AMP-activated protein kinase is activated by non-steroidal anti-inflammatory drugs.

Abstract:

:AMP-activated kinase (AMPK) is a cellular energy sensor, which is activated in stages of increased adenosine triphosphate (ATP) consumption. Its activation has been associated with a number of beneficial effects such as decrease of inflammatory processes and inhibition of disease progression of diabetes and obesity. A recent study suggested that salicylate, the active metabolite of the non-steroidal anti-inflammatory drug (NSAID) acetyl-salicylic acid (aspirin), is able to activate AMPK pharmacologically. This observation raised the question whether or not other NSAIDs might also act as AMPK activators and whether this action might contribute to their cyclooxygenase (COX)-independent anti-inflammatory properties. In this study, we investigated mouse and human neuronal cells and liver tissue of mice after treatment with various NSAIDs. Our results showed that the non-selective acidic NSAIDs ibuprofen and diclofenac induced AMPK activation similar to aspirin while the COX-2 selective drug etoricoxib and the non-opioid analgesic paracetamol, both drugs have no acidic structure, failed to activate AMPK. In conclusion, our results revealed that AMPK can be activated by specific non-steroidal anti-inflammatory drugs such as salicylic acid, ibuprofen or diclofenac possibly depending on the acidic structure of the drugs. AMPK might therefore contribute to their antinociceptive and anti-inflammatory properties.

journal_name

Eur J Pharmacol

authors

King TS,Russe OQ,Möser CV,Ferreirós N,Kynast KL,Knothe C,Olbrich K,Geisslinger G,Niederberger E

doi

10.1016/j.ejphar.2015.06.001

subject

Has Abstract

pub_date

2015-09-05 00:00:00

pages

299-305

eissn

0014-2999

issn

1879-0712

pii

S0014-2999(15)30066-2

journal_volume

762

pub_type

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