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注册: 2008-10-21
专业: 药物代谢与药物动力学

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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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