Glyoxal and Methylglyoxal as E-cigarette Vapor Ingredients-Induced Pro-Inflammatory Cytokine and Mucins Expression in Human Nasal Epithelial Cells

Glyoxal and Methylglyoxal as E-cigarette Vapor Ingredients-Induced Pro-Inflammatory Cytokine and Mucins Expression in Human Nasal Epithelial Cells

Background: Glyoxal (GO) and methylglyoxal (MGO) is among the majority of the toxic compounds emitted by electronic cigarettes (e-cigarettes) and cigarette smoke tobacco regularly. respiratory diseases presented mucus over production as their main pathophysiologic features. However, the effects of GO and MGO in pro-inflammatory cytokines and mucin expression in human nasal epithelial cells, as well as the underlying signaling pathway, has not been studied.


Objective: This study was to determine whether the GO and MGO induce pro-inflammatory cytokines, and expression of MUC5AC / 5B via MAPK (MAPK) and nuclear factor-kappa-light-chain-enhancer activated B cells (NF kB) signaling pathway.


Methods: The effect of GO and MGO in pro-inflammatory cytokines, mucins expression and signaling pathways of GO and MGO were investigated using enzyme immunoassay water-soluble tetrazolium salt-1, and immunoblot analysis with specific inhibitors and small interfering RNA.


Results: GO and MGO did not affect cell viability up to 2 mM in human nasal epithelial cells. GO and MGO increased production of pro-inflammatory such as interleukin (IL) -1β and IL-6) and MUC5AC / 5B. In addition, GO and MGO was significantly activated extracellular signal-regulated kinase 1/2 (ERK1 / 2), p38 MAPK and NF-kB. Do ERK1 / 2, p38 MAPK and NF-kB signaling pathway involved in the GO and MGO-induced production of pro-inflammatory cytokines (IL-1β and IL-6) and MUC5AC / 5B, we used specific inhibitors and siRNA transfection. This is significantly suppressed Go and MGO-induced expression of pro-inflammatory cytokines (IL-1β and IL-6) and MUC5AC / 5B.

Conclusions: GO and MGO-induced pro-inflammatory cytokines and expression of MUC5AC / 5B through ERK1 / 2, p38 MAPK and NF-kB in human nasal epithelial cells. These results indicate that GO and MGO may be involved in airway diseases related to hypersecretion of mucus.

Glyoxal and Methylglyoxal as E-cigarette Vapor Ingredients-Induced Pro-Inflammatory Cytokine and Mucins Expression in Human Nasal Epithelial Cells
Glyoxal and Methylglyoxal as E-cigarette Vapor Ingredients-Induced Pro-Inflammatory Cytokine and Mucins Expression in Human Nasal Epithelial Cells

Acyclic Triterpenoid Isolated from Alpinia katsumadai Relieves Chronic Formalin-Induced Rat Paw Inflammation by Inhibiting the phosphorylation of ERK and NF-kB

Chronic and excessive inflammation can damage organs and cause a host of inflammatory diseases such as inflammatory bowel disease, asthma, and rheumatoid arthritis. In this study, we investigated the anti-inflammatory effects of Alpinia katsumadai derived seed-pentahydroxy 2,3,5,22,23-2,6,10,15,19,23-hexamethyl-tetracosa-6,10,14, 18-tetraene (IPM) using lipopolysaccharide (LPS) -stimulated J774 cells and chronic foot rat model of formalin-induced inflammation. In vitro results showed that PHT showed no cytotoxicity and decreased LPS-induced NO secretion.

In addition, PHT inhibit LPS-induced inducible NO synthase (iNOS) and cyclooxygenase 2 expression (COX2) protein. Quantitative real-time PCR results showed that PHT downregulated gene expression of proinflammatory cytokine interleukin-1β (IL-1β) and interleukin-6 (IL-6) but not tumor necrosis factor α (TNF-α). IPM inhibit LPS-induced phosphorylation of extracellular signal-regulated kinase (ERK) and nuclear factor of kappa light chain enhancer activated B cells (NF-kB). In the mouse model, oral administration of 50 mg / kg PHT significantly reduced both the thickness and volume of mouse feet.

These results indicate that IPM has potential anti-inflammatory effects and should be considered as a possible functional material.Human podocytes (HPC) plays an important role in the pathogenesis of kidney disease. In this context, angiotensin II (Ang II) and nuclear factor kappa-light-chain-enhancer activated B cells (NF) plays an important role in Podosit injury.

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Description: A polyclonal antibody for detection of NF?B-p65 phospho Ser281) from Human, Mouse, Rat. This NF?B-p65 phospho Ser281) antibody is for IHC-P, ELISA. It is affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogenand is unconjugated. The antibody is produced in rabbit by using as an immunogen synthesized peptide derived from human NF?B-p65 around the phosphorylation site of S281

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ABP56026-02ml 0.2ml
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Description: A polyclonal antibody for detection of NF?B-p65 phospho Ser281) from Human, Mouse, Rat. This NF?B-p65 phospho Ser281) antibody is for IHC-P, ELISA. It is affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogenand is unconjugated. The antibody is produced in rabbit by using as an immunogen synthesized peptide derived from human NF?B-p65 around the phosphorylation site of S281

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Description: A Rabbit Polyclonal antibody against NF?B-p65 (phospho Ser281) from Human/Mouse/Rat. This antibody is tested and validated for IHC, WB, ELISA

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phospho-CREB (Ser133)

RA18008 100 ul
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DAPK1 (Phospho- Ser736) Antibody

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DAPK1 (Phospho- Ser289) Antibody

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NuaK1 (Phospho- Ser600) Antibody

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DSCR1 (Phospho- Ser108) Antibody

ABF8268 100 ug
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eEF2K (Phospho- Ser359) Antibody

ABF8269 100 ug
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HtrA2 (Phospho- Ser212) Antibody

ABF8275 100 ug
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More recently, transmembrane proteins (Tmem) 63C, a member of Tmem-family found to be expressed in the kidney and associated with Podosit function. In this study, we analyzed the expression and regulation of functional Tmem63c impact on cell viability and apoptosis in HPC in the context of activation of Ang II.

Tony

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