scholarly journals Inflammatory response in the mid colon of ICR mice treated with polystyrene microplastics for two weeks

2021 ◽  
Vol 37 (1) ◽  
Author(s):  
Yun Ju Choi ◽  
Ji Eun Kim ◽  
Su Jin Lee ◽  
Jeong Eun Gong ◽  
You Jeong Jin ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Oral Administration ◽  
Treated Group ◽  
Nuclear Factor ◽  
Icr Mice ◽  
Pyrin Domain ◽  
Tnf Α ◽  
Vehicle Treated Group ◽  
Light Chain Enhancer ◽  
Necrosis Factor

Abstract Background The oral administration of polystyrene-microplastics (PS-MPs) causes chronic constipation of ICR mice, but there are no reports on their effects on the inflammatory response in the colon. To determine if the oral administration of MPs causes inflammation in the colon, the changes in the apoptosis-associated speck like protein containing a caspase recruitment domain (ASC)-inflammasome pathway, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway, and inflammatory cytokine expression were evaluated in the mid colon of ICR mice treated with 0.5 μm size PS-MPs for two weeks. Results The thicknesses of the mucosa, muscle, flat luminal surface, and crypt layer were decreased significantly (p < 0.01) in the mid colon of the MPs treated group compared to the Vehicle treated group. On the other hand, a remarkable increase in the expression levels of NOD-like receptor pyrin domain-containing protein (NLRP) 3, ASC, and Cleaved Caspase (Cas)-1 protein was observed in the MPs treated group. In addition, similar increasing pattern in the levels of p-NF-κB and phospho-inhibitory subunit of NF-κB (p-IkB) α protein was detected. Four inflammatory cytokines, including NF-κB, interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1β, showed an increased expression level after the MPs treatment. Conclusions Therefore, the present study suggests that PS-MPs can be a novel cause of an inflammatory response in the mid colon of ICR mice.

scholarly journals Therapeutic effect and mechanism of action of quercetin in a rat model of osteoarthritis

2019 ◽  
Vol 48 (3) ◽  
pp. 030006051987346 ◽  
Author(s):  
Jun Zhang ◽  
Jing Yin ◽  
Daohong Zhao ◽  
Chaoran Wang ◽  
Yuhao Zhang ◽  
...  
Keyword(s):  
Therapeutic Effect ◽  
Mechanism Of Action ◽  
Rat Model ◽  
Dependent Manner ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Tnf Α ◽  
Dose Dependent ◽  
Light Chain Enhancer ◽  
Necrosis Factor

Objective To study the therapeutic effect and mechanism of action of quercetin in a rat model of osteoarthritis (OA). Methods The OA rat model was established by intra-articular injection of papain. Changes in knee diameter, toe volume and histopathology were measured. Levels of interleukin (IL)-β and tumor necrosis factor (TNF)-α were assessed by ELISA. Relative expression of Toll-like receptor (TLR)-4 and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) was evaluated by western blotting. Results Compared with rats treated with papain alone, changes in knee diameter, toe volume and Makin' s score were less apparent in OA rats treated with quercetin. Levels of serum IL-1β and TNF-α were also reduced in quercetin-treated OA rats. Expression of TLR-4 and NF-κB was significantly suppressed in a dose-dependent manner in quercetin-treated OA rats. Conclusion Quercetin exhibited a therapeutic effect in OA rats, which may be related to inhibition of IL-1β and TNF-α production via the TLR-4/NF-κB pathway.

Tumor Necrosis Factor, α-Induced Protein 3 Interacting Protein 2 is Involved in the Inflammatory Response in Sepsis via Inhibiting the Nuclear Factor-κB Pathway Activation

2020 ◽  
Vol 10 (4) ◽  
pp. 582-588
Author(s):  
Jia Li ◽  
Ye He ◽  
Yuping Li
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Responses ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Nuclear Factor ◽  
Interacting Protein ◽  
Raw264.7 Macrophages ◽  
Pathway Activation ◽  
Tnf Α ◽  
Necrosis Factor

