Nonsteroidal anti-inflammatory drugs (NSAIDs) comprise a heterogeneous group of pharmacological agents used for the symptomatic treatment of fever, pain, and inflammation. Although the main mechanism of action of NSAIDs consists of inhibiting prostaglandin synthesis by blocking the enzyme cyclooxygenase (COX), clinical, and experimental data strongly indicate the existence of additional mechanisms. Some of the COX-independent effects are related to the ability of NSAIDs to penetrate biological membranes and disrupt important molecular interactions necessary for a wide array of cellular functions, including cell adhesion. These effects, in particular those that interfere with L-selectin function in neutrophils during the inflammatory response, may contribute to the anti-inflammatory properties that NSAIDs exert in vivo. Recent contributions in this field have shown that the anti-L-selectin effect of NSAIDs is related to the NADPH-oxidase-dependent generation of superoxide anion at the plasma membrane. These findings might represent a novel approach for developing new and effective anti-inflammatory compounds with a better safety profile than the currently available NSAIDs.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/eji.201445222

NSAIDs: learning new tricks from old drugs.

Indomethacin sensitizes TRAIL-resistant melanoma cells to TRAIL-induced apoptosis through ROS-mediated upregulation of death receptor 5 and downregulation of survivin

Aspirin and indomethacin reduce lung inflammation of mice exposed to cigarette smoke.

Background: To determine in vitro if indomethacin inhibits proliferation and induces apoptosis in human retinoblastoma cell line Y79, and to explore possibly invo

Antiproliferative and apoptotic effects of indomethacin on human retinoblastoma cell line Y79 and the involvement of β-catenin, nuclear factor-κB and Akt signaling pathways.

Combined treatment of Caco-2 cells with butyrate and mesalazine inhibits cell proliferation and reduces Survivin protein level

Indomethacin is widely used to treat inflammatory and prevent adverse events which frequently accrue in biotherapy. In phase I clinical trial of recombinant human lymphotoxin alpha (rhLTalpha), indomethacin was premedicated to alleviate chill and fever. However, it is unknown whether indomethacin influences the therapeutic efficacy of rhLTalpha. In this study we found that pre-treatment with low dose of indomethacin enhanced the cytotoxicity of rhLTalpha and/or cisplatin/adriamycin on human tumor cells. Further investigation demonstrated that indomethacin dose-dependently suppressed the activation of nuclear factor kappa B (NFkappaB) by inhibiting phosphorylation and degradation of IkappaBalpha. In addition, indomethacin decreased the expression of NFkappaB-regulated gene products involved in rhLTalpha-induced anti-apoptosis (XIAP, cFLIP and cIAP-1), which may explain its sensitization of tumor cells to rhLTalpha and/or cisplatin/adriamycin.

Indomethacin enhances the cytotoxicity of recombinant human lymphotoxin alpha on tumor cells by suppressing NFkappaB signaling.

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Indomethacin enhances the cytotoxicity of recombinant human lymphotoxin alpha on tumor cells by suppressing NFkappaB signaling.