期刊
INFLAMMATION
卷 35, 期 3, 页码 1087-1093出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-011-9415-4
关键词
alveolar macrophages; heme oxygenase-1; anti-inflammatory; p38 MAPK
资金
- Priority Academic Program Development of Jiangsu Higher Education Institutions
- Peak of the six personnel in Jiangsu Province
- Jiangsu Province Graduate Education Innovation project [CX09S_035Z]
- Xuzhou Medical College [09KJZ07]
Alveolar macrophages (AMs) can initiate lung inflammation by producing pro-inflammatory cytokines and chemokines, but they participate actively in the prevention of inflammation during acute lung injury (ALI). Heme oxygenase-1 (HO-1) is mainly expressed in AMs and has anti-inflammatory properties in ALI, but the anti-inflammatory mechanisms of HO-1 are largely unknown. In this study, AMs were treated with saline, LPS (1 mu g/ml), hemin (10 mu M), zinc protoporphyrin (ZnPP; 10 mu M, 1 h prior to LPS and hemin), SB203580 (10 mu M, 1 h prior to LPS and hemin), or their combination up to 24 h. The specific HO-1 inhibitor ZnPP and SB203580 were used to inhibit the effects of HO-1 and the phosphorylated p38 mitogen-activated protein kinase (MAPK), respectively. The protein levels of HO-1 and p38 MAPK were analyzed by western blotting; arginase activity was measured in lysates obtained from cultured cells; nitric oxide production in the extracellular medium of AMs cultured for 24 h was monitored by assessing nitrite levels; the phagocytic ability of macrophage was measured by neutral red uptake. IL-10 of culture supernatants in AMs was determined by enzyme-linked immunosorbent assay. The results indicated that HO-1 induced by hemin increased arginase activity and phagocytic ability and decreased iNOS activity via p38 MAPK pathway in primary rat AMs. These changes and p38 MAPK may be the anti-inflammatory mechanism of HO-1 induced by hemin in primary rat AMs.
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