Key result
The adenosine analogue NECA inhibited LPS-induced reactive oxygen species production by equine neutrophils by up to 94.8% in a concentration- and cAMP-dependent manner.
Why the study?
Does the adenosine analogue NECA inhibit reactive oxygen species production in LPS-stimulated equine neutrophils?
Does the adenosine analogue NECA inhibit reactive oxygen species production in LPS-stimulated equine neutrophils?
Activation of adenosine A2A receptors inhibits ROS production by LPS-stimulated equine neutrophils in a cAMP-dependent manner, suggesting potential for stable adenosine A2A receptor agonists as anti-inflammatory drugs in horses.
Answers are grounded in this paper and cite their sources.
May inform equine anti-inflammatory drug development; leaves open clinical translation from this ex vivo model.
OBJECTIVE: To assess the anti-inflammatory effects of an adenosine analogue on lipopolysaccharide (LPS)-stimulated equine neutrophils. SAMPLE POPULATION: Neutrophils obtained from 10 healthy horses. PROCEDURES: An adenosine analogue (5'-N-ethylcarboxamidoadenosine [NECA]) was tested for its ability to inhibit production of reactive oxygen species (ROS) in LPS-stimulated equine neutrophils. Selective adenosine receptor antagonists were used to identify the receptor subtype responsible for effects. To assess the mechanism of action of NECA, cAMP concentrations were measured, and effects of dibutyryl cAMP (a stable analogue of cAMP) and rolipram (a type 4 phosphodiesterase inhibitor) were investigated. RESULTS: NECA elicited concentration-dependent inhibition of ROS production that was inhibited by ZM241385, a selective adenosine A(2A) receptor antagonist; this effect of NECA was not affected by the adenosine A(2B) receptor antagonist MRS1706. Also, ZM241385 blocked NECA-induced increases in cAMP concentrations, whereas MRS1706 did not alter this effect of NECA. Rolipram potentiated NECA-induced inhibition of ROS production, and dibutyryl cAMP also inhibited ROS production. CONCLUSIONS AND CLINICAL RELEVANCE: Activation of adenosine A(2A) receptors inhibited ROS production by LPS-stimulated equine neutrophils in a cAMP-dependent manner. These results suggest that stable adenosine A(2A) receptor agonists may be developed as suitable anti-inflammatory drugs in horses.
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Sun et al. (2007) studied Healthy (equine neutrophils) (n=10). 5'-N-ethylcarboxamidoadenosine (NECA) vs. LPS alone was evaluated on Inhibition of lipopolysaccharide (LPS)-induced production of reactive oxygen species (ROS) (p=<0.001). The adenosine analogue NECA inhibited LPS-induced reactive oxygen species production by equine neutrophils by up to 94.8% in a concentration- and cAMP-dependent manner.
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