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

Yuzhong Duan|Fanglin Chen|Anmei Zhang|Bo Zhu|Jian-guo Sun|Qichao Xie|Zheng-tang Chen
생화학분자생물학회 (Korean Society Of Biochemistry And Molecular Biology)|2014.01|BMB Reports|제47권 제1호|pp. 45-50

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참고문헌

키워드

Acute lung injuryProtein kinase CProtein tyrosine phosphataseAlveolar macrophages
주제분류화학

초록

Aspirin has been demonstrated to be effective in inhibiting COX-2 and PGE2 in Alveolar macrophages (AMs). However,the mechanisms have not been fully understood. In the presentstudy, we found that pretreatment with aspirin inhibitedLPS-induced COX-2 and PGE2 upregulation, IκBα degradation,NFκB activation and the increase of PKC activity, but elevatedLPS-induced the decrease of PTP activity. The PKC inhibitorcalphostin C dramatically reduced the COX-2 mRNA andPGE2 levels, but the PTP inhibitor peroxovanadium (POV)significantly increased the COX-2 mRNA and PGE2 levels. Furthermore, the PTP inhibitor mitigated the inhibitory effectof aspirin on COX-2 and PGE2 upregulation and NF-κBactivation, whereas the PKC inhibitor enhanced the inhibitoryeffects of aspirin on the production of COX-2 and PGE2. Ourdata indicate a novel mechanism by which aspirin acts as apotent anti-inflammatory agent in alveolus macrophages andALI.

Abstract

Aspirin has been demonstrated to be effective in inhibiting COX-2 and PGE2 in Alveolar macrophages (AMs). However,the mechanisms have not been fully understood. In the presentstudy, we found that pretreatment with aspirin inhibitedLPS-induced COX-2 and PGE2 upregulation, IκBα degradation,NFκB activation and the increase of PKC activity, but elevatedLPS-induced the decrease of PTP activity. The PKC inhibitorcalphostin C dramatically reduced the COX-2 mRNA andPGE2 levels, but the PTP inhibitor peroxovanadium (POV)significantly increased the COX-2 mRNA and PGE2 levels. Furthermore, the PTP inhibitor mitigated the inhibitory effectof aspirin on COX-2 and PGE2 upregulation and NF-κBactivation, whereas the PKC inhibitor enhanced the inhibitoryeffects of aspirin on the production of COX-2 and PGE2. Ourdata indicate a novel mechanism by which aspirin acts as apotent anti-inflammatory agent in alveolus macrophages andALI.

참고문헌 (29)

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