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6.6】Prof. Sudipta Seal
Topic: Nanoceria with engineered defects: Antioxidative Mimetic Enzymes
 
2019-05-31 | 文章来源:李薰奖办公室        【 】【打印】【关闭

  Lee Hsun Lecture Series

    Topic: Nanoceria with engineered defects: Antioxidative Mimetic Enzymes

  Speaker: Prof. Sudipta Seal

           University of Central Florida, USA

  Time: 14:00-16:00, (Thur.) Jun.6th, 2019

  Venue: Room 468,Lee Hsun Building, IMR CAS

  Abstract: Oxidative and nitrosative stress, the excessive generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), respectively, hinder the normal functioning and induces damaging effect to the cellular machinery. ROS and RNS are generated as byproducts of numerous metabolic reactions, in many disease states and under inflammatory conditions. Seal research group was the first one to show the specially engineered nanoceria (CNP) mimics the catalytic properties of antioxidative enzymes and induces protective effect through regenerative scavenging potential and ameliorates the disease states further. In general, CNP exhibits novel surface properties in terms of redox active Ce+3/Ce+4 ratios and change in nanoparticle morphology largely dependent on different synthesis, which will be covered in this lecture.

  We will discuss the role of CNP to accelerate the wound healing process through reducing the oxidative/nitrosative damage and inducing proliferative effect on the migration of keratinocytes, fibroblast and vascular endothelial cells. CNP activates angiogenesis, observed using both in vitro and in vivo model systems. Mechanistically, CNPs trigger angiogenesis by modulating the intracellular oxygen environment and stabilizing HIF-1 endogenously. Furthermore, correlations between angiogenesis induction and CNPs’ trafficking, depending on physicochemical properties including surface valence state ratio, surface charge, size, and shape.

  We have also successfully conjugated CNP with other biomolecules (i.e. mRNA), which promotes the wound healing in diabetic mice by reducing the oxidative stress environment and promoting macrophage transition. We hypothesize that treatment of macrophages with miR-146a conjugated nanoceria reduces ROS production and promotes expression of the M2 phenotype, important in wound healing. Will conclude the talk with few examples of CNP applications in reduction of chronic inflammation, protecting tissues against radiation protection, aid in inhibiting laser induced retinal damage, etc. Therefore, these inorganic nano-enzyme mimics can be used in nanomedicine, enabling unique ROS/RNS scavenging potential for mitigating oxidative and nitrosative stress. Highlights of the potential opportunities of nano-oxides technology commercialization from Seal research group will be presented.

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