Sesamin suppresses LPS-induced microglial activation via regulation of TLR4 expression

• Main Authors: Sasimol Udomruk, Chayanut Kaewmool, Peraphan Pothacharoen, Thanyaluck Phitak, Prachya Kongtawelert
• Format: Article
• Language: English
• Published: Elsevier 2018-10-01
• Series: Journal of Functional Foods
• Subjects: Sesamin; Toll-like receptor 4; Pro-inflammatory mediators; Neurodegeneration
• Online Access: http://www.sciencedirect.com/science/article/pii/S1756464618304407

Sesamin, one of the most abundant lignans in sesame seeds and oils, is well known for neuroprotective activity. However, its effects on toll-like-receptor 4 (TLR4), the key innate immune receptor implicated in microglia activation and neuroinflammation has not been reported. Our study demonstrated that sesamin significantly diminished LPS-stimulated TLR4 expression result in the reduction of nitric oxide (NO), prostaglandin E2 (PGE2) and pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) in BV2 microglia by suppressing JNK and NF-κB pathway. While conditioned medium from LPS-stimulated microglia-induced PC12 cell death, sesamin pre-treatment on microglia abrogated the cytotoxic effects of pro-inflammatory mediators. Our result also demonstrated the direct effect of sesamin in ameliorating PC12 cell death induced by activated microglial-conditioned medium. These results suggested that sesamin alleviated inflammation-induced neurodegeneration via inhibition of TLR4 expression and microglial activation resulting in diminishing the neurotoxicity effect. Sesamin might be a potential agent for neurodegenerative diseases prevention.