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Aspirin has been demonstrated to be effective in inhibiting COX-2 and PGE(2) in Alveolar macrophages (AMs). However, the mechanisms have not been fully understood. In the present study, we found that pretreatment with aspirin inhibited LPS-induced COX-2 and PGE(2) upregulation, IκBα degradation, NFκB activation and the increase of PKC activity, but elevated LPS-induced the decrease of PTP activity. The PKC inhibitor calphostin C dramatically reduced the COX-2 mRNA and PGE(2) levels, but the PTP inhibitor peroxovanadium (POV) significantly increased the COX-2 mRNA and PGE(2) levels. Furthermore, the PTP inhibitor mitigated the inhibitory effect of aspirin on COX-2 and PGE(2) upregulation and NF-κB activation, whereas the PKC inhibitor enhanced the inhibitory effects of aspirin on the production of COX-2 and PGE(2). Our data indicate a novel mechanism by which aspirin acts as a potent anti-inflammatory agent in alveolus macrophages and ALI.

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Aspirin inhibits lipopolysaccharide-induced COX-2 expression and PGE<sub>2</sub>production in porcine alveolar macrophages by modulating protein kinase C and protein tyrosine phosphatase activity

Aspirin inhibits lipopolysaccharide-induced COX-2 expression and PGE2production in porcine alveolar macrophages by modulating protein kinase C and protein tyrosine phosphatase activity

Aspirin inhibits lipopolysaccharide-induced COX-2 expression and PGE₂production in porcine alveolar macrophages by modulating protein kinase C and protein tyrosine phosphatase activity