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RISS 인기검색어
- 검색키워드
- 저자 : Ao Yuanyuan (검색결과 3 건)
- 무료
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- 유료
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Liu Jun,Zhang Junqing,Ao Yuanyuan 대한독성 유전단백체 학회 2023 Molecular & cellular toxicology Vol.19 No.2
Background Parkinson’s disease (PD) is a common neurodegenerative disorder associated with microglia-mediated neuroinfl ammation in pathogenesis. Regulatory T cells (Treg cells) are involved in the regulation of microglia activation and neuroinfl ammation. However, it is yet to be established whether exosomes derived from Treg cells (Treg-Exos) possess protective eff ect against MPP + -induced infl ammation 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 infl ammatory 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-κB 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 infl ammatory cytokines IL-β, IL-6, and TNF-α in MPP + -induced BV2 cells were also prevented by the treatment of Treg-Exos. Treg-Exos inhibited MPP + -induced activation of the TLR4/NF-κB 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 eff ect of Treg-Exos on MPP + -treated BV2 cells. Conclusions Collectively, Treg-Exos attenuated MPP + -induced oxidative stress and infl ammatory injury in BV-2 cells by inhibiting the TLR4/NF-κB signaling.
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Xia, Xiaojing,Che, Yanyi,Gao, Yuanyuan,Zhao, Shuang,Ao, Changjin,Yang, Hongjian,Liu, Juxiong,Liu, Guowen,Han, Wenyu,Wang, Yuping,Lei, Liancheng Korean Society for Molecular and Cellular Biology 2016 Molecules and cells Vol.39 No.5
During the lactation cycle of the bovine mammary gland, autophagy is induced in bovine mammary epithelial cells (BMECs) as a cellular homeostasis and survival mechanism. Interferon gamma ($IFN-{\gamma}$) is an important antiproliferative and apoptogenic factor that has been shown to induce autophagy in multiple cell lines in vitro. However, it remains unclear whether $IFN-{\gamma}$ can induce autophagy and whether autophagy affects milk synthesis in BMECs. To understand whether $IFN-{\gamma}$ affects milk synthesis, we isolated and purified primary BMECs and investigated the effect of $IFN-{\gamma}$ on milk synthesis in primary BMECs in vitro. The results showed that $IFN-{\gamma}$ significantly inhibits milk synthesis and that autophagy was clearly induced in primary BMECs in vitro within 24 h. Interestingly, autophagy was observed following $IFN-{\gamma}$ treatment, and the inhibition of autophagy can improve milk protein and milk fat synthesis. Conversely, upregulation of autophagy decreased milk synthesis. Furthermore, mechanistic analysis confirmed that $IFN-{\gamma}$ mediated autophagy by depleting arginine and inhibiting the general control nonderepressible-2 kinase (GCN2)/eukaryotic initiation factor $2{\alpha}$ ($eIF2{\alpha}$) signaling pathway in BMECs. Then, it was found that arginine supplementation could attenuate $IFN-{\gamma}$-induced autophagy and recover milk synthesis to some extent. These findings may not only provide a novel measure for preventing the $IFN-{\gamma}$-induced decrease in milk quality but also a useful therapeutic approach for $IFN-{\gamma}$-associated breast diseases in other animals and humans.
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Liancheng Lei,Xiaojing Xia,Yanyi Che,Yuanyuan Gao,Shuang Zhao,Changjin Ao,Hongjian Yang,Juxiong Liu,Guo-wen Liu,Wenyu Han,Yuping Wang 한국분자세포생물학회 2016 Molecules and cells Vol.39 No.5
During the lactation cycle of the bovine mammary gland, autophagy is induced in bovine mammary epithelial cells (BMECs) as a cellular homeostasis and survival mecha-nism. Interferon gamma (IFN-) is an important antiproliferative and apoptogenic factor that has been shown to induce autophagy in multiple cell lines in vitro. However, it remains unclear whether IFN- can induce autophagy and whether autophagy affects milk synthesis in BMECs. To understand whether IFN- affects milk synthesis, we isolated and purified primary BMECs and investigated the effect of IFN- on milk synthesis in primary BMECs in vitro. The results showed that IFN- significantly inhibits milk synthesis and that autophagy was clearly induced in primary BMECs in vitro within 24 h. Interestingly, autophagy was observed following IFN- treatment, and the inhibition of autophagy can improve milk protein and milk fat syn-thesis. Conversely, upregulation of autophagy decreased milk synthesis. Furthermore, mechanistic analysis con-firmed that IFN- mediated autophagy by depleting argi-nine and inhibiting the general control nonderepressible-2 kinase (GCN2)/eukaryotic initiation factor 2 (eIF2) signaling pathway in BMECs. Then, it was found that arginine supplementation could attenuate IFN--induced autophagy and recover milk synthesis to some extent. These findings may not only provide a novel measure for preventing the IFN--induced decrease in milk quality but also a useful therapeutic approach for IFN--associated breast diseases in other animals and humans.
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