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.