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Xanthoceraside inhibits pro-inflammatory cytokine expression in Aβ25-35/IFN-γ-stimulated microglia through the TLR2 receptor, MyD88, nuclear factor-κB, and mitogen-activated protein kinase signaling pathways.
J Pharmacol Sci. 2013; 122(4):305-17.JP

Abstract

An accumulating body of evidence suggests that Alzheimer's disease (AD) is associated with microglia-mediated neuroinflammation and pro-inflammatory cytokine expression. Therefore, the suppression of neuroinflammation and pro-inflammatory cytokine might theoretically slow down the progression of AD. Xanthoceraside, a novel triterpenoid saponin extracted from the husks of Xanthoceras sorbifolia Bunge, has potent antiinflammatory and neuroprotective effects. However, the molecular mechanism underlying its anti-inflammatory action remains unclear. In the present study, we attempted to determine the effects of xanthoceraside on the production of pro-inflammatory mediators in amyloid β25-35 (Aβ25-35)/interferon-γ (IFN-γ)-stimulated microglia. Our results indicated that xanthoceraside (0.01 and 0.1 μM) significantly inhibited the release of nitric oxide (NO) and pro-inflammatory cytokines interleukin-1β and tumor necrosis factor-α in a concentration-dependent manner. Reverse transcriptase-polymerase chain reaction and western blotting analyses showed that xanthoceraside decreased the Aβ25-35/IFN-γ-induced production of cyclooxygenase-2 and inducible NO synthase. These effects were accompanied by inhibited activities of nuclear factor-κB and mitogen-activated protein kinase through Toll-like receptor 2 in a myeloid differentiation protein 88-dependent manner. Our results provide support for the therapeutic potential of xanthoceraside in AD.

Authors+Show Affiliations

Department of Pharmacology, Life Science and Biopharmaceutics School, Shenyang Pharmaceutical University, Shenyang, PR China.No affiliation info availableNo affiliation info availableNo 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

23966052

Citation

Qi, Yue, et al. "Xanthoceraside Inhibits Pro-inflammatory Cytokine Expression in Aβ25-35/IFN-γ-stimulated Microglia Through the TLR2 Receptor, MyD88, Nuclear factor-κB, and Mitogen-activated Protein Kinase Signaling Pathways." Journal of Pharmacological Sciences, vol. 122, no. 4, 2013, pp. 305-17.
Qi Y, Zou LB, Wang LH, et al. Xanthoceraside inhibits pro-inflammatory cytokine expression in Aβ25-35/IFN-γ-stimulated microglia through the TLR2 receptor, MyD88, nuclear factor-κB, and mitogen-activated protein kinase signaling pathways. J Pharmacol Sci. 2013;122(4):305-17.
Qi, Y., Zou, L. B., Wang, L. H., Jin, G., Pan, J. J., Chi, T. Y., & Ji, X. F. (2013). Xanthoceraside inhibits pro-inflammatory cytokine expression in Aβ25-35/IFN-γ-stimulated microglia through the TLR2 receptor, MyD88, nuclear factor-κB, and mitogen-activated protein kinase signaling pathways. Journal of Pharmacological Sciences, 122(4), 305-17.
Qi Y, et al. Xanthoceraside Inhibits Pro-inflammatory Cytokine Expression in Aβ25-35/IFN-γ-stimulated Microglia Through the TLR2 Receptor, MyD88, Nuclear factor-κB, and Mitogen-activated Protein Kinase Signaling Pathways. J Pharmacol Sci. 2013;122(4):305-17. PubMed PMID: 23966052.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Xanthoceraside inhibits pro-inflammatory cytokine expression in Aβ25-35/IFN-γ-stimulated microglia through the TLR2 receptor, MyD88, nuclear factor-κB, and mitogen-activated protein kinase signaling pathways. AU - Qi,Yue, AU - Zou,Li-Bo, AU - Wang,Li-Hua, AU - Jin,Ge, AU - Pan,Jin-Jin, AU - Chi,Tian-Yan, AU - Ji,Xue-Fei, PY - 2013/8/23/entrez PY - 2013/8/24/pubmed PY - 2014/3/29/medline SP - 305 EP - 17 JF - Journal of pharmacological sciences JO - J. Pharmacol. Sci. VL - 122 IS - 4 N2 - An accumulating body of evidence suggests that Alzheimer's disease (AD) is associated with microglia-mediated neuroinflammation and pro-inflammatory cytokine expression. Therefore, the suppression of neuroinflammation and pro-inflammatory cytokine might theoretically slow down the progression of AD. Xanthoceraside, a novel triterpenoid saponin extracted from the husks of Xanthoceras sorbifolia Bunge, has potent antiinflammatory and neuroprotective effects. However, the molecular mechanism underlying its anti-inflammatory action remains unclear. In the present study, we attempted to determine the effects of xanthoceraside on the production of pro-inflammatory mediators in amyloid β25-35 (Aβ25-35)/interferon-γ (IFN-γ)-stimulated microglia. Our results indicated that xanthoceraside (0.01 and 0.1 μM) significantly inhibited the release of nitric oxide (NO) and pro-inflammatory cytokines interleukin-1β and tumor necrosis factor-α in a concentration-dependent manner. Reverse transcriptase-polymerase chain reaction and western blotting analyses showed that xanthoceraside decreased the Aβ25-35/IFN-γ-induced production of cyclooxygenase-2 and inducible NO synthase. These effects were accompanied by inhibited activities of nuclear factor-κB and mitogen-activated protein kinase through Toll-like receptor 2 in a myeloid differentiation protein 88-dependent manner. Our results provide support for the therapeutic potential of xanthoceraside in AD. SN - 1347-8648 UR - https://www.unboundmedicine.com/medline/citation/23966052/Xanthoceraside_inhibits_pro_inflammatory_cytokine_expression_in_Aβ25_35/IFN_γ_stimulated_microglia_through_the_TLR2_receptor_MyD88_nuclear_factor_κB_and_mitogen_activated_protein_kinase_signaling_pathways_ L2 - https://linkinghub.elsevier.com/retrieve/pii/DN/JST.JSTAGE/jphs/13031FP DB - PRIME DP - Unbound Medicine ER -