{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T12:22:31Z","timestamp":1788524551089,"version":"build-2803163510"},"reference-count":54,"publisher":"SAGE Publications","issue":"11","license":[{"start":{"date-parts":[[2015,11,1]],"date-time":"2015-11-01T00:00:00Z","timestamp":1446336000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Medicinal Food"],"published-print":{"date-parts":[[2015,11]]},"abstract":"<jats:p>\n                    A number of compounds isolated from mushrooms have exhibited disease-modifying effects. We sought to investigate the mechanisms responsible for the anti-inflammatory effects of an extract from the mushroom species\n                    <jats:italic toggle=\"yes\">Sarcodon asparatus<\/jats:italic>\n                    (SAE). Male BALB\/c mice (\n                    <jats:italic toggle=\"yes\">N<\/jats:italic>\n                    =42; 6 weeks old) were randomly assigned to four treatment groups. Intraperitoneal administration of SAE significantly attenuated lipopolysaccharide (LPS)-mediated increases in alanine aminotransferase (ALT) activity. LPS also increased serum levels of proinflammatory cytokines, including IL-1\n                    <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                    , IL-6, and TNF-\n                    <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                    , which were dose-dependently and significantly attenuated by SAE. Correlative relationships between serum ALT activity and proinflammatory cytokines suggested that SAE-mediated suppression of liver injury was partly attributable to the attenuation of serum inflammatory responses. SAE significantly decreased hepatic NO\n                    <jats:sup>\u2022<\/jats:sup>\n                    production and subsequent 3-nitrotyrosine formation, and the hepatic NO\n                    <jats:sup>\u2022<\/jats:sup>\n                    production significantly correlated with serum ALT and cytokine levels, suggesting that SAE mitigates liver injury in association with inflammatory processes, likely by suppressing NO\n                    <jats:sup>\u2022<\/jats:sup>\n                    production. Anti-inflammatory activity and further mechanisms of SAE were evaluated using RAW264.7 with LPS challenge. Noncytotoxic levels of SAE significantly attenuated NO\n                    <jats:sup>\u2022<\/jats:sup>\n                    production in RAW264.7 cells and also markedly suppressed the expression of iNOS and other proinflammatory mediators, including COX-2 and IL-6, which were upregulated in the presence of LPS. SAE inhibited the phosphorylation of p65, an observation that occurred independently of IKK\n                    <jats:italic toggle=\"yes\">\u03b1\u03b2<\/jats:italic>\n                    -mediated I\n                    <jats:italic toggle=\"yes\">\u03ba<\/jats:italic>\n                    B\n                    <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                    phosphorylation. Collectively, our results demonstrate that SAE suppressed NO\n                    <jats:sup>\u2022<\/jats:sup>\n                    -mediated inflammation by inhibiting p65 transcriptional activation without affecting IKK\n                    <jats:italic toggle=\"yes\">\u03b1\u03b2<\/jats:italic>\n                    -mediated I\n                    <jats:italic toggle=\"yes\">\u03ba<\/jats:italic>\n                    B\n                    <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                    phosphorylation. Further studies are warranted to examine the major compounds responsible for these effects and the mechanisms responsible for the p65 phosphorylation observed.\n                  <\/jats:p>","DOI":"10.1089\/jmf.2014.3422","type":"journal-article","created":{"date-parts":[[2015,4,2]],"date-time":"2015-04-02T16:03:58Z","timestamp":1427990638000},"page":"1198-1206","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":7,"title":["Ethanol Extract of\n                    <i>Sarcodon asparatus<\/i>\n                    Mitigates Inflammatory Responses in Lipopolysaccharide-Challenged Mice and Murine Macrophages"],"prefix":"10.1177","volume":"18","author":[{"given":"Min-Yu","family":"Chung","sequence":"first","affiliation":[{"name":"Korea Food Research Institute"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sung Keun","family":"Jung","sequence":"additional","affiliation":[{"name":"Korea Food Research Institute"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hye-Jin","family":"Lee","sequence":"additional","affiliation":[{"name":"Korea Food Research Institute"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dong Hwa","family":"Shon","sequence":"additional","affiliation":[{"name":"Korea Food Research Institute"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hyun-Ku","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Marine Life Science, Jeju National University, Jeju, Korea."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2015,11,1]]},"reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bioeng.8.061505.095708"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1002\/hep.1840190229"},{"key":"e_1_3_2_4_2","first-page":"53","article-title":"Changes in tissue antioxidant enzyme activities and lipid peroxides in endotoxin-induced multiple organ failure","volume":"42","author":"Yoshikawa T","year":"1994","unstructured":"Yoshikawa T, , Takano H, , Takahashi S, , Ichikawa H, , Kondo M: Changes in tissue antioxidant enzyme activities and lipid peroxides in endotoxin-induced multiple organ failure. 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