KMID : 1034820230190020283
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Molecular & Cellular Toxicology 2023 Volume.19 No. 2 p.283 ~ p.291
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Exosomes derived from regulatory T cells attenuates MPP+-induced inflammatory response and oxidative stress in BV-2 cells by inhibiting the TLR4/NF-¥êB signaling
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Jun Liu
Junqing Zhang Yuanyuan Ao
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Abstract
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Background : Parkinson¡¯s disease (PD) is a common neurodegenerative disorder associated with microglia-mediated neuroinflammation in pathogenesis. Regulatory T cells (Treg cells) are involved in the regulation of microglia activation and neuroinflammation. However, it is yet to be established whether exosomes derived from Treg cells (Treg-Exos) possess protective effect against MPP+-induced inflammation and oxidative stress in microglia.
Objective : In our study, we examined the function of Treg cells in the in vitro PD model. MTT assay was used to assess the viability of BV2 cells. ROS, MDA, and SOD activity were detected, and ELISA was performed to estimate the inflammatory response and oxidative stress of BV-2 cells. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting were applied to detect the level changes of genes involved in the TLR4/NF-¥êB signaling pathway.
Results : The results showed that Treg-Exos improved the cell viability of MPP+-treated BV2 cells. MPP+-induced increase in ROS and MDA production, as well as decrease in SOD activity in BV2 cells were attenuated by Treg-Exos. The increased levels of inflammatory cytokines IL-¥â, IL-6, and TNF-¥á in MPP+-induced BV2 cells were also prevented by the treatment of Treg-Exos. Treg-Exos inhibited MPP+-induced activation of the TLR4/NF-¥êB signaling, indicated by decreased protein level of TLR4 and p-p65/p65 ratio in BV2 cells. Further, we also found that upregulation of TLR4 blocks the protective effect of Treg-Exos on MPP+-treated BV2 cells.
Conclusions : Collectively, Treg-Exos attenuated MPP+-induced oxidative stress and inflammatory injury in BV-2 cells by inhibiting the TLR4/NF-¥êB signaling.
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KEYWORD
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Exosomes, Microglia activation, Neuroinflammation, Parkinson¡Çs disease, TLR4/NF-¥êB signaling, Treg cells, Treg-Exos
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