scholarly journals Protective Effects of Emodin-Induced Neutrophil Apoptosis via the Ca2+-Caspase 12 Pathway against SIRS in Rats with Severe Acute Pancreatitis

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Gui-Jun Wang ◽  
Yue Wang ◽  
Yong-Sheng Teng ◽  
Fa-Lv Sun ◽  
Hong Xiang ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Multiple Organ ◽  
Neutrophil Apoptosis ◽  
Protective Effects ◽  
Expression Levels ◽  
Beneficial Effects ◽  
Caspase 12 ◽  
Underlying Mechanisms ◽  
Active Fragments

Severe acute pancreatitis (SAP) results in high mortality. This is partly because of early multiple organ dysfunction syndromes that are usually caused by systemic inflammatory response syndrome (SIRS). Many studies have reported the beneficial effects of emodin against SAP with SIRS. However, the exact mechanism underlying the effect of emodin remains unclear. This study was designed to explore the protective effects and underlying mechanisms of emodin against SIRS in rats with SAP. In the present study, cytosolic Ca2+ levels, calpain 1 activity, and the expression levels of the active fragments of caspases 12 and 3 decreased in neutrophils from rats with SAP and increased after treatment with emodin. Delayed neutrophil apoptosis occurred in rats with SAP and emodin was able to reverse this delayed apoptosis and inhibit SIRS. The effect of emodin on calpain 1 activity, the expression levels of the active fragments of caspases 12 and 3, neutrophil apoptosis, and SIRS scores were attenuated by PD150606 (an inhibitor of calpain). These results suggest that emodin inhibits SIRS in rats with SAP by inducing circulating neutrophil apoptosis via the Ca2+-calpain 1-caspase 12-caspase 3 signaling pathway.

Protective Effects of Baicalin and Octreotide on Multiple Organ Injury in Severe Acute Pancreatitis

2007 ◽  
Vol 53 (2) ◽  
pp. 581-591 ◽  
Author(s):  
Xi Ping Zhang ◽  
Ling Zhang ◽  
Ping Yang ◽  
Rui Ping Zhang ◽  
Qi Hui Cheng
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Multiple Organ ◽  
Organ Injury ◽  
Protective Effects ◽  
Multiple Organ Injury

Research on Scutellarin Parenteral Solution’s Protective Effects in Rats with Severe Acute Pancreatitis and Multiple Organ Injuries

Inflammation ◽  
2011 ◽  
Vol 35 (3) ◽  
pp. 1005-1014 ◽  
Author(s):  
Chen Hanqing ◽  
Zhang Xiping ◽  
Ou Jingmin ◽  
Jiang Jun ◽  
Wu Dijiong
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Multiple Organ ◽  
Protective Effects

scholarly journals Protective Effects of Necrostatin-1 in Acute Pancreatitis: Partial Involvement of Receptor Interacting Protein Kinase 1

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1035
Author(s):  
Yulin Ouyang ◽  
Li Wen ◽  
Jane A. Armstrong ◽  
Michael Chvanov ◽  
Diane Latawiec ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Protein Kinase ◽  
Pancreatic Acinar Cell ◽  
Protective Effects ◽  
Interacting Protein ◽  
Beneficial Effects ◽  
Protective Actions ◽  
Underlying Mechanisms

Acute pancreatitis (AP) is a severe and potentially fatal disease caused predominantly by alcohol excess and gallstones, which lacks a specific therapy. The role of Receptor-Interacting Protein Kinase 1 (RIPK1), a key component of programmed necrosis (Necroptosis), is unclear in AP. We assessed the effects of RIPK1 inhibitor Necrostatin-1 (Nec-1) and RIPK1 modification (RIPK1K45A: kinase dead) in bile acid (TLCS-AP), alcoholic (FAEE-AP) and caerulein hyperstimulation (CER-AP) mouse models. Involvement of collateral Nec-1 target indoleamine 2,3-dioxygenase (IDO) was probed with the inhibitor Epacadostat (EPA). Effects of Nec-1 and RIPK1K45A were also compared on pancreatic acinar cell (PAC) fate in vitro and underlying mechanisms explored. Nec-1 markedly ameliorated histological and biochemical changes in all models. However, these were only partially reduced or unchanged in RIPK1K45A mice. Inhibition of IDO with EPA was protective in TLCS-AP. Both Nec-1 and RIPK1K45A modification inhibited TLCS- and FAEE-induced PAC necrosis in vitro. Nec-1 did not affect TLCS-induced Ca2+ entry in PACs, however, it inhibited an associated ROS elevation. The results demonstrate protective actions of Nec-1 in multiple models. However, RIPK1-dependent necroptosis only partially contributed to beneficial effects, and actions on targets such as IDO are likely to be important.

scholarly journals Involvement of the PI3K/Akt/NF-κB Signaling Pathway in the Attenuation of Severe Acute Pancreatitis-Associated Acute Lung Injury by Sedum sarmentosum Bunge Extract

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Yuepeng Jin ◽  
Lewei Liu ◽  
Bicheng Chen ◽  
Yongyu Bai ◽  
Fan Zhang ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Severe Acute Pancreatitis ◽  
Inflammatory Diseases ◽  
Interleukin 1 ◽  
Sodium Taurocholate ◽  
Beneficial Effects ◽  
Parallel Increase ◽  
Underlying Mechanisms

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-κB) 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-α (TNF-α) 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-κB activities.

