BACKGROUND: Severe acute pancreatitis (SAP) is a commonly seen acute abdominal syndrome characterized by sudden onset, rapid progression and high mortality rate. The damage in peripheral organs may be more severe than...BACKGROUND: Severe acute pancreatitis (SAP) is a commonly seen acute abdominal syndrome characterized by sudden onset, rapid progression and high mortality rate. The damage in peripheral organs may be more severe than that in the pancreas, and can even lead to multiple organ dysfunction. It is critical to recognize early pathological changes in multiple organs. This study aimed to assess the early pathological features of damaged organs in a rat model of SAP. METHODS: Thirty clean grade healthy male Sprague-Dawley rats weighing 250-300 g were randomly divided into a model control group (n=15) and a sham-operated group (n=15). The SAP rat model was induced by sodium taurocholate. Samples of blood and from multiple organs were collected 3 hours after operation. We assessed the levels of IL-6, TNF-alpha, PLA2, NO, ET-1, MDA, amylases and endotoxin in blood and observed the early pathological changes in multiple damaged organs. RESULTS: Levels of IL-6, TNF-alpha, PLA2, NO, ET-1 and MDA in serum and of amylase and endotoxin in plasma of the model control group rats were significantly higher than those of the sham-operated group (P<0.01). Different degrees of pathological change were observed in multiple damaged organs. CONCLUSION: Multiple organ injury may occur at the early stage of SAP in rats.展开更多
目的动态观察清热解毒中药黄芩对流感病毒感染所致小鼠气管、肺组织病理损伤的影响。方法建立流感病毒肺适应株(FM1)感染的肺炎小鼠模型,将96只BALB/c An N小鼠随机分为空白对照组、流感病毒感染模型组、黄芩组。在FM1株感染1、3、5、7...目的动态观察清热解毒中药黄芩对流感病毒感染所致小鼠气管、肺组织病理损伤的影响。方法建立流感病毒肺适应株(FM1)感染的肺炎小鼠模型,将96只BALB/c An N小鼠随机分为空白对照组、流感病毒感染模型组、黄芩组。在FM1株感染1、3、5、7 d,分别采用肉眼观察、光学显微镜、气管电镜扫描动态观察各组小鼠气管、肺组织病理学变化。结果肉眼观察,黄芩组在感染后肺组织充血、水肿,肺门见暗褐色实变区较模型组实变区面积减少。光镜下观察,黄芩组在感染后气管、肺组织病变程度较模型组明显减轻。气管电镜扫描观察,黄芩组气管内壁黏膜完整性、细胞的饱满度、纤毛数量、纤毛排列均好于模型组。结论清热解毒中药黄芩能够显著改善FM1株感染所致小鼠气管、肺组织的炎性病变,对FM1株感染所致小鼠肺组织病理损伤具有较强的修复作用。展开更多
BACKGROUND:The plasma concentration of paraquat is closely related to the prognosis of patients with paraquat toxication,and the most common cause of death from paraquat poisoning is multiple organ failure(MOF).This s...BACKGROUND:The plasma concentration of paraquat is closely related to the prognosis of patients with paraquat toxication,and the most common cause of death from paraquat poisoning is multiple organ failure(MOF).This study aimed to evaluate therapeutic effect of smecta on the plasma concentrations of paraquat and multi-organ injury induced by paraquat intoxication in rats.METHODS:A total of 76 healthy adult SD rats were randomly divided into group A(control group,/7=6),group B(poisoned group,n=30) and group C(smecta-treated group,n=30).Rats in groups B and C were treated intragastrically with PQ at 50 mg/kg,and rats in group A was treated intragastrically with saline(1 ml_).Rats in group C were given intragastrically smecta at 400 mg/kg 10 minutes after administration of PQ,while rats in other two groups were treated intragastrically with 1ml_ saline at the same time.Live rats in groups B and C were sacrificed at 2,6,24,48,72 hours after administration of PQ for the determination of paraquat plasma concentrations and for HE staining of the lung,stomach and jejunum.The rats were executed at the end of trial by the same way in group A.RESULTS:The plasma concentration of paraquat(ng/mL) ranged from 440.314±49.776 to4320.6150±413.947.Distinctive pathological changes were seen in the lung,stomach and jejunum in group B.Lung injuries deteriorated gradually,edema,leukocyte infiltration,pneumorrhagia,incrassated septa and lung consolidation were observed.Abruption of mucosa,hyperemic gastric mucosa and leukocyte infiltration were obvious in the stomach.The hemorrhage of jejunum mucosa,the abruption of villus,the gland damage with the addition of inflammatory cell infiltration were found.Compared to group B,the plasma concentration of paraquat reduced(P<0.01) and the pathological changes mentioned above were obviously alleviated in group C(P<0.05,P<0.01).CONCLUSION:Smecta reduced the plasma concentration of paraquat and alleviated pathologic injury of rats with PQ poisoning.展开更多
