Ginsenoside Rg1 reduced the invasion of S. aureus into respiratory epithelial cells involving pro-inflammatory cytokines and glucocorticoid receptor

doi:10.5246/jcps.2011.03.033

Abstract

Abstract:

The invasion of Staphylococcus aureus into respiratory epithelial cells and the followed inflammatory responses cause serious tissue damage. The aim of this study was to investigate the effects of ginsenoside Rg1 (Rg1) on S. aureus infection in vitro and its action mechanism. An internalization model was constructed to determine the effect of Rg1 on S. aureus invasion. The changes of expression of integrin β1, NF-κB and glucocorticoid receptor were analyzed by Western blot. Expression of pro-inflammatory genes was validated using RT-PCR. The results demonstrated that Rg1 treatment could reduce the invasion of S. aureus into rat pulmonary epithelial cells by down-regulating integrin β1. Its anti-inflammatory action was exerted through reducing NF-κB and expressions of intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-α (TNF-α), interleukin-2 (IL-2) and interleukin-6 (IL-6). The increased expression of glucocorticoid receptor was involved in this regulation. The results suggested that Rg1 could play a positive role in reducing S. aureus infections. Rg1 could be used for the treatment of S. aureus infection, potentially.

Key words: Staphylococcus aureus, Ginsenoside Rg1, Pulmonary epithelial cell

CLC Number:

Supporting:

Zhi-Yi Yuan, Zhen Meng, Yu-Shuang Chai, Jia-Qi Lan, Fan Lei, Hui-Ying Li, Dong-Ming Xing, Hui-Yu Li, Li-Jun Du^* . Ginsenoside Rg1 reduced the invasion of S. aureus into respiratory epithelial cells involving pro-inflammatory cytokines and glucocorticoid receptor [J]. , DOI: 10.5246/jcps.2011.03.033.

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