| 1. |
- Chen, Jiawei, et al.
(författare)
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Inhibition of aquaporin-9 ameliorates severe acute pancreatitis and associated lung injury by NLRP3 and Nrf2/HO-1 pathways
- 2024
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Ingår i: International Immunopharmacology. - 1567-5769. ; 137
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Tidskriftsartikel (refereegranskat)abstract
- Inflammation, apoptosis and oxidative stress play crucial roles in the deterioration of severe acute pancreatitis-associated acute respiratory distress syndrome (SAP-ARDS). Unfortunately, despite a high mortality rate of 45 %[1], there are limited treatment options available for ARDS outside of last resort options such as mechanical ventilation and extracorporeal support strategies[2]. This study investigated the potential therapeutic role and mechanisms of AQP9 inhibitor RG100204 in two animal models of severe acute pancreatitis, inducing acute respiratory distress syndrome: 1) a sodium-taurocholate induced rat model, and 2) and Cerulein and lipopolysaccharide induced mouse model. RG100204 treatment led to a profound reduction in inflammatory cytokine expression in pancreatic, and lung tissue, in both models. In addition, infiltration of CD68 + and CD11b + cells into these tissues were reduced in RG100204 treated SAP animals, and edema and SAP associated tissue damage were improved. Moreover, we demonstrate that RG100204 reduced apoptosis in the lungs of rat SAP animals, and reduces NF-κB signaling, NLRP3, expression, while profoundly increasing the Nrf2-dependent anti oxidative stress response. We conclude that AQP9 inhibition is a promising strategy for the treatment of pancreatitis and its systemic complications, such as ARDS.
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| 2. |
- Zhou, Mengtao, et al.
(författare)
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The efficiency of continuous regional intra-arterial infusion in the treatment of infected pancreatic necrosis
- 2013
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Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 13:3, s. 212-215
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Our aim was to investigate the efficiency of continuous regional intra-arterial infusion (CRAI) with antisecretory agents and antibiotics in the treatment of infected pancreatic necrosis. Materials and methods: CRAI was used as a new clinical technique to treat acute pancreatitis patients during a 4-year period at the First Affiliated Hospital, Wenzhou Medical College, China. In this retrospective study, thirty-four patients with proven infected pancreatic necrosis were included. Twelve patients were treated with CRAL and were matched according to age, sex, APACHE II scores, Ranson scores and remote organ dysfunction, with 22 patients with IPN treated surgically. The clinical outcome following surgery and CRAI were compared. Results: No difference was found between the two groups when comparing age, gender, APACHE II scores, Ranson scores and remote organ dysfunction (p > 0.05). The patients treated with CRAI had a lower incidence of complications (33.3% vs 72.7%), duration of hospitalization (27.1 +/- 4.7 days vs 43.0 +/- 12.0 days) and cost of hospitalization (4.09 +/- 1.64 thousand RMB vs 8.77 +/- 3.74 thousand RMB) as compared to patients treated with surgery (p < 0.05). The survival rate was significantly higher in the CRAI group as compared to the surgical group (91.7% vs 63.6%; p < 0.01). However, the two groups had similar rates of concomitant operative treatment and incidence of remote organ dysfunction (p > 0.05). Conclusions: CRAI or CRAI in combination with abscess drainage seemingly improve the clinical outcome in patients with infected pancreatic necrosis. Further confirmative prospective randomized multicenter studies are warranted prior to broad introduction of the CRAI concept. Copyright (C) 2013, IAP and EPC. Published by Elsevier India, a division of Reed Elsevier India Pvt. Ltd. All rights reserved.
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| 3. |
- Fan, Ke, et al.
(författare)
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Hollow Iron-Vanadium Composite Spheres : A Highly Efficient Iron-Based Water Oxidation Electrocatalyst without the Need for Nickel or Cobalt
- 2017
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Ingår i: Angewandte Chemie International Edition. - : WILEY-V C H VERLAG GMBH. - 1433-7851 .- 1521-3773. ; 56:12, s. 3289-3293
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Tidskriftsartikel (refereegranskat)abstract
- Noble-metal-free bimetal-based electrocatalysts have shown high efficiency for water oxidation. Ni and/or Co in these electrocatalysts are essential to provide a conductive, high-surface area and a chemically stable host. However, the necessity of Ni or Co limits the scope of low-cost electrocatalysts. Herein, we report a hierarchical hollow FeV composite, which is Ni- and Co-free and highly efficient for electrocatalytic water oxidation with low overpotential 390 mV (10 mA cm(-2) catalytic current density), low Tafel slope of 36.7 mV dec(-1), and a considerable durability. This work provides a novel and efficient catalyst, and greatly expands the scope of low-cost Fe-based electrocatalysts for water splitting without need of Ni or Co.
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| 4. |
- Jin, Yuepeng, et al.
