scholarly journals Mesenteric Lymph Duct Drainage Attenuates Lung Inflammatory Injury and Inhibits Endothelial Cell Apoptosis in Septic Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Yongjun Liu ◽  
Chuanxi Chen ◽  
Qing Sun ◽  
Huadong Sun ◽  
Ning Liu ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Inflammatory Mediators ◽  
Cell Apoptosis ◽  
Mrna Levels ◽  
Endothelial Cell Apoptosis ◽  
Lymph Drainage ◽  
Inflammatory Injury ◽  
Mesenteric Lymph ◽  
Tnf Α ◽  
Lymph Duct

The present study was to investigate the effect of mesenteric lymph duct drainage on lung inflammatory response, histological alteration, and endothelial cell apoptosis in septic rats. Animals were randomly assigned into four groups: control, sham surgery, sepsis, and sepsis plus mesenteric lymph drainage. We used the colon ascendens stent peritonitis (CASP) procedure to induce the septic model in rats, and mesenteric lymph drainage was performed with a polyethylene (PE) catheter inserted into mesenteric lymphatic. The animals were sacrificed at the end of CASP in 6 h. The mRNA expression levels of inflammatory mediators were measured by qPCR, and the histologic damage were evaluated by the pathological score method. It was found that mesenteric lymph drainage significantly reduced the expression of TNF-α, IL-1β, and IL-6 mRNA in the lung. Pulmonary interstitial edema and infiltration of inflammatory cells were alleviated by mesenteric lymph drainage. Moreover, increased mRNA levels of TNF-α, IL-1β, IL-6 mRNA, and apoptotic rate were observed in PMVECs treated with septic lymph. These results indicate that mesenteric lymph duct drainage significantly attenuated lung inflammatory injury by decreasing the expression of pivotal inflammatory mediators and inhibiting endothelial apoptosis to preserve the pulmonary barrier function in septic rats.

scholarly journals Effects of down-regulation of microRNA-23a on TNF-α-induced endothelial cell apoptosis through caspase-dependent pathways

2011 ◽  
Vol 93 (4) ◽  
pp. 623-632 ◽  
Author(s):  
Wei Ruan ◽  
Jun-mei Xu ◽  
Suo-bei Li ◽  
Ling-qing Yuan ◽  
Ru-ping Dai
Keyword(s):  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Endothelial Cell Apoptosis ◽  
Down Regulation ◽  
Tnf Α

Hemorrhagic shock induces endothelial cell apoptosis, which is mediated by factors contained in mesenteric lymph

2004 ◽  
Vol 32 (12) ◽  
pp. 2464-2470 ◽  
Author(s):  
Qi Lu ◽  
Da-Zhong Xu ◽  
Marson T. Davidson ◽  
György Haskó ◽  
Edwin A. Deitch
Keyword(s):  
Endothelial Cell ◽  
Hemorrhagic Shock ◽  
Cell Apoptosis ◽  
Endothelial Cell Apoptosis ◽  
Mesenteric Lymph

scholarly journals Endothelial cell apoptosis in brown adipose tissue of rats induced by hyperinsulinaemia: the possible role of TNF-α

2011 ◽  
Vol 55 (4) ◽  
pp. 34 ◽  
Author(s):  
M. Markelic ◽  
K. Velickovic ◽  
I. Golic ◽  
V. Otasevic ◽  
A. Stancic ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Endothelial Cell ◽  
Brown Adipose Tissue ◽  
Cell Apoptosis ◽  
Endothelial Cell Apoptosis ◽  
Brown Adipose ◽  
Tnf Α

Regulation of nicotine-induced apoptosis of pulmonary artery endothelial cells by treatment of N-acetylcysteine and vitamin E

2007 ◽  
Vol 26 (7) ◽  
pp. 595-602 ◽  
Author(s):  
R. Demiralay ◽  
N. Gürsan ◽  
H. Erdem
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Vitamin E ◽  
Pulmonary Artery ◽  
Cell Apoptosis ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Endothelial Cell Apoptosis ◽  
Antioxidant Agents ◽  
Tnf Α

This study investigated the frequency of apoptosis in rat pulmonary artery endothelial cells after intraperitoneal nicotine injection, examining the roles of the inflammatory markers myeloperoxidase (MPO), tumour necrosis factor alpha (TNF-α ), and vascular endothelial growth factor (VEGF) in nicotine-induced vascular damage and the protective effects of two known antioxidant agents, N-acetylcysteine (NAC) and vitamin E. Female Wistar rats were divided into four groups, each composed of nine rats: negative control group, positive control group, NACtreated group (500 mg/kg), and vitamin E-treated group (500 mg/kg). Nicotine was intraperitoneally injected at a dosage of 0.6 mg/kg for 21 days. Following nicotine injection, the antioxidants were administered orally; treatment was continued until the rats were killed. Lung tissue samples were stained with hematoxylin-eosin (H&E) for histopathological assessments. Apoptosis level in endothelial cells was determined by using TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick endlabelling) method. Staining of cytoplasmic TNF-α and VEGF in endothelial cells, and perivascular MPO activity were evaluated by immunohistochemistry. The treatments with NAC and vitamin E significantly reduced the rate of nicotine-induced endothelial cell apoptosis. NAC and vitamin E significantly reduced the increases in the local production of TNF-α and VEGF, and perivascular MPO activity. This findings suggest that NAC can be as effective as vitamin E in protecting against nicotine-induced endothelial cell apoptosis. Human & Experimental Toxicology (2007) 26: 595—602.

