendra subspinipes mutilans(SSM) on cerulein-induced acute pancreatitis(AP) in a mouse model.METHODS:SSM water extract(0.1,0.5,or 1 g/kg) was administrated intraperitoneally 1 h prior to the first injection of cerulein.Once AP developed,the stable cholecystokinin analogue,cerulein was injected hourly,over a 6 h period.Blood samples were taken 6 h later to determine serum amylase,lipase,and cytokine levels.The pancreas and lungs were rapidly removed for morphological examination,myeloperoxidase assay,and real-time reverse transcription polymerase chain reaction.To specify the role of SSM in pancreatitis,the pancreatic acinar cells were isolated using collagenase method.Then the cells were pre-treated with SSM,then stimulated with cerulein.The cell viability,cytokine productions and high-mobility group box protein-1(HMGB-1) were measured.Furthermore,the regulating mechanisms of SSM action were evaluated.RESULTS:The administration of SSM significantly attenuated the severity of pancreatitis and pancreatitis associated lung injury,as was shown by the reduction in pancreatic edema,neutrophil infiltration,vacuolization and necrosis.SSM treatment also reduced pancreatic weight/body weight ratio,serum amylase,lipase and cytokine levels,and mRNA expression of multiple inflammatory mediators such as tumor necrosis factor-α and interleukin-1β.In addition,treatment with SSM inhibited HMGB-1 expression in the pancreas during AP.In accordance with in vivo data,SSM inhibited the cerulein-induced acinar cell death,cytokine,and HMGB-1 release.SSM also inhibited the activation of c-Jun NH2-terminal kinase,p38 and nuclear factor(NF)-κB.CONCLUSION:These results suggest that SSM plays a protective role during the development of AP and pancreatitis associated lung injury via deactivating c-Jun NH2-terminal kinase,p38 and NF-κB.展开更多
糖尿病视网膜病变(diabetic retinopathy,DR)是由糖尿病所导致的最典型的微血管并发症之一。以往DR发病机制和治疗的研究主要集中在微血管;近年来,许多学者认为DR不仅仅是一种微血管病变,而且还伴有视网膜神经退行性变。近期研究表明,...糖尿病视网膜病变(diabetic retinopathy,DR)是由糖尿病所导致的最典型的微血管并发症之一。以往DR发病机制和治疗的研究主要集中在微血管;近年来,许多学者认为DR不仅仅是一种微血管病变,而且还伴有视网膜神经退行性变。近期研究表明,自噬与高迁移率族蛋白B1(high mobility group box protein 1,HMGB1)通过多条通路参与到糖尿病视网膜微血管病变和神经退行性变中,通过调控自噬或HMGB1可能为DR治疗提供一种新的思路。本文就自噬与HMGB1在糖尿病视网膜微血管病变和神经退行性变发病中的研究进展进行综述。展开更多
目的:探讨延迟的丙酮酸乙酯(EP)治疗对重症急性胰腺炎(SAP)大鼠血清高迁移率族蛋白1(HMGB1)水平和胰外脏器损伤的影响.方法:96只大鼠随机分为3组,假手术组(Sham组,n=32)、重症急性胰腺炎组(SAP组,n= 32)和丙酮酸乙酯延迟治疗组(EP组,n=3...目的:探讨延迟的丙酮酸乙酯(EP)治疗对重症急性胰腺炎(SAP)大鼠血清高迁移率族蛋白1(HMGB1)水平和胰外脏器损伤的影响.方法:96只大鼠随机分为3组,假手术组(Sham组,n=32)、重症急性胰腺炎组(SAP组,n= 32)和丙酮酸乙酯延迟治疗组(EP组,n=32),采用胰胆管逆行灌注人工胆汁的方法复制大鼠SAP模型.EP组建模12,18,30h分别尾静脉注射1次EP溶液30 mg/kg.建模后24和48h处死动物取材,取血清检测HMGB1水平及肝肾功能生化指标,取肺组织用于肺损伤检测.结果:延迟的EP治疗能有效降低SAP大鼠血清HMGB1水平.EP组血清丙氨酸转氨酶(ALT, 446±91 IU/L vs 53±98 IU/L.P<0.01)、天冬氨酸转氨酶(AS T.667±103 IU/L vs 1368±271 IU/L,P<0.01)、尿素氮(BUN,38±4 mg/ dL vs 41±4 mg/dL,P=0.05)和肌酐(Cr,1.2±0.3 mg/dL vs 1.8±0.3 mg/dL,P<0.01)水平以及肺湿/干比(8.22±0.42 vs 9.76±0.45,P<0.01)和组织学评分(7.1±0.7 vs 8.4±1.1,P<0.01)均明显低于SAP组.结论:延迟的EP治疗通过下调血清HMGB1水平减轻SAP大鼠胰外脏器损伤.EP可能是SAP患者抗炎治疗和脏器功能保护的有效选择.展开更多
