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zjandzq金虫 (正式写手)
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The possibility that the drug may affect asthmatic inflammation, through inhibition of the relevant inflammatory cytokines, has not been explored. The purpose of this study was, firstly, to investigate the ability of andrographolide to inhibit the release of inflammatory cytokines in vitro in a model of non-specificinflammation and subsequently to determine whether such effect can also be exerted in vivo in allergic lung inflammation. LPS-induced TNF-α and GM-CSF release from mouse peritoneal macrophages was inhibited by andrographolide in a concentration-dependent manner. The concentration of the drug producing 50% inhibition was 0.6 μM for TNF-α and 3.3 μM for GM-CSF. The maximal inhibition achieved (at 50 μM) was 77% and 94%, respectively, for the two cytokines. The drug was as efficacious as dexamethasone, but about 8–12 times less potent. The drug also suppressed LPS-induced expression of mRNA for the two cytokines, suggesting that this effect may contribute to the mechanism underlying its anti-inflammatory effects. In the in vivo study, intra-peritoneal treatment of ovalbumin-immunized and nasally-challenged mice with andrographolide significantly inhibited the elevation of bronchoalveolar fluid (BAF) levels of TNF-α and GM- CSF in a dose-dependent manner, with 30 mg/kg producing an inhibition of 92% and 65% of the cytokines, respectively) and almost completely abolishing the accumulation of lymphocytes and eosinophils. |
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