Name: Guoying Bing

Country: China

Affiliation:

Professor
Department of Anatomy and  Neurobiology

Room HSRB 426, College of Medicine

Email: Send an Email


Address:

Professor
Department of Anatomy and  Neurobiology

Room HSRB 426, College of Medicine

University of Kentucky

Lexington KY 40536

Office Phone: 859-323-9708

E-mail: :[email protected]

Research Interests:

Neuroinflammation   Mediated   Dopaminergic Cell Death

Parkinson’s   Disease (PD) is a neurodegenerative disease characterized by loss of the dopamine-containing   neurons in the substantia nigra pars compacta (SNpc). Although the cause of   neuronal death remains unclear, increasing evidence points to the role of chronic   inflammatory processes. In order to explore the possibility that microglial   activation causes dopaminergic cell death in the SNpc, lipopolysaccharide (LPS),   a bacterial endotoxin that activate microglia, was into the substantia nigra   (SN). The LPS injection not only caused the activation of microglia, but also   resulted in a dose-dependent, selective loss of dopaminergic neurons by apoptosis   in the SNpc. We therefore hypothesize that LPS activates microglia in the SN   resulting in the release of cytotoxic agents. These agents, in turn, activate   signal transduction pathways that cause neuronal degeneration of dopaminergic   neurons in the SN. The long-term goal of this study is to validate LPS injection   as a new animal model of PD that can be used to elucidate the etiology and molecular   mechanisms underlying PD and to develop novel therapeutic treatments for this   and other neurodegenerative diseases.

Influence of Xenobiotic   Metabolites on the Neuronal Cell Death
  Dr. Bing’s laboratory has recently found that a high level of microsomal   epoxide hydrolase (mEH) expression in the brain of patients with Alzheimer’s   disease as well as the rat brain following exposure to neurodegenerative agents   such as kainic acid and trimethyl-tin. Relatively little is known about the   expression and function of mEH in the CNS. However, the dual function of mEH   in the activation as well as the inactivation of various reactive compounds   from xenobiotic metabolites has important implications regarding its role in   brain toxicity. The hypothesize is that mEH plays a crucial role in the biotransformation   of endogenous xenobiotics and/or environmental chemicals into more toxic metabolites   which may cause neuronal degeneration in specific neuronal populations. The   identifying the exact role of mEH as well as the role of xenobiotic metabolites   in the brain will be critical in understanding the neurodegeneration induced   by exposure to toxic chemicals.

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