Multiple organ dysfunction associated with severe acute pancreatitis (SAP)

2001 ◽  
Vol 120 (5) ◽  
pp. A644-A645
Author(s):  
Kimmo I. Halonen ◽  
Ville Pettila ◽  
Ari K. Leppaniemi ◽  
Esko A. Kemppainen ◽  
Pauli A. Puolakkainen ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Organ Dysfunction ◽  
Severe Acute Pancreatitis ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction

scholarly journals NLRP3 Deficiency Alleviates Severe Acute Pancreatitis and Pancreatitis-Associated Lung Injury in a Mouse Model

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Qiang Fu ◽  
Zhensheng Zhai ◽  
Yuzhu Wang ◽  
Lixia Xu ◽  
Pengchong Jia ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Lung Injury ◽  
Severe Acute Pancreatitis ◽  
Nlrp3 Inflammasome ◽  
Early Death ◽  
Neutrophil Infiltration ◽  
Multiple Organ ◽  
Dependent Manner ◽  
Dose Dependent ◽  
Nlrp3 Expression

The rapid production and release of a large number of inflammatory cytokines can cause excessive local and systemic inflammation in severe acute pancreatitis (SAP) and multiple organ dysfunction syndrome (MODS), especially pancreatitis-associated acute lung injury (P-ALI), which is the main cause of early death in patients with SAP. The NLRP3 inflammasome plays an important role in the maturation of IL-1β and the inflammatory cascade. Here, we established a model of SAP using wild-type (NLRP3+/+) and NLRP3 knockout (NLRP3-/-) mice by intraperitoneal injections of caerulein (Cae) and lipopolysaccharide (LPS). Pathological injury to the pancreas and lungs, the inflammatory response, and neutrophil infiltration were significantly mitigated in NLRP3-/- mice. Furthermore, INF-39, an NLRP3 inflammasome inhibitor, could reduce the severity of SAP and P-ALI in a dose-dependent manner. Our results suggested that SAP and P-ALI were alleviated by NLRP3 deficiency in mice, and thus, reducing NLRP3 expression may mitigate SAP-associated inflammation and P-ALI.

scholarly journals Minimally invasive drainage versus open surgical debridement in SAP/SMAP – a network meta-analysis

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Kai Zhang ◽  
Xiaole Zhu ◽  
Chaoqun Hou ◽  
Chenyuan Shi ◽  
Yi Miao ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Minimally Invasive ◽  
Severe Acute Pancreatitis ◽  
Meta Analysis ◽  
Multiple Organ ◽  
Surgical Debridement ◽  
Percutaneous Catheter Drainage ◽  
Endoscopic Drainage ◽  
Percutaneous Catheter ◽  
Study Participants

Abstract Background The efficacy of some therapeutic methods (open surgical debridement (OSD), conservative treatment (CST) and minimally invasive drainage (MID)) for severe acute pancreatitis (SAP) and moderately severe acute pancreatitis (MSAP) has been widely evaluated. However, the results remained controversial. We performed this study to illuminate whether any difference in incidence exists on patients with SAP/MSAP treated with OSD and MID. Methods Eligible articles were collected base of a comprehensive review of PUBMED, EMBASE, COCHRANE, CKNI and WANGFANG for published randomized controlled trials. Two steps of meta-analysis were performed, routine pair-wise meta-analysis and network meta-analysis. Results Thirteen studies were included in this study. Participants were classed as 5 groups, CST, early MID (EMID), late MID (LMID), early OSD (EOSD) and late OSD (LOSD). And MID contains endoscopic drainage (ESD), percutaneous catheter drainage (PCD) and minimally invasive surgery (MIS). Compared with CST, MID could decrease both mortality and multiple organ dysfunction syndrome (MODS) rate but OSD couldn’t. Both EMID and MID can significantly decrease the mortality and MODS rate compared to CST. PCD might be most likely to have a benefit compared to CST. Conclusion Existing evidence for the use of MID in SAP/MSAP is reliable and it can be used as early treatment. OSD, if necessary, should be avoided or delayed as long as possible.

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