説明
Publisher Summary This chapter focuses on methods for studying chemokine expression in transgenic mice overexpressing human glutathione peroxidases. As a model of pathological conditions involving oxidative stress, kidney ischemiareperfusion is used. Both animal studies and clinical data strongly implement reactive oxygen species (ROS) in ischemia-reperfusion injury, whereas the inflammatory response is crucial for amplification of kidney malfunction. It has also become apparent that low levels of ROS play an important role in activation and recruitment of inflammatory cells through induction of adhesion receptors and regulation of the activity of lipoxygenases and cyclooxygenases, transcription factors, protein kinases, and other mediators. All this indicates that there are many ways in which ROS can influence the function of the immune system as well as its interaction with other tissues. The chapter presents methods by which to use genetically engineered animal models that are able to modulate the level of oxidative stress, to study the mechanisms of chemokine activation in pathological processes.
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キーワード
- Glutathione Peroxidase
- Blotting, Western
- Electrophoretic Mobility Shift Assay
- Mice, Transgenic
- Intercellular Adhesion Molecule-1
- Kidney
- Antioxidants
- Up-Regulation
- DNA-Binding Proteins
- Mice
- Oxidative Stress
- NF-KappaB Inhibitor alpha
- Polyribosomes
- Reperfusion Injury
- Animals
- Humans
- I-kappa B Proteins
- RNA, Messenger
- Chemokines
- Reactive Oxygen Species