Abstract
6-Shogaol, a pungent agent isolated from Zingiber officinale Roscoe, has been known to have anti-tumor and anti-inflammatory effects. However, the anti-inflammatory effects and biological mechanism of 6-Shogaol in LPS-activated BV2 microglia remains largely unknown. In this study, we evaluated the anti-inflammatory effects of 6-Shogaol in LPS-activated BV2 microglia. 6-Shogaol was administrated 1 h before LPS treatment. The production of inflammatory mediators were detected by ELISA. The expression of NF-κB and PPAR-γ were detected by western blot analysis. Our results revealed that 6-Shogaol inhibited LPS-induced TNF-α, IL-1β, IL-6, and PGE2 production in a concentration dependent manner. Furthermore, 6-Shogaol inhibited LPS-induced NF-κB activation by inhibiting phosphorylation and nuclear translocation of NF-κB p65. In addition, 6-Shogaol could increase the expression of PPAR-γ. Moreover, inhibition of PPAR-γ by GW9662 could prevent the inhibition of 6-Shogaol on LPS-induced inflammatory mediator production. In conclusion, 6-Shogaol inhibits LPS-induced inflammation by activating PPAR-γ.
Highlights
The incidence of neurodegenerative disease, Parkinson disease (PD) and Alzheimer’s disease, increased markedly in the last decades [1, 2]
6-Shogaol concentration dependently down-regulated the production of TNF-α, IL-1ß, IL-6, and PGE2 induced by LPS
Microglia has been known to play an important role in neurodegenerative diseases [12]
Summary
The incidence of neurodegenerative disease, Parkinson disease (PD) and Alzheimer’s disease, increased markedly in the last decades [1, 2]. The major immune cells in the brain, plays a key role in host defence response to injury or infectious agents [3]. Microglia is exquisitely sensitive to brain injury and disease [4]. Overactivation of microglia leads to the production of inflammatory mediators which plays a critical role in the development of neuroinflammation [5, 6]. Neuroinflammation has recently been implicated as an important mechanism responsible for the pathological processes of neurodegenerative diseases [7, 8]. The identification of agents to inhibit neuroinflammation might be an effective approach for the treatment of neurodegenerative diseases
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