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ObjectiveTo investigate the risk factors for open pancreatic necrosectomy (OPN), an effective treatment method for severe acute pancreatitis (SAP) after the failure of percutaneous catheter drainage (PCD), in patients with SAP. MethodsA retrospective analysis was performed for 156 patients with SAP who underwent surgical intervention based on the step-up approach in The Affiliated Hospital of Zunyi Medical University from January 1, 2010 to June 30, 2018, and according to whether OPN was performed, the patients were divided into PCD group with 126 patients and PCD+OPN group with 30 patients. Related clinical data were collected, including age, sex, etiology, blood calcium on admission, white blood cell count on admission, whether CTSI score was ＞7, APACHE-Ⅱ score, Ranson score, presence or absence of peripancreatic fluid accumulation, presence or absence of infection, presence or absence of multiple organ failure (MOF), and whether PCD was performed at more than 1 week after admission. The t-test was used for comparison of continuous data between groups, and the chi-square test was used for comparison of categorical data between groups; a multivariate logistic regression analysis was used to determine the independent predictive factors for OPN. ResultsThe probability of OPN was 19.2% for SAP patients in the later stage. Compared with the PCD+OPN group, the PCD group had a significantly lower proportion of patients with MOF on admission ［27.0% (34/126) vs 70.0% (21/30), χ2=19.642, P＜0.01］ and a significantly higher proportion of patients undergoing PCD at less than 1 week after admission ［61.9% (78/126) vs 20.0% (6/30), χ2=17.121, P＜0.01］. MOF on admission (odds ratio ［OR］=5.343, 95% confidence interval ［CI］: 1.832-15.583, P＜0.05), initial PCD performed at more than 1 week after admission (OR= 5.518, 95% CI: 1.742-17.477, P＜0.05), and infection on admission (OR=5.016, 95% CI: 1.322-19.378, P＜0.05) were independent risk factors for subsequent OPN in SAP patients. ConclusionSAP with MOF on admission, initial PCD performed at more than 1 week after admission, and SAP with infection on admission are independent risk factors for subsequent OPN in SAP patients undergoing PCD in the early stage based on the step-up approach. Timely identification of related risk factors helps to grasp the timing of OPN in clinical practice and improve the clinical prognosis of SAP patients.
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Hepatic ischemia-reperfusion injury (HIRI) is the main cause of liver damage and even multiple organ failure after complex liver surgery.When liver ischemia reperfusion occurs,the non-coding RNAs in the liver tissue is dysregulated and part of the non-coding RNAs with abnormal expression is involved in HIRI regulation.Non-coding RNAs to may be the intervention target for reducing HIRI.This article summarized the types and related functions of non-coding RNAs,the role of different non-coding RNAs in HIRI,and the interconnections between various non-coding RNAs in HIRI.
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High-mobility group box B1 (HMGB1) is a DNA-binding protein widely distributed in eukaryotic cells. When tissue damage occurs, HMGB1 acts as an endogenous risk signal to activate the body’s immune system and mediate aseptic inflammatory response. Current research findings have shown that HMGB1 plays a key role in hepatic ischemia-reperfusion injury. This article summarizes the recent research advances in the proinflammatory role of HMGB1 in hepatic ischemia-reperfusion and HMGB1 as a target for the treatment of hepatic ischemia-reperfusion injury.
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High-mobility group box B1 (HMGB1) is a DNA-binding protein widely distributed in eukaryotic cells. When tissue damage occurs, HMGB1 acts as an endogenous risk signal to activate the body’s immune system and mediate aseptic inflammatory response. Current research findings have shown that HMGB1 plays a key role in hepatic ischemia-reperfusion injury. This article summarizes the recent research advances in the proinflammatory role of HMGB1 in hepatic ischemia-reperfusion and HMGB1 as a target for the treatment of hepatic ischemia-reperfusion injury.