Flagellin is a potent activator of a broad range of cell types that are involved in innate and adaptive immunity. Therefore, it is a good adjuvant candidate for vaccines, and it might function as a biological protecta...Flagellin is a potent activator of a broad range of cell types that are involved in innate and adaptive immunity. Therefore, it is a good adjuvant candidate for vaccines, and it might function as a biological protectant against both major acute radiation syndrome during cancer radiotherapy and a mitigator of radiation emergencies. However, accumulating evidence has implicated flagellin in the occurrence of some inflammatory diseases, such as acute lung inflammation, cardiovascular collapse and inflammatory bowel disease. The aim of this study was to elucidate whether only flagellin-TLR5 signaling activation plays a role in the pathophysiology of liver or whether some other flagellin activity also contributes to liver injury either via bacterial infections or during clinical applications. Recombinant flagellin proteins with or without TLR5-stimulating activity were used to evaluate the role of flagellin-TLR5 signaling in liver injury in wild-type and TLR5 KO mice. Gross lesions and large areas of hepatocellular necrosis were observed in liver tissue 12 h after the intraperitoneal administration of 100 or 200 pg flagellin （FliC） in a dose-and time-dependent manner in wild-type mice, but not in TLR5 KO mice. Deletion of the N-terminal or TLR5 binding domain of flagellin inhibited flagellin-induced inflammatory responses and the subsequent acute liver function abnormality and damage. These data confirmed that flagellin is an essential determinant of liver injury and demonstrated that the over-activation of TLR5 signaling by high-dose flagellin caused acute inflammatory responses, neutrophil accumulation and oxidative stress in the liver, which contributes to the progression and severity of flagellin-induced liver injury.展开更多
BACKGROUND: Remote organ failure occurs in cases of acute pancreatitis (AP); however, the reports on AP induced by pancreatic duct obstruction are rare. In this study we determined the effect of L-cysteine on pancreat...BACKGROUND: Remote organ failure occurs in cases of acute pancreatitis (AP); however, the reports on AP induced by pancreatic duct obstruction are rare. In this study we determined the effect of L-cysteine on pancreaticobiliary inflammation and remote organ damage in rats after pancreaticobiliary duct ligation (PBDL). METHODS: AP was induced by PBDL in rats with 5/0 silk Sixty rats were randomly divided into 4 groups. Groups A and B were sham-operated groups that received injections of saline or L-cysteine (10 mg/kg) intraperitoneally (15 rats in each group). Groups C and D were PBDL groups that received injections of saline or L-cysteine (10 mg/kg) intraperitoneally (15 rats in each group). The tissue samples of the pancreas and remote organs such as the lung, liver, intestine and kidney were subsequently examined for pathological changes under a light microscope. The samples were also stored for the determination of malondialdehyde and glutathione levels. Blood urea nitrogen (BUN), plasma amylase, ALT and AST levels were determined spectrophotometrically using an automated analyzer. Also, we evaluated the effect of L-cysteine on remote organ injury in rats with AP induced by retrograde infusion of 3.5% sodium taurocholate (NaTc) into the bile-pancreatic duct. RESULTS: Varying degrees of injury in the pancreas, lung, liver intestine and kidney were observed in the rats 24 hours after PBDL. The severity of injury to the lung, liver and intestine was attenuated, while injury status was not changed significantly in the pancreas and kidney after L-cysteine treatment. Oxidativestress was also affected by L-cysteine in PBDL-treated rats. The concentration of tissue malondialdehyde decreased in the pancreas and remote organs of PBDL and L-cysteine administrated rats, and the concentration of glutathione increased more significantly than that of the model control group. However, L-cysteine administration reduced the severity of injury in remote organs but not in the pancreas in rats with NaTc-induced AP. CONCLUSION: L-c展开更多