The study aimed to explore the role of TNFAIP3 interacting protein 2 (TNIP2) in lipopolysaccharide (LPS) induced RAW264.7 macrophages or septic mice. TNIP2 level was detected using quantitative real time polymerase chain reaction (qRT-PCR) and western blotting. LPS-stimulated RAW264.7 macrophages were used to investigate the effects of TNIP2 on sepsis in vitro. In addition, septic mice model was established to validate the regulation of TNIP2 during inflammation response in vivo. The levels of inflammatory cytokines were assessed by enzyme-linked immunosorbent assay (ELISA). The data indicated that TNIP2 mRNA was down-regulated in the peripheral blood from sepsis patients. Interleukin (IL)-1β, IL-6 and tumour necrosis factor (TNF)-α levels were significantly increased and the level of TNIP2 was suppressed in LPS-stimulated macrophages compared to the control group. TNIP2-plasmid promoted the TNIP2 expression in RAW 264.7 macrophages and reversed the effects of LPS on inflammatory factors and Nuclear factor-κ B (NFκ- B) pathway. The results also showed that TNIP2-plasmid alleviated inflammatory responses in septic mice, evidenced by the reduction in the levels of TNF-α , IL-1β and IL-6. TNIP2-plasmid also reduced the secretion of organ damage markers in septic mice serum. Our data indicated that TNIP2 was involved in the inflammatory response in sepsis via inhibiting the NF-κ B pathway activation.

scholarly journals Re-expression of HPV16 E2 in SiHa (human cervical cancer) cells potentiates NF-κB activation induced by TNF-α concurrently increasing senescence and survival

2015 ◽  
Vol 35 (1) ◽  
Author(s):  
Devan Prabhavathy ◽  
Chandrasekaran Karthik Subramanian ◽  
Devarajan Karunagaran
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Tumour Necrosis ◽  
Nuclear Factor ◽  
Tnf Α ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Light Chain Enhancer ◽  
Necrosis Factor ◽  
Human Cervical Cancer

Human papillomavirus (HPV)16 E2 potentiates NF-κB (nuclear factor kappa-light-chain-enhancer of activated B-cells) activation induced by tumour necrosis factor (TNF)-α in SiHa (human cervical cancer) cells and significantly influences cell viability, apoptosis and expression of pro-survival genes regulated by NF-κB.

Tumor necrosis factor induces neuroendocrine differentiation in small cell lung cancer cell lines

1998 ◽  
Vol 275 (2) ◽  
pp. L311-L321 ◽  
Author(s):  
Kathleen J. Haley ◽  
Kirit Patidar ◽  
Fan Zhang ◽  
Rodica L. Emanuel ◽  
Mary E. Sunday
Keyword(s):  
Cell Differentiation ◽  
Cell Lines ◽  
Nuclear Factor Κb ◽  
Neuroendocrine Cell ◽  
Acid Decarboxylase ◽  
Nuclear Factor ◽  
Small Cell Lung ◽  
Amino Acid Decarboxylase ◽  
Tnf Α ◽  
Necrosis Factor

We studied tumor necrosis factor (TNF)-α as a candidate cytokine to promote neuroendocrine cell differentiation in a nitrosamine-hyperoxia hamster lung injury model. Differential screening identified expression of the genes modulated by TNF-α preceding neuroendocrine cell differentiation. Undifferentiated small cell lung carcinoma (SCLC) cell lines NCI-H82 and NCI-H526 were treated with TNF-α for up to 2 wk. Both cell lines demonstrated rapid induction of gastrin-releasing peptide (GRP) mRNA; H82 cells also expressed aromatic-l-amino acid decarboxylase mRNA within 5 min after TNF-α was added. Nuclear translocation of nuclear factor-κB immunostaining occurred with TNF-α treatment, suggesting nuclear factor-κB involvement in the induction of GRP and/or aromatic-l-amino acid decarboxylase gene expression. We also demonstrated dense core neurosecretory granules and immunostaining for proGRP and neural cell adhesion molecule in H82 cells after 7–14 days of TNF-α treatment. We conclude that TNF-α can induce phenotypic features of neuroendocrine cell differentiation in SCLC cell lines. Similar effects of TNF-α in vivo may contribute to the neuroendocrine cell differentiation/hyperplasia associated with many chronic inflammatory pulmonary diseases.

scholarly journals EKSPRESI Tumor Necrosis Factor alpha (TNF-α) DAN Transforming growth factors beta (TGF-β) PADA PERIODONTITIS APIKALIS KRONIS AKIBAT INDUKSI Enterococcus faecalis PADA TIKUS WISTAR

