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http://dx.doi.org/10.5483/BMBRep.2014.47.1.089

Aspirin inhibits lipopolysaccharide-induced COX-2 expression and PGE2 production in porcine alveolar macrophages by modulating protein kinase C and protein tyrosine phosphatase activity  

Duan, Yuzhong (Cancer Institute of PLA, Xinqiao Hospital, Third Military Medical University)
Chen, Fanglin (Cancer Institute of PLA, Xinqiao Hospital, Third Military Medical University)
Zhang, Anmei (Cancer Institute of PLA, Xinqiao Hospital, Third Military Medical University)
Zhu, Bo (Cancer Institute of PLA, Xinqiao Hospital, Third Military Medical University)
Sun, Jianguo (Cancer Institute of PLA, Xinqiao Hospital, Third Military Medical University)
Xie, Qichao (Cancer Institute of PLA, Xinqiao Hospital, Third Military Medical University)
Chen, Zhengtang (Cancer Institute of PLA, Xinqiao Hospital, Third Military Medical University)
Publication Information
BMB Reports / v.47, no.1, 2014 , pp. 45-50 More about this Journal
Abstract
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, $I{\kappa}B{\alpha}$ degradation, NF-${\kappa}B$ 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-${\kappa}B$ 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.
Keywords
Acute lung injury; Alveolar macrophages; Protein kinase C; Protein tyrosine phosphatase;
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