scholarly journals Nicaraven Attenuates Postoperative Systemic Inflammatory Responses-Induced Tumor Metastasis

2019 ◽  
Vol 27 (4) ◽  
pp. 1068-1074 ◽  
Author(s):  
Xu Zhang ◽  
Takahito Moriwaki ◽  
Tsuyoshi Kawabata ◽  
Shinji Goto ◽  
Ke-Xiang Liu ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Tumor Metastasis ◽  
Intestinal Ischemia ◽  
Cancer Metastasis ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Inflammatory Cells ◽  
Major Surgery ◽  
Lewis Lung Cancer ◽  
Intestinal Ischemia Reperfusion

Abstract Background Inflammation has been demonstrated to promote cancer metastasis. Due to the well-known systemic inflammatory responses (SIR) after major surgery, it is critical to investigate and attenuate SIR-induced tumor metastasis of cancer patients suffering surgical procedures. Methods C57BL/6 mice were intravenously injected with Lewis lung cancer cells at 6, 24, and 72 h after the induction of intestinal ischemia/reperfusion (I/R) injury. We found that the number of tumor nodules significantly increased in lungs of mice injected with cancer cells at 6 h but not at 24 and 72 h after I/R injury. The administration of nicaraven 30 min before and 24 h after I/R injury effectively attenuated the enhanced tumor metastasis to lungs. Protein array showed the increase of various cytokines in plasma of mice at 6 h after I/R injury, but many of them were attenuated by the administration of nicaraven. Immunostaining indicated the increase of Ly6g-, CD206-, and CD11c-positive inflammatory cells in the lungs, but it was also attenuated by nicaraven administration. Conclusions Postoperative SIR-induced tumor metastasis have been clearly evidenced in our experimental model, and the administration of nicaraven may ameliorate the SIR-induced tumor metastasis by suppressing inflammatory responses.

scholarly journals Translocation of 99mTc labelled bacteria after intestinal ischemia and reperfusion

2004 ◽  
Vol 19 (4) ◽  
pp. 328-333 ◽  
Author(s):  
Samir Assi João ◽  
Suelene Suassuna Silvestre de Alencar ◽  
Aldo da Cunha Medeiros ◽  
Simone Otília Fernandes Diniz ◽  
Valbert Nascimento Cardoso ◽  
...  
Keyword(s):  
Bacterial Translocation ◽  
Intestinal Ischemia ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Ischemia And Reperfusion ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph ◽  
Colony Forming Units ◽  
Male Wistar Rats ◽  
Intestinal Ischemia Reperfusion

PURPOSE: Ischemia and reperfusion of the small intestine disrupts gut barrier, causes bacterial translocation and activates inflammatory responses. An experimental study was planned to evaluate if 99mTc labelled Escherichia coli translocates to mesenteric lymph nodes, liver, spleen, lung and serum of rats submitted to mesenteric ischemia/reperfusion. Additionally, it was observed if the time of reperfusion influences the level of translocation. METHODS: Forty male Wistar rats underwent 45 minutes of gut ischemia by occlusion of the superior mesenteric artery. The translocation of labelled bacteria to different organs and portal serum was determined in rats reperfused for 30 minutes, 24 hours, sham(S) and controls(C), using radioactivity count and colony forming units/g (CFU). RESULTS: All the organs from rats observed for 24 hours after reperfusion had higher levels of radioactivity and positive cultures (CFU) than did the organs of rats reperfused for 30 minutes, C and S, except in the spleen (p<0,01). CONCLUSION: The results of this study indicated that intestinal ischemia/reperfusion led to bacterial translocation, mostly after 24 hours of reperfusion.

scholarly journals Amelioration of Coagulation Disorders and Inflammation by Hydrogen-Rich Solution Reduces Intestinal Ischemia/Reperfusion Injury in Rats through NF-κB/NLRP3 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Ling Yang ◽  
Yan Guo ◽  
Xin Fan ◽  
Ye Chen ◽  
Bo Yang ◽  
...  
Keyword(s):  
Survival Rate ◽  
Intestinal Ischemia ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Intestinal Injury ◽  
Inflammasome Activation ◽  
Coagulation Disorders ◽  
Poor Survival ◽  
Rich Solution ◽  
Intestinal Ischemia Reperfusion