2019 ◽  
Vol 7 (2) ◽  
pp. 66
Author(s):  
Richard Fritzgerald ◽  
Cecilia Lunardhi ◽  
Ruslan Effendy ◽  
Tamara Yuanita
Keyword(s):  
Tissue Damage ◽  
Treated Group ◽  
Positive Control ◽  
Negative Control ◽  
Control Group ◽  
Transforming Growth Factors ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background. Root canal treatment is a main role in decreasing infection from root canal and pulp. The main cause of periapical damage mostly are bacteries. E.faecalis is a bactery that is found as an etiology of endodontic treatment failure. Cell wall of this bacteria is containing Lipoteichoic acid (LTA). LTA can penetrate into the periradicular tissue, act as endotoxin in host and cause periradicular inflammation then lead to bone destruction. LTA stimulates immunology reaction that produce Tumor Necrosis Factor alpha (TNF-α) and Transforming growth factors beta (TGF-ß). TNF-α is a main mediator and also have an important role in inflamation response otherwise TGF-ß is working as a multifunction  regulator of cell growth and differentiation during reforming and remodelling.  Purpose. The aim of this study is to know about the expression of TNF-α and TGF-ß during the periapical tissue damage due to induction of E.faecalis. Method. This study used laboratory experimental with the post test only control group design. A total of 30 male rats were randomly divided into 3 main groups, Group A (control negative) : normal tooth. Group B (control positive) : every tooth was induced only by sterile BHI-b. Group C (treated group) : every tooth  was induced by 10 μl BHI-b E.faecalis ATCC212(106 CFU). The animals were sacrificed 21 days later and prepared for histological examination of tissue damage, then we did the immunohistochemistry  followed by calculation on the light microscope. Result. The analysis revealed that the expression of TNF-α at treated group are higher than negative control and positive control but the expression of  TGF-ß at treated group are higher than the negative control group but lower than positive control. Conclusion. From this study we know that the expression of TNF-α and TGF-ß are changing during the periapical tissue damage that induced by E.faecalis.

scholarly journals Laxative Effect of Spicatoside A by Cholinergic Regulation of Enteric Nerve in Loperamide-Induced Constipation: ICR Mice Model

Molecules ◽  
2019 ◽  
Vol 24 (5) ◽  
pp. 896 ◽  
Author(s):  
Ji Kim ◽  
Ji Park ◽  
Mi Kang ◽  
Hyeon Choi ◽  
Su Bae ◽  
...  
Keyword(s):  
Chronic Constipation ◽  
Water Channel ◽  
Treated Group ◽  
Histological Structure ◽  
Neural Cells ◽  
Mice Model ◽  
Icr Mice ◽  
Cholinergic Regulation ◽  
Spicatoside A ◽  
Vehicle Treated Group

Researches on spicatoside A (SpiA)-containing natural products suggest the possibility of SpiA as a potential laxative to alleviate chronic constipation. However, no studies have been conducted with single compound administration of SpiA. To verify the laxative effects and mechanism of action of SpiA on chronic constipation, we investigated alterations in the excretion parameters, histological structure, and cholinergic regulation of the enteric nerve in the colons of Institute of Cancer Research (ICR) mice with loperamide (Lop)-induced constipation after exposure to 20 mg/kg of SpiA. Decrease in the number, weight and water contents of stools in the Lop+Vehicle treated group significantly recovered after SpiA treatment, and alterations in the histological structure and transmission electron microscopy (TEM) images were improved in the Lop+SpiA treated group. Similar recovery effects were observed in the ability for mucin secretion and expression of the membrane water channel gene (aquaporin 8, AQP8). Furthermore, significant improvements were observed in the acetylcholinesterase (AChE) activity and acetylcholine receptors’ (AChRs) downstream signaling pathway after treatment of SpiA. The levels of gastrointestinal (GI) hormones including cholecystokinin (CCK) and gastrin were also remarkably enhanced in the Lop+SpiA treated group as compared to the Lop+Vehicle treated group. The expression of receptor tyrosine kinase (C-kit) and protein gene product 9.5 (PGP9.5) in Cajal and neural cells, as well as the phosphorylation of myosin light chain (MLC) in smooth muscle cells, were recovered after SpiA exposure. Taken together, the results of the present study provide the first strong evidence that SpiA improves chronic constipation through muscarinic cholinergic regulation of the enteric nerve in a Lop-induced constipation ICR mice model.

scholarly journals POPing the fire into the pyrin?

2003 ◽  
Vol 373 (1) ◽  
pp. e1-e2
Author(s):  
Sanjeev MARIATHASAN ◽  
Domagoj VUCIC
Keyword(s):  
Inflammatory Response ◽  
Adaptor Proteins ◽  
Nuclear Factor Κb ◽  
Scaffold Proteins ◽  
Interleukin 1Β ◽  
Nuclear Factor ◽  
Complex Assembly ◽  
Inflammatory Disorders ◽  
Pyrin Domain ◽  
Biochemical Journal

Initiation of an inflammatory response requires the co-ordinated participation of proteins within a scaffold in the cytosol of responding cells. The scaffold proteins contain members of a newly discovered family of pyrin-domain adaptor proteins that regulate complex assembly for initiation of nuclear factor κB and interleukin-1β signalling. A paper in this issue of the Biochemical Journal by Stehlik et al. identifies a new member of the pyrin family that may control signalling by sequestering pro-inflammatory components, shedding light on the origin of human inflammatory disorders.

