Article Publish Status: FREE
Abstract Title:

Stigmasterol attenuates inflammatory response of microglia via NF-κB and NLRP3 signaling by AMPK activation.

Abstract Source:

Biomed Pharmacother. 2022 Jun 27 ;153:113317. Epub 2022 Jun 27. PMID: 35772378

Abstract Author(s):

Fan Jie, Xuan Yang, Bowen Yang, Yan Liu, Lipeng Wu, Baiyi Lu

Article Affiliation:

Fan Jie


Alzheimer's disease (AD) is the most common cause of dementia in the elderly. Although its pathogenesis remains unclear, studies have indicated microglia-mediated neuroinflammation playing an important role. Phytosterols are a class of natural compounds presented in food, and have anti-inflammatory abilities. Recent studies suggested that phytosterols can traverse the blood-brain barrier and enter the brain, however, it remains largely unknown that whether phytosterols affect neuroinflammation in the AD pathogenesis. Here, we used APP/PS1mice as the animal model of AD, and found that stigmasterol treatment attenuated cognitive deficits, and decreased Aβconcentration in cortex and hippocampus. Stigmasterol treatment also suppressed neuroinflammation, by reducing pro-inflammatory cytokine levels and microglia activation. Next, we simulated BV2 cells with Aβoligomers, which induced inflammatory responses of microglia. Stigmasterol protected BV2 cells against Aβoligomers induced inflammation, and mediated secretion of pro-inflammatory cytokines via NF-κB and NLRP3 signaling pathways by AMPK activation. Stigmasterol also alleviated the M1 polarization of BV2 cells. In general, our study demonstrates that stigmasterol ameliorated neuroinflammation in APP/PS1 mice, and suppressed inflammatory response of microglia to Aβoligomers via AMPK/NF-κB and AMPK/NLRP3 signaling, which provides a mechanistic insight for stigmasterol in anti-inflammation and AD therapy.

Study Type : Animal Study, In Vitro Study

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