Shaohua Yang, M.D., Ph.D.
Permanent URI for this communityhttps://hdl.handle.net/20.500.12503/31682
Member, Institute for Healthy Aging
Professor, Pharmacology & Neuroscience
Email: Shaohua.Yang@unthsc.edu
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Browsing Shaohua Yang, M.D., Ph.D. by Author "Li, Wenjun"
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Item Artemisinin Prevents Glutamate-Induced Neuronal Cell Death Via Akt Pathway Activation(Frontiers Media S.A., 2018-04-20) Lin, Shao-Peng; Li, Wenjun; Winters, Ali; Liu, Ran; Yang, ShaohuaArtemisinin is an anti-malarial drug that has been in use for almost half century. Recently, novel biological effects of artemisinin on cancer, inflammation-related disorders and cardiovascular disease were reported. However, neuroprotective actions of artemisinin against glutamate-induced oxidative stress have not been investigated. In the current study, we determined the effect of artemisinin against oxidative insult in HT-22 mouse hippocampal cell line. We found that pretreatment of artemisinin declined reactive oxygen species (ROS) production, attenuated the collapse of mitochondrial membrane potential induced by glutamate and rescued HT-22 cells from glutamate-induced cell death. Furthermore, our study demonstrated that artemisinin activated Akt/Bcl-2 signaling and that neuroprotective effect of artemisinin was blocked by Akt-specific inhibitor, MK2206. Taken together, our study indicated that artemisinin prevented neuronal HT-22 cell from glutamate-induced oxidative injury by activation of Akt signaling pathway.Item Hyperglycemia Alters Astrocyte Metabolism and Inhibits Astrocyte Proliferation(JKL International, 2018-08-01) Li, Wenjun; Roy Choudhury, Gourav; Winters, Ali; Prah, Jude; Lin, Wenping; Liu, Ran; Yang, ShaohuaDiabetes milieu is a complex metabolic disease that has been known to associate with high risk of various neurological disorders. Hyperglycemia in diabetes could dramatically increase neuronal glucose levels which leads to neuronal damage, a phenomenon referred to as glucose neurotoxicity. On the other hand, the impact of hyperglycemia on astrocytes has been less explored. Astrocytes play important roles in brain energy metabolism through neuron-astrocyte coupling. As the component of blood brain barrier, glucose might be primarily transported into astrocytes, hence, impose direct impact on astrocyte metabolism and function. In the present study, we determined the effect of high glucose on the energy metabolism and function of primary astrocytes. Hyperglycemia level glucose (25 mM) induced cell cycle arrest and inhibited proliferation and migration of primary astrocytes. Consistently, high glucose decreased cyclin D1 and D3 expression. High glucose enhanced glycolytic metabolism, increased ATP and glycogen content in primary astrocytes. In addition, high glucose activated AMP-activated protein kinase (AMPK) signaling pathway in astrocytes. In summary, our in vitro study indicated that hyperglycemia might impact astrocyte energy metabolism and function phenotype. Our study provides a potential mechanism which may underlie the diabetic cerebral neuropathy and warrant further in vivo study to determine the effect of hyperglycemia on astrocyte metabolism and function.