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

Stevioside inhibits inflammation and apoptosis by regulating TLR2 and TLR2-related proteins in S. aureus-infected mouse mammary epithelial cells.
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DOI:
10.1016/j.intimp.2014.06.015
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发表时间:
2014-09
影响因子:
5.6
通讯作者:
Tiancheng Wang;Xiaojin Song;Ze-cai Zhang;Meng-yao Guo;Haichao Jiang;Wei Wang;Yongguo Cao;Lianqin Zhu;Naisheng Zhang
Tiancheng Wang;Xiaojin Song;Ze-cai Zhang;Meng-yao Guo;Haichao Jiang;Wei Wang;Yongguo Cao;Lianqin Zhu;Naisheng Zhang
中科院分区:
医学2区
文献类型:
--
作者:
Tiancheng Wang;Xiaojin Song;Ze-cai Zhang;Meng-yao Guo;Haichao Jiang;Wei Wang;Yongguo Cao;Lianqin Zhu;Naisheng Zhang

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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 withS. 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-κB, 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-α, IL-6 and IL-1β dose-dependently inS. aureus-stimulated MMECs. Stevioside suppressed theS. aureus-induced expression of TLR2 and proteins of the NF-κB and MAPK pathways as well as apoptosis. The mRNA levels of IκBα, 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-κB and MAPK signaling pathways, as well as caspase-3 and Bax.