基金Supported by National Research Foundation of Korea grant funded by the Korea government MEST,No. 2010-0029498
文摘AIM:To evaluate the inhibitory effects of Scolopendra subspinipes mutilans(SSM) on cerulein-induced acute pancreatitis(AP) in a mouse model.METHODS:SSM water extract(0.1,0.5,or 1 g/kg) was administrated intraperitoneally 1 h prior to the first injection of cerulein.Once AP developed,the stable cholecystokinin analogue,cerulein was injected hourly,over a 6 h period.Blood samples were taken 6 h later to determine serum amylase,lipase,and cytokine levels.The pancreas and lungs were rapidly removed for morphological examination,myeloperoxidase assay,and real-time reverse transcription polymerase chain reaction.To specify the role of SSM in pancreatitis,the pancreatic acinar cells were isolated using collagenase method.Then the cells were pre-treated with SSM,then stimulated with cerulein.The cell viability,cytokine productions and high-mobility group box protein-1(HMGB-1) were measured.Furthermore,the regulating mechanisms of SSM action were evaluated.RESULTS:The administration of SSM significantly attenuated the severity of pancreatitis and pancreatitis associated lung injury,as was shown by the reduction in pancreatic edema,neutrophil infiltration,vacuolization and necrosis.SSM treatment also reduced pancreatic weight/body weight ratio,serum amylase,lipase and cytokine levels,and mRNA expression of multiple inflammatory mediators such as tumor necrosis factor-α and interleukin-1β.In addition,treatment with SSM inhibited HMGB-1 expression in the pancreas during AP.In accordance with in vivo data,SSM inhibited the cerulein-induced acinar cell death,cytokine,and HMGB-1 release.SSM also inhibited the activation of c-Jun NH2-terminal kinase,p38 and nuclear factor(NF)-κB.CONCLUSION:These results suggest that SSM plays a protective role during the development of AP and pancreatitis associated lung injury via deactivating c-Jun NH2-terminal kinase,p38 and NF-κB.
文摘糖尿病视网膜病变(diabetic retinopathy,DR)是由糖尿病所导致的最典型的微血管并发症之一。以往DR发病机制和治疗的研究主要集中在微血管;近年来,许多学者认为DR不仅仅是一种微血管病变,而且还伴有视网膜神经退行性变。近期研究表明,自噬与高迁移率族蛋白B1(high mobility group box protein 1,HMGB1)通过多条通路参与到糖尿病视网膜微血管病变和神经退行性变中,通过调控自噬或HMGB1可能为DR治疗提供一种新的思路。本文就自噬与HMGB1在糖尿病视网膜微血管病变和神经退行性变发病中的研究进展进行综述。
文摘目的:探讨延迟的丙酮酸乙酯(EP)治疗对重症急性胰腺炎(SAP)大鼠血清高迁移率族蛋白1(HMGB1)水平和胰外脏器损伤的影响.方法:96只大鼠随机分为3组,假手术组(Sham组,n=32)、重症急性胰腺炎组(SAP组,n= 32)和丙酮酸乙酯延迟治疗组(EP组,n=32),采用胰胆管逆行灌注人工胆汁的方法复制大鼠SAP模型.EP组建模12,18,30h分别尾静脉注射1次EP溶液30 mg/kg.建模后24和48h处死动物取材,取血清检测HMGB1水平及肝肾功能生化指标,取肺组织用于肺损伤检测.结果:延迟的EP治疗能有效降低SAP大鼠血清HMGB1水平.EP组血清丙氨酸转氨酶(ALT, 446±91 IU/L vs 53±98 IU/L.P<0.01)、天冬氨酸转氨酶(AS T.667±103 IU/L vs 1368±271 IU/L,P<0.01)、尿素氮(BUN,38±4 mg/ dL vs 41±4 mg/dL,P=0.05)和肌酐(Cr,1.2±0.3 mg/dL vs 1.8±0.3 mg/dL,P<0.01)水平以及肺湿/干比(8.22±0.42 vs 9.76±0.45,P<0.01)和组织学评分(7.1±0.7 vs 8.4±1.1,P<0.01)均明显低于SAP组.结论:延迟的EP治疗通过下调血清HMGB1水平减轻SAP大鼠胰外脏器损伤.EP可能是SAP患者抗炎治疗和脏器功能保护的有效选择.
