Aspirin-triggered lipoxin A4 attenuates lipopolysaccharide induced inflammatory response in primary astrocytes

•Effects of aspirin-triggered-lipoxin A4 (ATL) on astrocytes inflammatory response were evaluated.•Inflammatory response was induced by lipopolysaccharide in cultured cortical astrocytes.•ATL inhibited production of nitric oxide and prostaglandin E2.•ATL reduced the expression of cyclooxygenase 2 and inducible nitric oxide synthase.•ATL attenuated NF-κB signal transducer pathway.

The activation of astrocytes contributes to inflammatory responses underlying brain injury and neurodegenerative diseases. Lipoxins have emerged as mediators of endogenous anti-inflammatory events. However, the involvement of aspirin-triggered-lipoxin A4 (ATL) in astrocyte-induced neuroinflammatory responses has not been investigated. Here, we examined the anti-inflammatory effects of ATL in the central nervous system using rat astrocyte cultures stimulated with lipopolysaccharide (LPS). We found that pretreatment with ATL exerted potent anti-inflammatory effects by inhibiting LPS-induced production of nitric oxide and prostaglandin E2. ATL also reduced the expression of cyclooxygenase 2 and inducible nitric oxide synthase mRNA and protein. Furthermore, ATL suppressed the LPS-induced translocation of the NF-κB p65 subunit to the nucleus and prevented LPS-induced IκBα phosphorylation in a dose-dependent manner. These findings suggest that ATL attenuates neuroinflammation by inhibiting the NF-κB signal transducer pathway in cultured cortical astrocytes.