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AIM To investigate the protective effects of polysaccharides from Dendrobium nobile Lindl.on cerebra ischemia/reperfusion injury in rats and its possible mechanism of action.METHODS One hundred and five SD rats were divided into sham group,model group,Nimodipine group (10 mg/kg) and treatment groups with low-,medium-,and high dose (50,100,and 200 mg/kg) of polysaccharides from D.nobile.The right middle cerebral artery of rats was occluded by inserting a.thread through internal carotid artery for 2 h,and was sampled after reperfusion for 24 h.The rats received gavage once a day for 7 d before operation.Neurological deficits score,brain index,brain water content and infarct size in rats were conducted at the end of reperfusion;the activity of superoxide dismutase (SOD),glutathione peroxidase (GSH-Px),myeloperoxidase (MPO) and the content of malondialdehyde (MDA) of brain tissue and blood serum were measured by chemical colorimetry;the infiltration of neutrophile granulocyte in rat ischemic cortex were detected with immune-fluorescence staining.RESULTS Sham group had no neurological deficit,but the model group showed severe neurological deficits,meanwhile,the infarct size,brain index and brain water content rose markedly,the content of MDA and the activity of MPO of the brain tissue and the blood serum increased remarkably,while the activity of SOD and GSH-Px apparently decreased;compared with the model group,neurological deficits of rats were improved significantly in polysaccharides from D.nobile dose groups,moreover,the infarct size,brain index and brain water content markedly declined,the MDA level and the activity of MPO significantly decreased,but the activity of SOD,GSH-Px increased remarkably;the infiltration of neutrophile granulocyte in the high dose group significantly decreased compared with the model group.CONCLUSION Polysaccharides from D.nobile has some neuroprotective effects on local cerebral ischemia/reperfusion injury,and that may be related to the remove of oxygen free radicals and the decrease in inflammation reaction.
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Objective To explore the anti-inflammatory effect of erythropoietin (EPO) on hepatic ischemia reperfusion (IR) injury in fatty liver rats.Methods A total of 100 male SD rats were fed with high-fat diet for 12 weeks.After the model was successfully established,the fatty liver rats were randomly divided into sham-operation (SHAM),the ischemia-reperfusion (IR) and EPO preconditioning group.Serum ALT and AST as well as hepatic histopathological changes were measured.Xanthine oxidase method was used to detect the liver tissue SOD.Thiobarbituric acid method was used to detect the MDA.Enzyme-linked immunosorbent adsorption assay (ELISA) was used to detect the plasma tumor necrosis factor alpha (TNFαt) and interleukin 1 (IL-1).Results In the EPO preconditioning groups the swelling hepatocytes was observed,but the inflammatory cell infiltration was significantly decreased and no necrosis of hepatocytes was found.ALT and AST in the EPO preconditioning groups were significantly lower than those in IR group (P ＜ 0.05).The levels of SOD activity in the EPO preconditioning groups were significantly higher,but MDA were significantly lower than that in IR group (P ＜ 0.05).The TNF-α and IL-1 in the EPO preconditioning groups were significantly lower than those in IR group (P ＜0.05).The values of ALT,AST,TNF-α,IL-1 and MDA in the EPO groups were:EPO-1 ＞ EPO-2 ＞ EPO-3 (P ＜ 0.05);but the values of SOD in the EPO groups were:EPO-1 ＜ EPO-2 ＜ EPO-3 (P ＜ 0.05).Conclusions EPO preconditioning has a protective effect against hepatic IR injury in fatty liver rats,possibly through inhibiting the inflammatory reaction to prevent the IR injury.The anti-inflammatory effect of high-dose EPO is better than that of low-dose EPO.
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Objective To study the effects of monocyte chemotactic protein-1(MCP-1) on the growth of human umbilical vein endothelial cells (hUVEC). Methods hUVEC were cultured in vitro and identified. hUVEC that grew vigorously were stimulated for 24 h or 48 h respectively with MCP-1(0.1, 1.0, 10, and 100 ?g/L). The survival rate of hUVEC was first detected by MTT assay. The cell cycle and DNA content were detected and analyzed by flow cytometry. Results hUVEC were isolated from human umbilical veins and cultured, and then identified by immunofluorescence and immunohistochemistry with factor Ⅷ and KDR. MCP-1 induced the apoptosis of hUVEC in a dose-dependentmanner and a time-dependentmanner (P
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Aim To study the inhibition of genistein on proliferation and transcription of c-fos mRNA in human umbilical vascular smooth muscle cells(hUVSMC) induced by monocyte chemotactic protein-1(MCP-1). Methods Growth-arrested hUVSMC were stimulated with MCP-1(10 ?g?L-1) prior to co-treatment with different concentrations of genistein (10,30,90 ?mol?L-1). The response of hUVMSC to these treatments was observed in comparison with that of control group. The proliferation of hUVMSC was evaluated by cell counting. The expression of c-fos mRNA was detected by RT-PCR. Results Low concentration of genistein(10 ?mol?L-1) inhibited the proliferation of hUVSMC and high concentration of genistein(30,90 ?mol?L-1) inhibited the expression of c-fos in hUVSMC induced by MCP-1. Conclusions Genistein could suppress the proliferation of hUVSMC induced by of MCP-1. Its mechanisms may involve the down-regulation of c-fos mRNA expression.