4.7 Article

Stevioside inhibits inflammation and apoptosis by regulating TLR2 and TLR2-related proteins in S. aureus-infected mouse mammary epithelial cells

Journal

INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 22, Issue 1, Pages 192-199

Publisher

ELSEVIER
DOI: 10.1016/j.intimp.2014.06.015

Keywords

Stevioside; TLR2; Anti-inflammatory; Anti-apoptosis; Staphylococcus aureus; Mouse mammary epithelial cells

Funding

  1. National Natural Science Foundation of China [31272622, 31201925]
  2. Research Fund for the Doctoral Program of Higher Education of China [20110061130010, 20120061120098]
  3. Jilin Province Science Foundation for Youths [20130522087JH]

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Stevioside is a natural sweetener that is commonly used in traditional medicine and as a food additive. The object of this study was to investigate the anti-inflammatory and anti-apoptosis function of stevioside and the possible molecular mechanisms for such activity in Staphylococcus aureus (S. aureus)-infected mouse mammary epithelial cells (MMECs). The cells were treated with varying doses of stevioside before infection with S. aureus. The live/dead cells were detected by immunofluorescence microscopy. The pro-inflammatory cytokines were determined by ELISA. The mRNA of TLR2 and proteins related to NF-kappa B, MAPK and apoptosis were analyzed by q-PCR. The relative protein expression levels were determined by Western blot. The results indicated that stevioside inhibited the mRNA and protein expression of TNF-alpha, IL-6 and IL-1 beta dose-dependently in S. aureus-stimulated MMECs. Stevioside suppressed the S. aureus-induced expression of TLR2 and proteins of the NF-kappa B and MAPK pathways as well as apoptosis. The mRNA levels of I kappa B alpha, p38, ERK, JNK, p65, caspase-3 and Bax were not influenced by the stevioside treatment. Stevioside exerts anti-inflammatory and anti-apoptotic properties by inhibiting the release of cytokines and the activation of TLR2 and proteins of the NF-kappa B and MAPK signaling pathways, as well as caspase-3 and Bax. (C) 2014 Elsevier B.V. All rights reserved.

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