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Tanshinone IIA inhibits LPS-induced NF-kappaB activation in RAW 264.7 cells: possible involvement of the NIK-IKK, ERK1/2, p38 and JNK pathways.
Eur J Pharmacol. 2006 Aug 07; 542(1-3):1-7.EJ

Abstract

Nuclear factor kappaB (NF-kappaB) activation by NF-kappaB-inducing kinase (NIK)-IkappaB alpha kinase (IKK) pathway and mitogen-activated protein kinases (MAPKs) pathway are important in inflammation. We recently found that the tanshinone IIA, a diterpene isolated from Salvia miltiorrhiza (S. miltiorrhiza), reduced the production of pro-inflammatory mediators in RAW 264.7 cells stimulated with lipopolysaccharide (LPS). However, little is known about the inhibitory mechanisms of tanshinone IIA on the production of pro-inflammatory mediators. To investigate the inhibitory mechanism, we determined the inhibitory effects of tanshinone IIA on the activation of NF-kappaB and IkappaB alpha phosphorylation, and also examined phosphorylation of NIK and IKK as well as the activation of MAPKs such as p38 MAPK (p38), extracellular signal-regulated kinases 1/2 (ERK1/2), and c-Jun N-terminal kinase (JNK) in RAW 264.7 cells stimulated with LPS. Tanshinone IIA inhibited NF-kappaB-DNA complex, NF-kappaB binding activity, and the phosphorylation of IkappaB alpha in a dose dependent manner. Tanshinone IIA also inhibited the translocation of NF-kappaB from cytosol to nucleus. Moreover, the phosphorylation of NIK and IKK as well as the phosphorylation of p38, ERK1/2, and JNK in the LPS-stimulated RAW 264.7 cells were suppressed by the tanshinone IIA in a dose dependent manner. These results suggest that tanshinone IIA may inhibit LPS-induced IkappaB alpha degradation and NF-kappaB activation via suppression of the NIK-IKK pathway as well as the MAPKs (p38, ERK1/2, and JNK) pathway in RAW 264.7 cells and these properties may provide a potential mechanism that explains the anti-inflammatory activity of tanshinone IIA.

Authors+Show Affiliations

Department of Skin and Beauty, Seojeong College, Yangju city, Gyeonggi 482-860, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16797002

Citation

Jang, Seon Il, et al. "Tanshinone IIA Inhibits LPS-induced NF-kappaB Activation in RAW 264.7 Cells: Possible Involvement of the NIK-IKK, ERK1/2, P38 and JNK Pathways." European Journal of Pharmacology, vol. 542, no. 1-3, 2006, pp. 1-7.
Jang SI, Kim HJ, Kim YJ, et al. Tanshinone IIA inhibits LPS-induced NF-kappaB activation in RAW 264.7 cells: possible involvement of the NIK-IKK, ERK1/2, p38 and JNK pathways. Eur J Pharmacol. 2006;542(1-3):1-7.
Jang, S. I., Kim, H. J., Kim, Y. J., Jeong, S. I., & You, Y. O. (2006). Tanshinone IIA inhibits LPS-induced NF-kappaB activation in RAW 264.7 cells: possible involvement of the NIK-IKK, ERK1/2, p38 and JNK pathways. European Journal of Pharmacology, 542(1-3), 1-7.
Jang SI, et al. Tanshinone IIA Inhibits LPS-induced NF-kappaB Activation in RAW 264.7 Cells: Possible Involvement of the NIK-IKK, ERK1/2, P38 and JNK Pathways. Eur J Pharmacol. 2006 Aug 7;542(1-3):1-7. PubMed PMID: 16797002.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tanshinone IIA inhibits LPS-induced NF-kappaB activation in RAW 264.7 cells: possible involvement of the NIK-IKK, ERK1/2, p38 and JNK pathways. AU - Jang,Seon Il, AU - Kim,Hyung Jin, AU - Kim,Young-Jun, AU - Jeong,Seung-Il, AU - You,Yong-Ouk, Y1 - 2006/05/06/ PY - 2006/01/03/received PY - 2006/04/12/revised PY - 2006/04/28/accepted PY - 2006/6/27/pubmed PY - 2006/12/15/medline PY - 2006/6/27/entrez SP - 1 EP - 7 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 542 IS - 1-3 N2 - Nuclear factor kappaB (NF-kappaB) activation by NF-kappaB-inducing kinase (NIK)-IkappaB alpha kinase (IKK) pathway and mitogen-activated protein kinases (MAPKs) pathway are important in inflammation. We recently found that the tanshinone IIA, a diterpene isolated from Salvia miltiorrhiza (S. miltiorrhiza), reduced the production of pro-inflammatory mediators in RAW 264.7 cells stimulated with lipopolysaccharide (LPS). However, little is known about the inhibitory mechanisms of tanshinone IIA on the production of pro-inflammatory mediators. To investigate the inhibitory mechanism, we determined the inhibitory effects of tanshinone IIA on the activation of NF-kappaB and IkappaB alpha phosphorylation, and also examined phosphorylation of NIK and IKK as well as the activation of MAPKs such as p38 MAPK (p38), extracellular signal-regulated kinases 1/2 (ERK1/2), and c-Jun N-terminal kinase (JNK) in RAW 264.7 cells stimulated with LPS. Tanshinone IIA inhibited NF-kappaB-DNA complex, NF-kappaB binding activity, and the phosphorylation of IkappaB alpha in a dose dependent manner. Tanshinone IIA also inhibited the translocation of NF-kappaB from cytosol to nucleus. Moreover, the phosphorylation of NIK and IKK as well as the phosphorylation of p38, ERK1/2, and JNK in the LPS-stimulated RAW 264.7 cells were suppressed by the tanshinone IIA in a dose dependent manner. These results suggest that tanshinone IIA may inhibit LPS-induced IkappaB alpha degradation and NF-kappaB activation via suppression of the NIK-IKK pathway as well as the MAPKs (p38, ERK1/2, and JNK) pathway in RAW 264.7 cells and these properties may provide a potential mechanism that explains the anti-inflammatory activity of tanshinone IIA. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/16797002/Tanshinone_IIA_inhibits_LPS_induced_NF_kappaB_activation_in_RAW_264_7_cells:_possible_involvement_of_the_NIK_IKK_ERK1/2_p38_and_JNK_pathways_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(06)00464-X DB - PRIME DP - Unbound Medicine ER -