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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.
Densification Mechanism of Warm Compaction for Iron-based Powder Materials
Qu Shengguan,Li Yuanyuan,Xia Wei,Chen Weiping 한국분말야금학회 2006 한국분말야금학회 학술대회논문집 Vol.2006 No.1
An apparatus measuring changes of various forces directly and continuously was developed by a way of direct touch between powders and transmitting force component, which can be used to study forces state of powders during warm compaction. Using the apparatus, warm compaction processes of iron-based powder materials containing different lubricants at different temperatures were studied. Results show that densification of the iron-based powder materials can be divided into four stages, in which powder movement changes from robustness to weakness, while its degree of plastic deformation changes from weakness to robustness.
Jingying Gao,Lixia Xia,Yuanyuan Wei 대한약리학회 2022 The Korean Journal of Physiology & Pharmacology Vol.26 No.3
As the mechanism underlying glucose metabolism regulation by oxymatrine is unclear, this study investigated the effects of oxymatrine on pyroptosis in INS-1 cells. Flow cytometry was employed to examine cell pyroptosis and reactive oxygen species (ROS) production. Cell pyroptosis was also investigated via transmission electron microscopy and lactate dehydrogenase (LDH) release. Protein levels were detected using western blotting and interleukin (IL)-1β and IL-18 secretion by enzyme-linked immunosorbent assay. The caspase-1 activity and DNA-binding activity of nuclear factor kappa B (NF-κB) and nuclear factor (erythroid-derived 2)-like 2 protein (Nrf2) were also assessed. In the high glucose and high fat-treated INS-1 cells (HG + PA), the caspase-1 activity and LDH content, as well as Nod-like receptor family pyrin domain containing 3, Gsdmd-N, caspase-1, apoptosis-associated specklike protein containing a CARD, IL-1β, and IL-18 levels were increased. Moreover, P65 protein levels increased in the nucleus but decreased in the cytoplasm. Oxymatrine attenuated these effects and suppressed high glucose and high fat-induced ROS production. The increased levels of nuclear Nrf2 and heme oxygenase-1 (HO-1) in the HG + PA cells were further elevated after oxymatrine treatment, whereas cytoplasmic Nrf2 and Keleh-like ECH-associated protein levels decreased. Additionally, the elevated transcriptional activity of p65 in HG + PA cells was reduced by oxymatrine, whereas that of Nrf2 increased. The results indicate that the inhibition of pyroptosis in INS- 1 cells by oxymatrine, a key factor in its glucose metabolism regulation, involves the suppression of the NF-κB pathway and activation of the Nrf2/HO-1 pathway.
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.