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Phytomedicine. 2018 Dec 1;51:226-232. doi: 10.1016/j.phymed.2018.06.014. Epub 2018 Jun 23.

Andalucin from Artemisia lannta suppresses the neuroinflammation via the promotion of Nrf2-mediated HO-1 levels by blocking the p65-p300 interaction in LPS-activated BV2 microglia.

Author information

1
Department of pharmacy, The Affiliated Hospital of Nanjing University Medical School, 321 Zhong Shan Road, Nanjing 210008, China.
2
Institute of Botany, Jiangsu Province and Chinese Academy of Sciences, Nanjing 210014, China.
3
Department of anesthesiology, The Affiliated Hospital of Nanjing University Medical School, Nanjing 210008, China.
4
Department of pharmacy, The Affiliated Hospital of Nanjing University Medical School, 321 Zhong Shan Road, Nanjing 210008, China. Electronic address: 20031269@qq.com.

Abstract

BACKGROUND:

Neuroinflammation plays an important role in many neurodegenerative conditions such as Alzheimer's disease (AD) and Parkinson disease (PD). Andalucin (ADL), a sesquiterpene lactone from Artemisia lannta, has been reported to exhibit NO inhibition in vitro. However, the effect of ADL on microglia-mediated neuroinflammation has not been investigated.

PURPOSE:

This study was designed to determine the anti-neuroinflammatory effect of ADL against LPS-activated BV2 microglial cells and to explore the underlying mechanisms.

METHODS:

The production of pro-inflammatory mediators and cytokines were measured by ELISA. The relevant mechanisms were analyzed by qRT-PCR, Luciferase assay, Western blot and Co-immunoprecipitation Assay.

RESULTS:

ADL inhibited the LPS-induced release of NO, PGE2, TNF-α, IL-6 and IL-1β. In addition, ADL reduced the mRNA and protein levels of iNOS and COX-2. Mechanism studies found that ADL activated Nrf2/HO-1 signaling pathway and suppressed NF-κB signaling pathway. Further investigation showed that the stimulative effect of ADL on Nrf2 transcriptional activity and the inhibitory effect of ADL on RelA transcriptional activity were due to its regulation on p300-Nrf2/p65 interaction.

CONCLUSION:

ADL displayed anti-neuroinflammatory activity in LPS-activated BV2 cells. The mechanism concerns its regulatory effect on the crosstalk between Nrf2 and p65.

KEYWORDS:

Andalucin; Neuroinflammatory; Nrf2; P300; P65

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