Intestinal ischemia/reperfusion (I/R) injury often causes inflammatory responses and coagulation disorders, which is further promoting the deterioration of the disease. Hydrogen has anti-inflammatory, antioxidative, and antiapoptotic properties against various diseases. However, the effect of hydrogen on coagulation dysfunction after intestinal I/R and the underlying mechanism remains unclear. The purpose of this study was to explore whether hydrogen-rich solution (HRS) could attenuate coagulation disorders and inflammation to improve intestinal injury and poor survival following intestinal I/R. The rat model of intestinal I/R injury was established by clamping the superior mesenteric artery for 90 min and reperfusion for 2 h. HRS (10 or 20 mL/kg) or 20 mL/kg 0.9% normal saline was intravenously injected at 10 min before reperfusion, respectively. The samples were harvested at 2 h after reperfusion for further analyses. Moreover, the survival rate was observed for 24 h. The results showed that HRS improved the survival rate and alleviated serum diamine oxidase activities, intestinal injury, edema, and apoptosis. Interestingly, HRS markedly improved intestinal I/R-mediated coagulation disorders as evidenced by abnormal conventional indicators of coagulation and thromboelastography. Additionally, HRS attenuated inflammatory responses and the elevated tissue factor (TF) and inhibited nuclear factor kappa beta (NF-κB) and nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation in peripheral blood mononuclear cells. Moreover, inflammatory factors and myeloperoxidase were closely associated with TF level. This study thus emphasized upon the amelioration of coagulation disorders and inflammation by HRS as a mechanism to improve intestinal I/R-induced intestinal injury and poor survival, which might be partially related to inhibition of NF-κB/NLRP3 pathway.

scholarly journals Complement regulates TLR4-mediated inflammatory responses during intestinal ischemia reperfusion

2010 ◽  
Vol 48 (1-3) ◽  
pp. 356-364 ◽  
Author(s):  
Michael R. Pope ◽  
Sara M. Hoffman ◽  
Stephen Tomlinson ◽  
Sherry D. Fleming
Keyword(s):  
Intestinal Ischemia ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

Role of JNK phosphorylation in intestinal ischemia/reperfusion injury in mice

2010 ◽  
Vol 30 (2) ◽  
pp. 140-143
Author(s):  
De-yi ZHENG ◽  
Jian-ming WNAG ◽  
Yi-tao JIA ◽  
Jin-feng FU ◽  
Kai-yang LU ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

scholarly journals Ginsenoside Rb1 Treatment Attenuates Pulmonary Inflammatory Cytokine Release and Tissue Injury following Intestinal Ischemia Reperfusion Injury in Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Ying Jiang ◽  
Zhen Zhou ◽  
Qing-tao Meng ◽  
Qian Sun ◽  
Wating Su ◽  
...  
Keyword(s):  
Lung Injury ◽  
Signaling Pathway ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Weight Ratio ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Ginsenoside Rb1 ◽  
Intestinal Ischemia Reperfusion

Objective. Intestinal ischemia reperfusion (II/R) injury plays a critical role in remote organ dysfunction, such as lung injury, which is associated with nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. In the present study, we tested whether ginsenoside Rb1 attenuated II/R induced lung injury by Nrf2/HO-1 pathway.Methods. II/R injury was induced in male C57BL/6J mice by 45 min of superior mesenteric artery (SMA) occlusion followed by 2 hours of reperfusion. Ginsenoside Rb1 was administrated prior to reperfusion with or without ATRA (all-transretinoic acid, the inhibitor of Nrf2/ARE signaling pathway) administration before II/R.Results. II/R induced lung histological injury, which is accompanied with increased levels of malondialdehyde (MDA), interleukin- (IL-) 6, and tumor necrosis factor- (TNF-)αbut decreased levels of superoxide dismutase (SOD) and IL-10 in the lung tissues. Ginsenoside Rb1 reduced lung histological injury and the levels of TNF-αand MDA, as well as wet/dry weight ratio. Interestingly, the increased Nrf2 and HO-1 expression induced by II/R in the lung tissues was promoted by ginsenoside Rb1 treatment. All these changes could be inhibited or prevented by ATRA.Conclusion. Ginsenoside Rb1 is capable of ameliorating II/R induced lung injuries by activating Nrf2/HO-1 pathway.

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