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        Curcumin suppresses oxidative stress via regulation of ROS/NF-κB signaling pathway to protect retinal vascular endothelial cell in diabetic retinopathy

        Huang Jiang,Yi Quanyong,You Yuhong,Chen Yao,Niu Tongtong,Yi Li,Zhang Ji,Ji Xiaoyan,Xu Guoxu,Zou Weijie,Ji Fangfang,Luo Weifeng 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.3

        Background The retinal vascular endothelial cells can be damaged by oxidative stress even in the early stage of diabetic retinopathy (DR). This study aimed to investigate the protective effect of curcumin on the rat retinal vascular endothelial cells (RRVECs) in high glucose circumstance. Objective The cultured RRVECs were identified and characterized by both of vWF and CD31 immunofluorescence expression. The activation of ROS/NF-κB signal pathway was examined by electrophoretic Mobility Shift Assay (EMSA), immunohistochemistry and Western blot; the apoptosis of RRVECs was tested by flow cytometry. Results We found that curcumin reduced the reactive oxygen species (ROS) and relieved the apoptosis in RRVECs exposed to the high glucose by flow cytometry. It was revealed that the increased activity of NF-κB and phosphorylated NF-κB in RRVECs induced by high glucose concentration was significantly suppressed by curcumin. Conclusion We concluded that curcumin could suppress the oxidative stress via regulation of NF-κB signal to protect the RRVECs in DR. Background The retinal vascular endothelial cells can be damaged by oxidative stress even in the early stage of diabetic retinopathy (DR). This study aimed to investigate the protective effect of curcumin on the rat retinal vascular endothelial cells (RRVECs) in high glucose circumstance. Objective The cultured RRVECs were identified and characterized by both of vWF and CD31 immunofluorescence expression. The activation of ROS/NF-κB signal pathway was examined by electrophoretic Mobility Shift Assay (EMSA), immunohistochemistry and Western blot; the apoptosis of RRVECs was tested by flow cytometry. Results We found that curcumin reduced the reactive oxygen species (ROS) and relieved the apoptosis in RRVECs exposed to the high glucose by flow cytometry. It was revealed that the increased activity of NF-κB and phosphorylated NF-κB in RRVECs induced by high glucose concentration was significantly suppressed by curcumin. Conclusion We concluded that curcumin could suppress the oxidative stress via regulation of NF-κB signal to protect the RRVECs in DR.

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        Sodium nitrate modified SBA-15 and fumed silica for efficient production of acrylic acid and 2,3-pentanedione from lactic acid

        Junfeng Zhang,Weijie Ji,Chak-Tong Au,Xinzhen Feng,Yuling Zhao 한국공업화학회 2014 Journal of Industrial and Engineering Chemistry Vol.20 No.4

        The catalytic conversion of lactic acid to acrylic acid and 2,3-pentanedione over sodium nitrate-supported mesoporous SBA-15 and fumed silica was studied. The yields of acrylic acid, 2,3-pentanedione, and acetaldehyde are 44.8%, 25.1%, and 13.3%, respectively, over the 23%NaNO3/SBA-15 catalyst. The performance of the catalysts is strongly affected by NaNO3 loading, catalyst texture and porosity, and product diffusion efficiency. A proper control of NaNO3 loading can result in modification catalyst structure for improvement of 2,3-pentanedione selectivity. Under certain reaction conditions, the surface NaNO3 species can readily transform to sodium lactate that functions as active component to catalyze the target reactions.

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        miR-98 suppresses melanoma metastasis through a negative feedback loop with its target gene IL-6

        Fei Li,Xin-ji Li,Li Qiao,Fei Shi,Wen Liu,You Li,Yu-ping Dang,Weijie Gu,Xiao-gang Wang,Wei Liu 생화학분자생물학회 2014 Experimental and molecular medicine Vol.46 No.-

        Dysregulated microRNA (miRNA) expression has a critical role in tumor development and metastasis. However, the mechanism by which miRNAs control melanoma metastasis is unknown. Here, we report reduced miR-98 expression in melanoma tissues with increasing tumor stage as well as metastasis; its expression is also negatively associated with melanoma patient survival. Furthermore, we demonstrate that miR-98 inhibits melanoma cell migration in vitro as well as metastatic tumor size in vivo. We also found that IL-6 is a target gene of miR-98, and IL-6 represses miR-98 levels via the Stat3-NF-κB-lin28B pathway. In an in vivo melanoma model, we demonstrate that miR-98 reduces melanoma metastasis and increases survival in part by reducing IL-6 levels; it also decreases Stat3 and p65 phosphorylation as well as lin28B mRNA levels. These results suggest that miR-98 inhibits melanoma metastasis in part through a novel miR-98-IL-6-negative feedback loop.

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