Differential effect of MLC kinase in TNF-α-induced endothelial cell apoptosis and barrier dysfunction

2001 ◽  
Vol 280 (6) ◽  
pp. L1168-L1178 ◽  
Author(s):  
Irina Petrache ◽  
Alexander D. Verin ◽  
Michael T. Crow ◽  
Anna Birukova ◽  
Feng Liu ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Electrical Resistance ◽  
Stress Fiber ◽  
Fiber Formation ◽  
Endothelial Cell Apoptosis ◽  
Gap Formation ◽  
Barrier Dysfunction ◽  
Tnf Α ◽  
Mlc Phosphorylation

Tumor necrosis factor (TNF)-α is released in acute inflammatory lung syndromes linked to the extensive vascular dysfunction associated with increased permeability and endothelial cell apoptosis. TNF-α induced significant decreases in transcellular electrical resistance across pulmonary endothelial cell monolayers, reflecting vascular barrier dysfunction (beginning at 4 h and persisting for 48 h). TNF-α also triggered endothelial cell apoptosis beginning at 4 h, which was attenuated by the caspase inhibitor Z-Val-Ala-Asp-fluoromethylketone. Exploring the involvement of the actomyosin cytoskeleton in these important endothelial cell responses, we determined that TNF-α significantly increased myosin light chain (MLC) phosphorylation, with prominent stress fiber and paracellular gap formation, which paralleled the onset of decreases in transcellular electrical resistance and enhanced apoptosis. Reductions in MLC phosphorylation by the inhibition of either MLC kinase (ML-7, cholera toxin) or Rho kinase (Y-27632) dramatically attenuated TNF-α-induced stress fiber formation, indexes of apoptosis, and caspase-8 activity but not TNF-α-induced barrier dysfunction. These studies indicate a central role for the endothelial cell cytoskeleton in TNF-α-mediated apoptosis, whereas TNF-α-induced vascular permeability appears to evolve independently of contractile tension generation.

Effects and mechanism of arachidonic acid against TNF-α induced apoptosis of endothelial cells

2020 ◽  
pp. 1-7
Author(s):  
Ji-Xiong Chen ◽  
Xiao-Yan Huang ◽  
Ping Wang ◽  
Wen-Ting Lin ◽  
Wen-Xing Xu ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Umbilical Vein ◽  
Arachidonic Acid Metabolite ◽  
Apoptotic Cells ◽  
Endothelial Cell Apoptosis ◽  
Tnf Α

This study aimed to investigate the effects of arachidonic acid metabolite epoxyeicosatrienoic acid (EETs) in the apoptosis of endothelial cells induced by tumor necrosis factor-alpha (TNF-α). After human umbilical vein endothelial cells were cultured, TNF-α/ActD, 14, 15-EET, and HMR-1098 were added, respectively, into the culture medium. The apoptosis level of endothelial cells was detected by flow cytometry. After TNF-α/ActD induced endothelial cell apoptosis, flow cytometry staining showed that endothelial cell apoptosis increased significantly, and the apoptotic cells were significantly reduced after the addition of 14, 15-EET. However, the apoptotic cells significantly increased after the addition of HMR-1098. Western Blot results showed that the phosphorylation levels of LC3-II and AMPK were increased after TNF-α/ActD induction, and the increase was noticeable after the addition of 14, 15-EET. However, the phosphorylation levels of LC3-II and AMPK significantly decreased after the addition of HMR-1098. The activity of Caspase-8 and -9 decreased significantly after the addition of 14, 15-EET but increased after the addition of HMR-1098. Arachidonic acid can inhibit TNF-α induced endothelial cell apoptosis by upregulating autophagy.

scholarly journals IGFBP-3 and TNF-α Regulate Retinal Endothelial Cell Apoptosis

2013 ◽  
Vol 54 (8) ◽  
pp. 5376 ◽  
Author(s):  
Qiuhua Zhang ◽  
Youde Jiang ◽  
Matthew J. Miller ◽  
Bonnie Peng ◽  
Li Liu ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Endothelial Cell Apoptosis ◽  
Tnf Α ◽  
Retinal Endothelial Cell ◽  
Igfbp 3
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