Effect of Antrodia cinnamomea's fruiting bodies' extracts on the decrease of LPS- induced inflammation in mouse macrophage cell line

碩士 === 國立東華大學 === 生命科學系 === 103 === Antrodia cinnamomea ( AC ) is a traditional medicinal mushroom which grows only on the old trunk cavity of the endemic species Cinnamomum kanehirae ( Bull camphor tree )of Taiwan. On folk remedies, AC has been used for the treatment of diarrhea, vomiting and food...

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Bibliographic Details
Main Authors: I-Chun Wang, 王奕鈞
Other Authors: Tzong-Zeng Wu
Format: Others
Published: 2015
Online Access:http://ndltd.ncl.edu.tw/handle/94270125631050727993
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Summary:碩士 === 國立東華大學 === 生命科學系 === 103 === Antrodia cinnamomea ( AC ) is a traditional medicinal mushroom which grows only on the old trunk cavity of the endemic species Cinnamomum kanehirae ( Bull camphor tree )of Taiwan. On folk remedies, AC has been used for the treatment of diarrhea, vomiting and food poisoning etc. Recent studies have demonstrated a variety of physiological activities, including antioxidant and anticancer. In the present study, the lipopolysaccharide(LPS) induced mouse macrophage RAW 264.7 acute inflammation model was used to evaluate the anti-inflammatory activity of AC extract, named as “ME”, and its mechanism of action. The results showed that ME could significantly inhibit LPS-induced inflammatory on intracellular radical production, nitric oxide(NO), prostaglandin E2(PGE2) and cytokines, and also showed the capability to inhibit the synthesis of nitric oxide enzymes (iNOS) and cyclooxygenase 2 (COX-2) protein expression. As we all know the nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPK) play important roles in inflammation. The result showed that ME could inhibit NF-κB activation through the prevention of inhibitor IKK phosphorylation, IκBα degradation and NF-κB nuclear translocation. In addition, ME also inhibited MAPK activation through the prevention of inhibitor ERK, p38, JNK phosphorylation. Based on the above results, we conclude that the AC isolates ME should be through both the inhibition of NF-κB and MAPK pathway to suppress the production of pre-inflammatory substances.