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Sesamin suppresses advanced glycation end products induced microglial reactivity using BV2 microglial cell line as a
Sasimol Udomruk1, Benjawan Wudtiwai1, Thuzar Hla Shwe1
1Thailand Excellence Center for Tissue Engineering and Stem Cells, Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.
Abstract:
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.
Insights
Advanced glycation end products (AGEs) worsen neuroinflammation in Type 2 diabetes, increasing Alzheimer's risk. Sesamin, from sesame seeds, shows potential in reducing this inflammation by targeting key pathways.
Area of Science:
- Neuroscience
- Immunology
- Endocrinology
Background:
- Type 2 diabetes mellitus (T2DM) is linked to increased Alzheimer's disease (AD) risk, with neuroinflammation playing a key role.
- Advanced glycation end products (AGEs), elevated in diabetes, contribute to brain injury by inducing microglial reactivity.
Purpose of the Study:
- To investigate the effects of AGEs on microglial reactivity using a BV2 cell model.
- To explore the potential anti-inflammatory effects of sesamin on AGEs-induced microglial activation.
Main Methods:
- Utilized BV2 cells as a model for microglial reactivity.
- Investigated the roles of NF-κB, p38, and JNK signaling pathways in AGEs-induced inflammation.
- Assessed the inhibitory effects of specific pathway inhibitors (BAY-11-7082, SB203580, SP600125) on nitric oxide (NO) production.
- Evaluated sesamin's impact on AGEs-induced microglial activation, including phosphorylation of key pathways and receptor for advanced glycation end products (RAGE) expression.
Main Results:
- AGEs induced microglial reactivity in BV2 cells, involving the NF-κB, p38, and JNK pathways.
- Inhibitors of NF-κB, p38, and JNK pathways reduced AGEs-induced NO production.
- Sesamin suppressed AGEs-induced microglial reactivity by inhibiting the phosphorylation of NF-κB, p38, and JNK pathways.
- Sesamin also reduced AGEs-induced RAGE expression.
Conclusions:
- Sesamin demonstrates anti-inflammatory properties against AGEs-induced microglial activation.
- Sesamin may be a promising phytochemical to mitigate AGEs-driven neuroinflammation in T2DM-associated AD.
- Targeting AGEs-induced microglial reactivity presents a potential therapeutic strategy for neuroinflammation in T2DM-linked AD.