(författare)
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Involvement of the PI3K/Akt/NF- B Signaling Pathway in the Attenuation of Severe Acute Pancreatitis-Associated Acute Lung Injury by Sedum sarmentosum Bunge Extract
- 2017
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Ingår i: BioMed Research International. - : Hindawi Limited. - 2314-6133 .- 2314-6141. ; 2017
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Tidskriftsartikel (refereegranskat)abstract
- Sedum sarmentosum Bunge possesses excellent anti-inflammatory properties and was used in the treatment of inflammatory diseases. The aim of the present study was to investigate the efficiency of Sedum sarmentosum Bunge extract (SSBE) on severe acute pancreatitis-associated (SAP-associated) acute lung injury (ALI) in rats and to explore the underlying mechanisms. Here, we used a sodium taurocholate-induced SAP rat model to determine the role of SSBE in ALI. During the course of pancreatitis, the expressions of phosphorylated phosphoinositide 3-kinases (PI3K)/protein kinase B (Akt) and nuclear factor-kappa B (NF-B) p65 in the lungs were upregulated. Meanwhile, a parallel increase in the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor- (TNF-) in the lungs was observed after the induction of SAP. Treatment with SSBE significantly reduced the expression of p-Akt and p-p65 in the lungs and attenuated the severity of SAP-associated ALI compared to the SAP group at 12 h and 24 h. In summary, this study showed that SSBE has beneficial effects on SAP-associated ALI, probably through the PI3-K/Akt signaling pathways by suppressing the NF-B activities.
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| 5. |
- Lv, Wanzhi, et al.
(författare)
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Lipoxin A4 attenuation of endothelial inflammation response mimicking pancreatitis-induced lung injury
- 2013
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Ingår i: Experimental Biology and Medicine. - : SAGE Publications. - 1535-3702 .- 1535-3699. ; 238:12, s. 1388-1395
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Tidskriftsartikel (refereegranskat)abstract
- Lipoxins (LXs) and their analogues are known to display potent anti-inflammatory actions. Previously, we reported that lipoxin A4 (LXA4) possessed powerful anti-inflammatory properties in acute pancreatitis in rats and that it may ameliorate the concomitant acute lung injury by reducing cytokine generation and inhibiting neutrophil activation. Considering that the vascular endothelium plays an important role during adherence, migration and activation of leukocytes, the present study was designed to investigate the effects of LXA4 on the inflammatory response induced by tumor necrosis factor a (TNF-alpha) in human pulmonary microvascular endothelial cells (HPMECs) and explore the potential mechanisms involved in these processes. We found that LXA4 markedly down-regulated the expression of monocyte chemotactic protein-1 (MCP-1), E-selectin, and interleukin-6 (IL-6) mRNA, as well as intercellular adhesion molecule-1 (ICAM-1) in TNF-alpha-exposed HPMECs. Moreover, LXA4 inhibited the phosphorylation and nuclear translocation of nuclear factor-kappa B/p65 (NF-kappa B/p65) and phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) in HPMECs following TNF-alpha stimulation. Heme oxygenase-1 (HO-1), a cytoprotective enzyme, was up-regulated by LXA4 in both non- and TNF-alpha-stimulated HPMECs. In conclusion, the protective effects of LXA4 to ALI may be executed through inhibition inflammation pathways of NF-kappa B and p38 MAPK and up-regulation of cytoprotective HO-1.
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| 6. |
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| 7. |
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| 8. |
- Zhou, Mengtao, et al.
(författare)
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The protective effects of Lipoxin A(4) during the early phase of severe acute pancreatitis in rats
- 2011
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Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 46:2, s. 211-219
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Tidskriftsartikel (refereegranskat)abstract
- Objective. Our aim was to investigate the protective effects of a Lipoxin A(4) analogue (LXA(4)) in the early phase of acute pancreatitis in rats. Materials and methods. Severe acute pancreatitis (SAP) was induced by injection of 5% sodium taurocholate into the pancreatic duct. Rats with SAP were treated with LXA(4) (0.1 mg/kg), 10 min after the 5% sodium taurocholate injection, after which LXA(4) was administrated every 8 hours, three times (LXA(4) group). The sham group was only given the vehicle after operation. Plasma amylase activity, serum levels of interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-alpha) were measured at 4, 12, and 24 h after induction of SAP. The pancreatic index and histopathologic observations were evaluated and the expression of intercellular adhesion molecule-1 (ICAM-1) and NF-kappa B p65 in the pancreas, and the expression of ICAM-1 in the lungs were detected by immunohistochemistry. Results. LXA(4) treated rats had lower serum levels of TNF-alpha, IL-1, and IL-6 at all time points measured (p < 0.05), but significantly differed in plasma amylase activity only at 24 h as compared with the SAP group. The pancreatic index and the scores of pancreatitic histopathologic evaluations were lower in the LXA(4) group as compared to the SAP group. Immunohistochemistry showed that LXA(4) attenuated the expression of ICAM-1 and NF-kappa B p65 in the pancreas, as well as the expression of ICAM-1 in the lungs in animals with pancreatitis (p < 0.05). Conclusions. We demonstrate that LXA(4) has protective effects in experimental SAP, which may be achieved by inhibiting the NF-kappa B signalling pathway, thereby reducing the production of proinflammatory cytokines.
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