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  • Title: In vitro anti-inflammatory effects of beta-carboline alkaloids, isolated from Picrasma quassioides, through inhibition of the iNOS pathway.
    Author: Zhao F, Gao Z, Jiao W, Chen L, Chen L, Yao X.
    Journal: Planta Med; 2012 Dec; 78(18):1906-11. PubMed ID: 23115019.
    Abstract:
    In our previous study, fourty-eight compounds have been isolated and identified from the roots of Picrasma quassioides, which have been widely used as a traditional Chinese medicine for clearing heat and for detoxification as described in the Chinese Pharmacopoeia. β-Carboline alkaloids are commonly considered as main active constituents of P. quassioides, but the molecular mechanism remains yet unknown. In the present paper, one new β-carboline alkaloid together with two known β-carboline alkaloids have been investigated for their anti-inflammatory effect and mechanism of action in cultured macrophage RAW 264.7 cells. Griess assay was used to evaluate the inhibitory effect on the overproduction of nitric oxide. ELISA was used to determine the level of proinflammatory cytokines including TNF-α and IL-6. The inhibitory effect on the enzymatic activity of COX-2 and inducible nitric oxide synthase were tested by colorimetric and fluorimetric methods, respectively. Western blot was used to detect the expression of inducible nitric oxide synthase and COX-2. All three β-carboline alkaloids suppressed LPS-stimulated nitric oxide production and proinflammatory cytokines secretion, including TNF-α and IL-6 in a dose-dependent manner. They also strongly inhibited the expression of inducible nitric oxide synthase and inducible nitric oxide synthase enzymatic activity, whereas the expression of COX-2 and COX-2 enzymatic activity were not affected. These results indicated that potent inhibition of nitric oxide, TNF-α, and IL-6, but not COX-2 expression and COX-2 activity, might constitute the anti-inflammatory mechanism of β-carboline alkaloids. β-Carboline alkaloids suppressed the overproduction of nitric oxide through downregulation of inducible nitric oxide synthase expression and inducible nitric oxide synthase enzymatic activity in an LPS-stimulated macrophage.
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