芝麻素
神经炎症
小胶质细胞
糖基化
化学
药理学
p38丝裂原活化蛋白激酶
促炎细胞因子
内科学
内分泌学
糖尿病
信号转导
炎症
医学
生物化学
MAPK/ERK通路
食品科学
作者
Sasimol Udomruk,Benjawan Wudtiwai,Thuzar Hla Shwe,Thanyaluck Phitak,Peraphan Pothacharoen,Mattabhorn Phimphilai,Prachya Kongtawelert
标识
DOI:10.1016/j.brainresbull.2021.04.012
摘要
Neuroinflammation-mediated microglial reactivity is a major process, which explains the increased risk of Alzheimer's disease (AD) development in patients with Type 2 diabetes mellitus (T2DM). Advanced glycation end products (AGEs), formed by hyperglycemic condition in diabetes, is characterized as an intermediary of brain injury with diabetes through induction of microglial reactivity. Here, we explored the effect of AGEs on microglial reactivity using BV2 as a model. The NF-κB, p38 and JNK pathways were found to be important mechanism in AGEs-induced BV2 microglial reactivity. NF-κB inhibitor (BAY-11-7082), p38 inhibitor (SB203580) and JNK inhibitor (SP600125) exhibited the potential inhibition of AGEs-induced NO production. We also found that the sesamin, a major lignan found in sesame seed oils, exerts an anti-inflammatory effect under AGEs-induced microglial reactivity via suppressing the phosphorylation of NF-κB, p38 and JNK pathways. Moreover, sesamin also ameliorated AGEs-induced-receptor for advanced glycation end products (RAGE) expression. Taken together, sesamin may be a promising phytochemical compound to delay inflammatory progress by AGEs microglia function. Similarly, inhibition of AGEs-induced microglial reactivity might be potential therapeutic targets of neuroinflammation-based mechanisms in T2DM link progressive AD.
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