{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T01:48:41Z","timestamp":1773452921739,"version":"3.50.1"},"reference-count":40,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2008,8,29]],"date-time":"2008-08-29T00:00:00Z","timestamp":1219968000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2008,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Activated microglia participate in neuroinflammation which contributes to neuronal damage in neurodegenerative diseases. Inhibition of microglial activation may have potential anti\u2010inflammatory effects. Our laboratory has previously reported that triptolide, a natural biologically active compound extracted from <jats:italic>Tripterygium wilfordii<\/jats:italic>, could protect dopaminergic neurons from inflammation\u2010mediated damage. However, the mechanism by which triptolide inhibits inflammation remains unknown. We reported here that inhibition of prostaglandin E<jats:sub>2<\/jats:sub> (PGE<jats:sub>2<\/jats:sub>) production could be a potential mechanism of triptolide to suppress inflammation. Triptolide suppressed c\u2010<jats:italic>jun<\/jats:italic> NH2\u2010terminal kinase (JNK) phosphorylation, cyclooxygenase 2 (COX\u20102) expression and PGE<jats:sub>2<\/jats:sub> production in microglial cultures treated with lipopolysaccharide (LPS). Triptolide also greatly inhibited the transcriptional activity, but not the DNA\u2010binding activity of nuclear factor\u2010\u03baB (NF\u2010\u03baB) in microglia following LPS stimulation. These results indicate that triptolide might suppress NF\u2010\u03baB activity to down\u2010regulate COX\u20102 expression. The LPS\u2010stimulated transcriptional activity of NF\u2010\u03baB was suppressed by inhibition of p38MAPK, but not by that of JNK and extracellular signal\u2010regulated kinase. Furthermore, the LPS\u2010induced PGE<jats:sub>2<\/jats:sub> production was reduced by inhibiting these kinases. Taken together, these results suggest that triptolide may suppress neuroinflammation via a mechanism that involves inactivation of two parallel signaling pathways: p38\u2010NF\u2010\u03baB\u2010COX\u20102\u2010PGE<jats:sub>2<\/jats:sub> and JNK\u2010PGE<jats:sub>2<\/jats:sub>.<\/jats:p>","DOI":"10.1111\/j.1471-4159.2008.05653.x","type":"journal-article","created":{"date-parts":[[2008,8,30]],"date-time":"2008-08-30T03:06:16Z","timestamp":1220065576000},"page":"779-788","source":"Crossref","is-referenced-by-count":80,"title":["Triptolide inhibits COX\u20102 expression and PGE<sub>2<\/sub> release by suppressing the activity of NF\u2010\u03baB and JNK in LPS\u2010treated microglia"],"prefix":"10.1111","volume":"107","author":[{"given":"Yuntao","family":"Gong","sequence":"first","affiliation":[]},{"given":"Bing","family":"Xue","sequence":"additional","affiliation":[]},{"given":"Jian","family":"Jiao","sequence":"additional","affiliation":[]},{"given":"Liming","family":"Jing","sequence":"additional","affiliation":[]},{"given":"Xiaomin","family":"Wang","sequence":"additional","affiliation":[]}],"member":"311","published-online":{"date-parts":[[2008,10,14]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1001\/jama.289.21.2819"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.phytochem.2006.11.029"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.3109\/10428190109064582"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neures.2006.02.013"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.1.264"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.12.12.1063"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrd1225"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-6147(03)00176-7"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119056"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.neuro.22.1.219"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.274.5291.1383"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.21.12901"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.7.2774"},{"key":"e_1_2_7_15_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI12466"},{"key":"e_1_2_7_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-2952(97)00154-8"},{"key":"e_1_2_7_17_1","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2199-3-16"},{"key":"e_1_2_7_18_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2004.04.040"},{"key":"e_1_2_7_19_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-004-0555-y"},{"key":"e_1_2_7_20_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.19.13451"},{"key":"e_1_2_7_21_1","first-page":"387","article-title":"Primary rat mesencephalic neuron\u2010glia, neuron\u2010enriched, microglia\u2010enriched, and astroglia\u2010enriched cultures","volume":"79","author":"Liu B.","year":"2003","journal-title":"Methods Mol. 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