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RISS 인기검색어
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- 저자 : Rongchang Chen (검색결과 3 건)
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Chen Shuyu,Yu Li,Deng Yao,Liu Yuanyuan,Wang Lingwei,Li Difei,Yang Kai,Liu Shengming,Tao Ailin,Chen Rongchang 대한천식알레르기학회 2022 Allergy, Asthma & Immunology Research Vol.14 No.5
Purpose: Interleukin (IL)-17A plays a critical role in the pathogenesis of allergic airway inflammation. Yet, the exact roles of IL-17A in asthma are still controversial. Thus, the aim of this study was to dissect the roles of IL-17A in toluene diisocyanate (TDI)-induced mixed granulocytic asthma and to assess the effects of neutralizing antibody in different effector phases on TDI-induced asthma. Methods: IL-17A functions in allergic airway inflammation were evaluated using mice deficient in IL-17A (Il17a−/−) or IL-17A monoclonal antibody (IL-17A mab, intraperitoneally, 50 μg per mouse, 100 μg per mouse). Moreover, the effects of exogenous recombinant IL (rIL)-17A in vivo (murine rIL-17A, intranasally, 1 μg per mouse) and in vitro (human rIL-17A, 100 ng/mL) were investigated. Results: TDI-induced mixed granulocytic airway inflammation was IL-17A-dependent because airway hyperreactivity, neutrophil and eosinophil infiltration, airway smooth muscle thickness, epithelium injury, dysfunctional T helper (Th) 2 and Th17 responses, granulocytic chemokine production and mucus overproduction were more markedly reduced in the Il17a−/− mice or by IL-17A neutralization during the sensitization phase of wild-type (WT) mice. By contrast, IL-17A neutralization during the antigen-challenge phase aggravated TDI-induced eosinophils recruitment, with markedly elevated Th2 response. In line with this, instillation of rIL-17 during antigen sensitization exacerbated airway inflammation by promoting neutrophils aggregation, while rIL-17A during the antigen-challenge phase protected the mice from TDI-induced airway eosinophilia. Moreover, rIL-17A exerted distinct effects on eosinophil- or neutrophil-related signatures in vitro. Conclusions: Our data demonstrated that IL-17A was required for the initiation of TDI-induced asthma, but functioned as a negative regulator of established allergic inflammation, suggesting that early abrogation of IL-17A signaling, but not late IL-17A neutralization, may prevent the progression of TDI-induced asthma and could be used as a therapeutic strategy for severe asthmatics in clinical settings.
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Yingli Yu,MinWang,Rongchang Chen,Xiao Sun,Guibo Sun,Xiaobo Sun 고려인삼학회 2021 Journal of Ginseng Research Vol.45 No.6
Background: Effective strategies are dramatically needed to prevent and improve the recovery frommyocardialischemia and reperfusion (I/R) injury. Direct interactions between the mitochondria and endoplasmic reticulum(ER) during heart diseases have been recently investigated. This study was designed to explore the cardioprotectiveeffects of gypenoside XVII (GP-17) against I/R injury. The roles of ER stress, mitochondrial injury,and their crosstalk within I/R injury and in GP-17einduced cardioprotection are also explored. Methods: Cardiac contractility function was recorded in Langendorff-perfused rat hearts. The effects ofGP-17 on mitochondrial function including mitochondrial permeability transition pore opening, reactiveoxygen species production, and respiratory function were determined using fluorescence detection kitson mitochondria isolated from the rat hearts. H9c2 cardiomyocytes were used to explore the effects ofGP-17 on hypoxia/reoxygenation. Results: We found that GP-17 inhibits myocardial apoptosis, reduces cardiac dysfunction, and improvescontractile recovery in rat hearts. Our results also demonstrate that apoptosis induced by I/R is predominantlymediated by ER stress and associated with mitochondrial injury. Moreover, the cardioprotectiveeffects of GP-17 are controlled by the PI3K/AKT and P38 signaling pathways. Conclusion: GP-17 inhibits I/R-induced mitochondrial injury by delaying the onset of ER stress throughthe PI3K/AKT and P38 signaling pathways.
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Genomic analysis of Sheldrake origin goose hemorrhagic polyomavirus, China
Chunhe Wan,Cuiteng Chen,Longfei Cheng,Rongchang Liu,Guanghua Fu,Shaohua Shi,Hongmei Chen,Qiuling Fu,Yu Huang 대한수의학회 2018 Journal of Veterinary Science Vol.19 No.6
Goose hemorrhagic polyomavirus (GHPV) is not a naturally occurring infection in geese in China; however, GHPV infection has been identified in Pekin ducks, a domestic duck species. Herein, we investigated the prevalence of GHPV in five domestic duck species (Liancheng white ducks, Putian black ducks, Shan Sheldrake, Shaoxing duck, and Jinyun Sheldrake) in China. We determined that the Jinyun Sheldrake duck species could be infected by GHPV with no clinical signs, whereas no infection was identified in the other four duck species. We sequenced the complete genome of the Jinyun Sheldrake origin GHPV. Genomic data comparison suggested that GHPVs share a conserved genomic structure, regardless of the host (duck or geese) or region (Asia or Europe). Jinyun Sheldrake origin GHPV genomic characterization and epidemiological studies will increase our understanding of potential heterologous reservoirs of GHPV.
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