基金supported by grants from the Intensive Foundation Project for Technology of Hangzhou (2004Z006)
文摘BACKGROUND: Severe acute pancreatitis (SAP) is a commonly seen acute abdominal syndrome characterized by sudden onset, rapid progression and high mortality rate. The damage in peripheral organs may be more severe than that in the pancreas, and can even lead to multiple organ dysfunction. It is critical to recognize early pathological changes in multiple organs. This study aimed to assess the early pathological features of damaged organs in a rat model of SAP. METHODS: Thirty clean grade healthy male Sprague-Dawley rats weighing 250-300 g were randomly divided into a model control group (n=15) and a sham-operated group (n=15). The SAP rat model was induced by sodium taurocholate. Samples of blood and from multiple organs were collected 3 hours after operation. We assessed the levels of IL-6, TNF-alpha, PLA2, NO, ET-1, MDA, amylases and endotoxin in blood and observed the early pathological changes in multiple damaged organs. RESULTS: Levels of IL-6, TNF-alpha, PLA2, NO, ET-1 and MDA in serum and of amylase and endotoxin in plasma of the model control group rats were significantly higher than those of the sham-operated group (P<0.01). Different degrees of pathological change were observed in multiple damaged organs. CONCLUSION: Multiple organ injury may occur at the early stage of SAP in rats.
文摘目的动态观察清热解毒中药黄芩对流感病毒感染所致小鼠气管、肺组织病理损伤的影响。方法建立流感病毒肺适应株(FM1)感染的肺炎小鼠模型,将96只BALB/c An N小鼠随机分为空白对照组、流感病毒感染模型组、黄芩组。在FM1株感染1、3、5、7 d,分别采用肉眼观察、光学显微镜、气管电镜扫描动态观察各组小鼠气管、肺组织病理学变化。结果肉眼观察,黄芩组在感染后肺组织充血、水肿,肺门见暗褐色实变区较模型组实变区面积减少。光镜下观察,黄芩组在感染后气管、肺组织病变程度较模型组明显减轻。气管电镜扫描观察,黄芩组气管内壁黏膜完整性、细胞的饱满度、纤毛数量、纤毛排列均好于模型组。结论清热解毒中药黄芩能够显著改善FM1株感染所致小鼠气管、肺组织的炎性病变,对FM1株感染所致小鼠肺组织病理损伤具有较强的修复作用。
文摘BACKGROUND:The plasma concentration of paraquat is closely related to the prognosis of patients with paraquat toxication,and the most common cause of death from paraquat poisoning is multiple organ failure(MOF).This study aimed to evaluate therapeutic effect of smecta on the plasma concentrations of paraquat and multi-organ injury induced by paraquat intoxication in rats.METHODS:A total of 76 healthy adult SD rats were randomly divided into group A(control group,/7=6),group B(poisoned group,n=30) and group C(smecta-treated group,n=30).Rats in groups B and C were treated intragastrically with PQ at 50 mg/kg,and rats in group A was treated intragastrically with saline(1 ml_).Rats in group C were given intragastrically smecta at 400 mg/kg 10 minutes after administration of PQ,while rats in other two groups were treated intragastrically with 1ml_ saline at the same time.Live rats in groups B and C were sacrificed at 2,6,24,48,72 hours after administration of PQ for the determination of paraquat plasma concentrations and for HE staining of the lung,stomach and jejunum.The rats were executed at the end of trial by the same way in group A.RESULTS:The plasma concentration of paraquat(ng/mL) ranged from 440.314±49.776 to4320.6150±413.947.Distinctive pathological changes were seen in the lung,stomach and jejunum in group B.Lung injuries deteriorated gradually,edema,leukocyte infiltration,pneumorrhagia,incrassated septa and lung consolidation were observed.Abruption of mucosa,hyperemic gastric mucosa and leukocyte infiltration were obvious in the stomach.The hemorrhage of jejunum mucosa,the abruption of villus,the gland damage with the addition of inflammatory cell infiltration were found.Compared to group B,the plasma concentration of paraquat reduced(P<0.01) and the pathological changes mentioned above were obviously alleviated in group C(P<0.05,P<0.01).CONCLUSION:Smecta reduced the plasma concentration of paraquat and alleviated pathologic injury of rats with PQ poisoning.
