Effects of Feiyanning Decoction, a compound traditional Chinese medicine, on iNOS and COX-2 expressions induced by tumor necrosis factor-α in lung adenocarcinoma cell line

The beneficial effect of n-3 fatty acids can be related to anti-inflammatory properties. The aim of the study was to analyzed the effect of eicosapentaenoic acid (EPA) on 3T3-L1 cells (murine embryonic fibroblasts‒preadipocytes) activated with inflammatory factors (IF). Cells were incubated with 50 µmol of EPA for 48 h, and then activated with lipopolysaccharide (LPS) or tumor necrosis factor-α (TNF-α). The level of cycloxygenase-2 (Prostaglandin-Endoperoxide Synthase 2, PTGS2, COX-2), cytosolic prostaglandin synthase E2 (cPGES), fatty acid binding protein 4 (FABP4), toll-like receptor 4 (TLR4), glucose receptor type 4 (GLUT-4), and cannabinoid receptor 2 (CB2) was determined using Western blot analysis. The phospholipase A2 (Pla2g4a), and prostaglandin-Endoperoxide Synthase 2 (Ptgs2) gene expression was analyzed by real-time qPCR. After EPA and IF activation, a significant decrease in the COX-2, cPGES, and TRL4 protein levels was observed. Incubation of cells with EPA and IF resulted in a decrease in Ptgs2 and an increase in the Pla2g4a gene. A significant increase in the CB2 protein was observed in adipocytes co-treated with EPA and IF. The results indicated an anti-inflammatory properties of EPA. Interestingly, the activation of the GLUT4 receptor by EPA suggests an unique role of this FA in the regulation of the adipocyte metabolism and prevention of insulin resistance.

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Differential regulation of cyclooxygenase-2 (COX-2) mRNA stability by interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in human in vitro differentiated macrophages

Biochemical Pharmacology ◽

10.1016/s0006-2952(99)00312-3 ◽

2000 ◽

Vol 59 (2) ◽

pp. 187-194 ◽

Cited By ~ 88

Author(s):

Zai-Feng Huang ◽

John B Massey ◽

David P Via

Keyword(s):

Tumor Necrosis Factor ◽

Mrna Stability ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Differential Regulation ◽

Tnf Α ◽

Cox 2 ◽

Factor Α ◽

Necrosis Factor

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Immediate and delayed potentiating effects of tumor necrosis factor-α on TRPV1 sensitivity of rat vagal pulmonary sensory neurons

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00235.2016 ◽

2017 ◽

Vol 313 (2) ◽

pp. L293-L304 ◽

Cited By ~ 6

Author(s):

Chun-Chun Hsu ◽

You Shuei Lin ◽

Ruei-Lung Lin ◽

Lu-Yuan Lee

Keyword(s):

Tumor Necrosis Factor ◽

Sensory Neurons ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Transient Receptor Potential ◽

Receptor Potential ◽

Transient Receptor Potential Vanilloid ◽

Cox 2 ◽

Factor Α ◽

Necrosis Factor

We studied acute effects of tumor necrosis factor-α (TNFα) on the sensitivity of isolated rat vagal pulmonary sensory neurons. Our results showed the following. First, a brief pretreatment with a low dose of TNFα (1.44 nM, 9 min) enhanced the sensitivity of transient receptor potential vanilloid type 1 (TRPV1) receptors in these neurons in two distinct phases: the inward current evoked by capsaicin was amplified (Δ = 247%) immediately following the TNFα pretreatment, which gradually declined toward control and then increased again reaching another peak (Δ = 384%) after 60–90 min. Second, the immediate phase of this potentiating effect of TNFα was completely abolished by a pretreatment with a selective cyclooxygenase-2 (COX-2) inhibitor, NS-398, whereas the delayed potentiation was only partially attenuated. Third, in sharp contrast, TNFα did not generate any potentiating effect on the responses to non-TRPV1 chemical activators of these neurons. Fourth, the selectivity of the TNFα action on TRPV1 was further illustrated by the responses to acid (pH 6.0); TNFα did not affect the rapid transient current mediated by acid-sensing ion channels but significantly augmented the slow sustained current mediated by TRPV1 in the same neurons. Fifth, in anesthetized rats, a similar pattern of acute sensitizing effects of TNFα on pulmonary C-fiber afferents and the involvement of COX-2 were also clearly shown. In conclusion, a brief pretreatment with TNFα induced both immediate and delayed potentiating effects on the TRPV1 sensitivity in pulmonary sensory neurons, and the production of COX-2 arachidonic acid metabolites plays a major role in the immediate sensitizing effect of TNFα.

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Inhibition of cyclooxygenase-2 activity in subchondral bone modifies a subtype of osteoarthritis

Bone Research ◽

10.1038/s41413-019-0071-x ◽

2019 ◽

Vol 7 (1) ◽

Cited By ~ 8

Author(s):

Manli Tu ◽

Mi Yang ◽

Nanxi Yu ◽

Gehua Zhen ◽

Mei Wan ◽

...

Keyword(s):

Subchondral Bone ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Joint Destruction ◽

Cartilage Degeneration ◽

Cyclooxygenase 2 ◽

Disease Modifying Therapy ◽

Cox 2 ◽

Factor Α ◽

Necrosis Factor

Abstract Osteoarthritis (OA) causes the destruction of joints. Its pathogenesis is still under investigation, and there is no effective disease-modifying therapy. Here, we report that elevated cyclooxygenase-2 (COX-2) expression in the osteocytes of subchondral bone causes both spontaneous OA and rheumatoid arthritis (RA). The knockout of COX-2 in osteocytes or treatment with a COX-2 inhibitor effectively rescues the structure of subchondral bone and attenuates cartilage degeneration in spontaneous OA (STR/Ort) mice and tumor necrosis factor-α transgenic RA mice. Thus, elevated COX-2 expression in subchondral bone induces both OA-associated and RA-associated joint cartilage degeneration. The inhibition of COX-2 expression can potentially modify joint destruction in patients with arthritis.

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