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      저자 : Jiaxi Wu (검색결과 2 건)
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        Investigation into the antibacterial activity of monodisperse BSA-conjugated zinc oxide nanoparticles

        Dudu Wu,Zhi Chen,Kangrong Cai,Dongling Zhuo,Jiaxi Chen,Bin Jiang 한국물리학회 2014 Current Applied Physics Vol.14 No.11

        The antibacterial behavior of bovine serum albumin conjugated zinc oxide nanoparticles against Escherichia coli was investigated. The zinc oxide nanoparticles were synthesized by using bovine serum albumin as the structure directing agent. And the morphology and crystal phase of the zinc oxide nanoparticles were determined by transmission electron microscopy, X-ray diffractograms and Fourier transform infrared spectrograph techniques. The synthesized zinc oxide nanoparticles showed high antibacterial activity when compared with plain zinc oxide. And the antibacterial activity was assessed by measuring the growth inhibition and testing the zone of inhibition. Furthermore, the plausible mechanism of antibacterial behavior was attributed to the generation of reactive oxygen species by zinc oxide nanoparticles.

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        Honokiol ameliorates endothelial dysfunction through suppression of PTX3 expression, a key mediator of IKK/IκB/NF-κB, in atherosclerotic cell model

        Ling Qiu,Rong Xu,Siyang Wang,Shuijun Li,Hongguang Sheng,Jiaxi Wu,Yi Qu 생화학분자생물학회 2015 Experimental and molecular medicine Vol.47 No.-

        Pentraxin 3 (PTX3) was identified as a marker of the inflammatory response and overexpressed in various tissues and cells related to cardiovascular disease. Honokiol, an active component isolated from the Chinese medicinal herb Magnolia officinalis, was shown to have a variety of pharmacological activities. In the present study, we aimed to investigate the effects of honokiol on palmitic acid (PA)-induced dysfunction of human umbilical vein endothelial cells (HUVECs) and to elucidate potential regulatory mechanisms in this atherosclerotic cell model. Our results showed that PA significantly accelerated the expression of PTX3 in HUVECs through the IκB kinase (IKK)/IκB/nuclear factor-κB (NF-κB) pathway, reduced cell viability, induced cell apoptosis and triggered the inflammatory response. Knockdown of PTX3 supported cell growth and prevented apoptosis by blocking PA-inducted nitric oxide (NO) overproduction. Honokiol significantly suppressed the overexpression of PTX3 in PA-inducted HUVECs by inhibiting IκB phosphorylation and the expression of two NF-κB subunits (p50 and p65) in the IKK/IκB/NF-κB signaling pathway. Furthermore, honokiol reduced endothelial cell injury and apoptosis by regulating the expression of inducible NO synthase and endothelial NO synthase, as well as the generation of NO. Honokiol showed an antiinflammatory effect in PA-inducted HUVECs by significantly inhibiting the generation of interleukin-6 (IL-6), IL-8 and monocyte chemoattractant protein-1. In summary, honokiol repaired endothelial dysfunction by suppressing PTX3 overexpression in an atherosclerotic cell model. PTX3 may be a potential therapeutic target for atherosclerosis.

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