scholarly journals MON-721 Crude Protein of Pyropia Yezoensis Protects Against Tumor Necrosis Factor-á-Induced Myotube Atrophy by Regulating the Mitogen-Activated Protein Kinase and Nuclear Factor-Kappab Signaling Pathways in C2C12 Myotubes

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Min-Kyeong Lee ◽  
Nam Taek-Jeong ◽  
Youn Hee Choi
Keyword(s):  
Muscle Atrophy ◽  
Crude Protein ◽  
Tumor Necrosis ◽  
Mitogen Activated Protein Kinase ◽  
C2c12 Myotubes ◽  
Nuclear Factor Kappab ◽  
Nuclear Factor ◽  
Tnf Α ◽  
Mitogen Activated Protein ◽  
Necrosis Factor

Abstract Proinflammatory cytokines induce ubiquitin-proteasome-dependent proteolysis by activating intracellular factors in skeletal muscle, leading to muscle atrophy. Therefore, we investigated the protective effect of Pyropia yezoensis crude protein (PYCP) on tumor necrosis factor (TNF)-α-induced muscle atrophy in vitro. Mouse skeletal muscle C2C12 myotubes were treated for 48 h with TNF-α (20 ng/mL) in the presence or absence of PYCP (25, 50, and 100 μg/mL). PYCP at concentrations up to 100 μg/mL did not affect cell viability. Exposure to TNF-α for 48 h significantly decreased the diameter of myotubes, which was increased by treatment with 25, 50, and 100 μg/mL PYCP. PYCP inhibited TNF-α-induced intracellular reactive oxygen species accumulation in C2C12 myotubes. In addition, PYCP significantly reduced the levels of phosphorylated p38 and JNK. Moreover, by inhibiting the degradation of inhibitor of kappaB-α, PYCP significantly suppressed the TNF-α-induced increased transcriptional activity and nuclear translocation of nuclear factor-kappaB (NF-κB). Furthermore, PYCP inhibited E3-ubiquitin ligases in TNF-α-treated C2C12 myotubes. In conclusion, PYCP ameliorated TNF-α-induced muscle atrophy by inhibiting the mitogen-activated protein kinase-mediated NF-κB pathway, indicating that it has therapeutic potential for related disorders.

scholarly journals Shiga Toxin 1-Induced Inflammatory Response in Lipopolysaccharide-Sensitized Astrocytes Is Mediated by Endogenous Tumor Necrosis Factor Alpha

2009 ◽  
Vol 78 (3) ◽  
pp. 1193-1201 ◽  
Author(s):  
Verónica I. Landoni ◽  
Marcelo de Campos-Nebel ◽  
Pablo Schierloh ◽  
Cecilia Calatayud ◽  
Gabriela C. Fernandez ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Response ◽  
Tumor Necrosis Factor Alpha ◽  
Shiga Toxin ◽  
Tumor Necrosis ◽  
Brain Inflammation ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Hemolytic-uremic syndrome (HUS) is generally caused by Shiga toxin (Stx)-producing Escherichia coli. Endothelial dysfunction mediated by Stx is a central aspect in HUS development. However, inflammatory mediators such as bacterial lipopolysaccharide (LPS) and polymorphonuclear neutrophils (PMN) contribute to HUS pathophysiology by potentiating Stx effects. Acute renal failure is the main feature of HUS, but in severe cases, patients can develop neurological complications, which are usually associated with death. Although the mechanisms of neurological damage remain uncertain, alterations of the blood-brain barrier associated with brain endothelial injury is clear. Astrocytes (ASTs) are the most abundant inflammatory cells of the brain that modulate the normal function of brain endothelium and neurons. The aim of this study was to evaluate the effects of Stx type 1 (Stx1) alone or in combination with LPS in ASTs. Although Stx1 induced a weak inflammatory response, pretreatment with LPS sensitized ASTs to Stx1-mediated effects. Moreover, LPS increased the level of expression of the Stx receptor and its internalization. An early inflammatory response, characterized by the release of tumor necrosis factor alpha (TNF-α) and nitric oxide and PMN-chemoattractant activity, was induced by Stx1 in LPS-sensitized ASTs, whereas activation, evidenced by higher levels of glial fibrillary acid protein and cell death, was induced later. Furthermore, increased adhesion and PMN-mediated cytotoxicity were observed after Stx1 treatment in LPS-sensitized ASTs. These effects were dependent on NF-κB activation or AST-derived TNF-α. Our results suggest that TNF-α is a pivotal effector molecule that amplifies Stx1 effects on LPS-sensitized ASTs, contributing to brain inflammation and leading to endothelial and neuronal injury.

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