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- 저자 : Huang Feiyun (검색결과 2 건)
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Yang Zhen,Xie Jiqin,Huang Feiyun,Yang Yu,Zhang Xiuyue,Yue Bisong 한국곤충학회 2022 Entomological Research Vol.52 No.2
Edible insects are alternative sources of high protein. Southeast Asia, South America, Africa, and Europe have recorded edible insects and, especially in Europe and America, there are factories that produce insects as food. In some areas of China, there has also been the habit of eating insects since ancient times. Periplaneta americana is an insect with the homology of medicine and food. In recent years, its medicinal and nutritional functions have attracted extensive attention and research. Its adult powder has been certified as a health product. It not only contains a variety of proteins but also is rich in fatty acids. The composition and antioxidant function of adult powder extract was analyzed in this study. Using adult P. americana powder as the raw material, it was extracted with n-Hexane, dichloromethane, and ethyl acetate, respectively. Gas chromatography–mass spectrometry (GC–MS) removed a total of 60 compounds, and many active components were extracted from P. americana powder for the first time. The parts and relative content of each extracted sample were obtained, and the total antioxidant capacity (T-AOC) of each extracted piece was determined, among which the antioxidant activity of ethyl acetate was the highest.
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The Role of Macrophage Migration Inhibitory Factor (MIF) in Asthmatic Airway Remodeling
Li Ruyi,Wang Feiyun,Wei Jianghong,Lin Yun,Tang Guofang,Rao Lizong,Ma Libing,Xu Qing,Wu Jingjie,Lv Qian,Zhou Rui,Lei Huiren,Zhao Xueqiang,Yao Dong,Xiao Bo,Huang Haiming,Zhang Jiange,Mo Biwen 대한천식알레르기학회 2021 Allergy, Asthma & Immunology Research Vol.13 No.1
Purpose: Recent studies have demonstrated that macrophage migration inhibitory factor (MIF) is of importance in asthmatic inflammation. The role of MIF in modulating airway remodeling has not yet been thoroughly elucidated to date. In the present study, we hypothesized that MIF promoted airway remodeling by intensifying airway smooth muscle cell (ASMC) autophagy and explored the specific mechanisms. Methods: MIF knockdown in the lung tissues of C57BL/6 mice was conducted by instilling intratracheally adeno-associated virus (AAV) vectors (MIF-mutant AAV9) into mouse lung tissues. Mice genetically deficient in the autophagy marker ATG5 (ATG5+/−) was used to detect the role of autophagy in ovalbumin (OVA)-asthmatic murine models. Moreover, to block the expression of MIF and CD74 in vitro models, inhibitors, antibodies and lentivirus transfection techniques were employed. Results: First, MIF knockdown in the lung tissues of mice showed markedly reduced airway remodeling in OVA murine mice models. Secondly, ASMC autophagy was increased in the OVA-challenged models. Mice genetically deficient in the autophagy marker ATG5 (ATG5+/−) that were primed and challenged with OVA showed lower airway remodeling than genetically wild-type asthmatic mice. Thirdly, MIF can induce ASMC autophagy in vitro. Moreover, the cellular source of MIF which promoted ASMC autophagy was macrophages. Finally, MIF promoted ASMC autophagy in a CD74-dependent manner. Conclusions: MIF can increase asthmatic airway remodeling by enhancing ASMC autophagy. Macrophage-derived MIF can promote ASMC autophagy by targeting CD74.
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