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Xanthii fructus inhibits inflammatory responses in LPS-stimulated RAW 264.7 macrophages through suppressing NF-κB and JNK/p38 MAPK.
J Ethnopharmacol. 2015 Dec 24; 176:394-401.JE

Abstract

ETHNOPHARMACOLOGICAL RELEVANCE

Xanthii fructus (XF) has long been used to treat a variety of inflammatory conditions in Korean traditional medicine, but the underlying mechanisms that could explain the anti-inflammatory actions of XF remain largely unknown.

AIM OF THE STUDY

This study aimed to elucidate the anti-inflammatory effects of X. fructus (XF) and to examine its underlying molecular mechanisms in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages.

MATERIALS AND METHODS

The effect of XF on LPS-induced mRNA and protein expressions of inflammatory mediators and cytokines were determined. Moreover, the activation of the nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways and the expression of heme oxygenase-1 (HO-1) were explored to elucidate the anti-inflammatory mechanisms.

RESULTS

XF significantly inhibited LPS-induced production of inflammatory mediators, interleukin-6 (IL-6), nitric oxide (NO), and prostaglandin E2 (PGE2), without any cytotoxicity. However, it did not affect tissue necrosis factor (TNF)-α or IL-1β production in LPS-stimulated RAW 264.7 cells. Expression levels of inducible nitric oxide synthase (iNOS) mRNA and protein were inhibited dose-dependently by XF in LPS-stimulated RAW 264.7 cells, but there were no changes in cyclooxygenase-2 (COX-2) mRNA and protein. XF significantly attenuated LPS-induced phosphorylation and degradation of inhibitory kappa Bα (IκBα) and consequently reduced the nuclear translocation of p65 NF-κB. Pretreatment with XF also strongly inhibited the LPS-induced phosphorylation of p38 kinase and JNK, whereas the phosphorylation of ERK1/2 was not affected. In addition, XF led to an increase in HO-1 expression.

CONCLUSION

Taken together, our findings support that XF inhibits LPS-induced inflammatory responses by blocking NF-κB activation, inhibiting JNK/p38 MAPK phosphorylation, and enhancing HO-1 expression in macrophages, suggesting that it could be an attractive therapeutic candidate for various inflammatory diseases.

Authors+Show Affiliations

Acupuncture and Meridian Science Research Center, College of Korean Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.Department of Anatomy, College of Korean Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.Department of Anatomy, College of Korean Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.Inuri Medical Group, Seoul 137-877, Republic of Korea.Department of Anatomy, College of Korean Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.Department of Anatomy, College of Korean Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea. Electronic address: youngjoos@khu.ac.kr.

Pub Type(s)

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

Language

eng

PubMed ID

26560439

Citation

Yeom, Mijung, et al. "Xanthii Fructus Inhibits Inflammatory Responses in LPS-stimulated RAW 264.7 Macrophages Through Suppressing NF-κB and JNK/p38 MAPK." Journal of Ethnopharmacology, vol. 176, 2015, pp. 394-401.
Yeom M, Kim JH, Min JH, et al. Xanthii fructus inhibits inflammatory responses in LPS-stimulated RAW 264.7 macrophages through suppressing NF-κB and JNK/p38 MAPK. J Ethnopharmacol. 2015;176:394-401.
Yeom, M., Kim, J. H., Min, J. H., Hwang, M. K., Jung, H. S., & Sohn, Y. (2015). Xanthii fructus inhibits inflammatory responses in LPS-stimulated RAW 264.7 macrophages through suppressing NF-κB and JNK/p38 MAPK. Journal of Ethnopharmacology, 176, 394-401. https://doi.org/10.1016/j.jep.2015.11.020
Yeom M, et al. Xanthii Fructus Inhibits Inflammatory Responses in LPS-stimulated RAW 264.7 Macrophages Through Suppressing NF-κB and JNK/p38 MAPK. J Ethnopharmacol. 2015 Dec 24;176:394-401. PubMed PMID: 26560439.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Xanthii fructus inhibits inflammatory responses in LPS-stimulated RAW 264.7 macrophages through suppressing NF-κB and JNK/p38 MAPK. AU - Yeom,Mijung, AU - Kim,Jae-Hyun, AU - Min,Ju-Hee, AU - Hwang,Man Ki, AU - Jung,Hyuk-Sang, AU - Sohn,Youngjoo, Y1 - 2015/11/10/ PY - 2015/07/23/received PY - 2015/10/12/revised PY - 2015/11/06/accepted PY - 2015/11/13/entrez PY - 2015/11/13/pubmed PY - 2016/10/7/medline KW - Inflammation KW - MAPKs KW - NF-κB KW - Xanthii fructus KW - Xanthium strumarium (Asteraceae) KW - iNOS SP - 394 EP - 401 JF - Journal of ethnopharmacology JO - J Ethnopharmacol VL - 176 N2 - ETHNOPHARMACOLOGICAL RELEVANCE: Xanthii fructus (XF) has long been used to treat a variety of inflammatory conditions in Korean traditional medicine, but the underlying mechanisms that could explain the anti-inflammatory actions of XF remain largely unknown. AIM OF THE STUDY: This study aimed to elucidate the anti-inflammatory effects of X. fructus (XF) and to examine its underlying molecular mechanisms in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. MATERIALS AND METHODS: The effect of XF on LPS-induced mRNA and protein expressions of inflammatory mediators and cytokines were determined. Moreover, the activation of the nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways and the expression of heme oxygenase-1 (HO-1) were explored to elucidate the anti-inflammatory mechanisms. RESULTS: XF significantly inhibited LPS-induced production of inflammatory mediators, interleukin-6 (IL-6), nitric oxide (NO), and prostaglandin E2 (PGE2), without any cytotoxicity. However, it did not affect tissue necrosis factor (TNF)-α or IL-1β production in LPS-stimulated RAW 264.7 cells. Expression levels of inducible nitric oxide synthase (iNOS) mRNA and protein were inhibited dose-dependently by XF in LPS-stimulated RAW 264.7 cells, but there were no changes in cyclooxygenase-2 (COX-2) mRNA and protein. XF significantly attenuated LPS-induced phosphorylation and degradation of inhibitory kappa Bα (IκBα) and consequently reduced the nuclear translocation of p65 NF-κB. Pretreatment with XF also strongly inhibited the LPS-induced phosphorylation of p38 kinase and JNK, whereas the phosphorylation of ERK1/2 was not affected. In addition, XF led to an increase in HO-1 expression. CONCLUSION: Taken together, our findings support that XF inhibits LPS-induced inflammatory responses by blocking NF-κB activation, inhibiting JNK/p38 MAPK phosphorylation, and enhancing HO-1 expression in macrophages, suggesting that it could be an attractive therapeutic candidate for various inflammatory diseases. SN - 1872-7573 UR - https://www.unboundmedicine.com/medline/citation/26560439/Xanthii_fructus_inhibits_inflammatory_responses_in_LPS_stimulated_RAW_264_7_macrophages_through_suppressing_NF_κB_and_JNK/p38_MAPK_ DB - PRIME DP - Unbound Medicine ER -