基金This work was financially supported by the National S＆T Major Project on Major Infectious Diseases （Grant 2012ZX10001-008 and 2008ZX10001-010）, the National Basic Research Program of China （973 Program） （Grant 2012CB518904） from the Ministry of Science and Technology of the People＇s Republic of China, and the National Natural Science Foundation of China （Grant 81202381）. We sincerely thank Dr George Dacai Liu for his critical comments and revision of the article. We are thankful to the Core Facility and Technical Support, Wuhan Institute of Virology and Xuefang An for valuable assistance in the animal studies, as well as Ying Sun, Rong Bao and Benxia He for their help with the sample collection.
文摘Flagellin is a potent activator of a broad range of cell types that are involved in innate and adaptive immunity. Therefore, it is a good adjuvant candidate for vaccines, and it might function as a biological protectant against both major acute radiation syndrome during cancer radiotherapy and a mitigator of radiation emergencies. However, accumulating evidence has implicated flagellin in the occurrence of some inflammatory diseases, such as acute lung inflammation, cardiovascular collapse and inflammatory bowel disease. The aim of this study was to elucidate whether only flagellin-TLR5 signaling activation plays a role in the pathophysiology of liver or whether some other flagellin activity also contributes to liver injury either via bacterial infections or during clinical applications. Recombinant flagellin proteins with or without TLR5-stimulating activity were used to evaluate the role of flagellin-TLR5 signaling in liver injury in wild-type and TLR5 KO mice. Gross lesions and large areas of hepatocellular necrosis were observed in liver tissue 12 h after the intraperitoneal administration of 100 or 200 pg flagellin （FliC） in a dose-and time-dependent manner in wild-type mice, but not in TLR5 KO mice. Deletion of the N-terminal or TLR5 binding domain of flagellin inhibited flagellin-induced inflammatory responses and the subsequent acute liver function abnormality and damage. These data confirmed that flagellin is an essential determinant of liver injury and demonstrated that the over-activation of TLR5 signaling by high-dose flagellin caused acute inflammatory responses, neutrophil accumulation and oxidative stress in the liver, which contributes to the progression and severity of flagellin-induced liver injury.
基金supported by grants from the National Natural Science Foundation of China(30971359)the Shanghai Key Laboratory of Pancreatic Diseases for open research project(P2012001)
文摘BACKGROUND: Remote organ failure occurs in cases of acute pancreatitis (AP); however, the reports on AP induced by pancreatic duct obstruction are rare. In this study we determined the effect of L-cysteine on pancreaticobiliary inflammation and remote organ damage in rats after pancreaticobiliary duct ligation (PBDL). METHODS: AP was induced by PBDL in rats with 5/0 silk Sixty rats were randomly divided into 4 groups. Groups A and B were sham-operated groups that received injections of saline or L-cysteine (10 mg/kg) intraperitoneally (15 rats in each group). Groups C and D were PBDL groups that received injections of saline or L-cysteine (10 mg/kg) intraperitoneally (15 rats in each group). The tissue samples of the pancreas and remote organs such as the lung, liver, intestine and kidney were subsequently examined for pathological changes under a light microscope. The samples were also stored for the determination of malondialdehyde and glutathione levels. Blood urea nitrogen (BUN), plasma amylase, ALT and AST levels were determined spectrophotometrically using an automated analyzer. Also, we evaluated the effect of L-cysteine on remote organ injury in rats with AP induced by retrograde infusion of 3.5% sodium taurocholate (NaTc) into the bile-pancreatic duct. RESULTS: Varying degrees of injury in the pancreas, lung, liver intestine and kidney were observed in the rats 24 hours after PBDL. The severity of injury to the lung, liver and intestine was attenuated, while injury status was not changed significantly in the pancreas and kidney after L-cysteine treatment. Oxidativestress was also affected by L-cysteine in PBDL-treated rats. The concentration of tissue malondialdehyde decreased in the pancreas and remote organs of PBDL and L-cysteine administrated rats, and the concentration of glutathione increased more significantly than that of the model control group. However, L-cysteine administration reduced the severity of injury in remote organs but not in the pancreas in rats with NaTc-induced AP. CONCLUSION: L-c
