Su‐Lan Liao

Taichung Veterans General Hospital

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Wen‐Ying Chen

Xuzhou Medical College

Chun‐Jung Chen

National Synchrotron Radiation Research Center

Cheng-Yi Chang

Wan Fang Hospital

Yen‐Chuan Ou

Taichung Veterans General Hospital

Chun‐Jung Chen

China Medical University

Shih‐Yi Lin

National Yang Ming Chiao Tung University

Chih-Cheng Wu

Providence University

Shue‐Ling Raung

Taichung Veterans General Hospital

Yu‐Hsiang Kuan

Chung Shan Medical University Hospital

Jian‐Ri Li

Taichung Veterans General Hospital

Cooperative Institutions

Taichung Veterans General Hospital

National Chung Hsing University

National Yang Ming Chiao Tung University

China Medical University

National Cheng Kung University

Institute of Physics, Academia Sinica

National Taiwan University

National Tsing Hua University

Hungkuang University

Academia Sinica

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Investigation of Japanese encephalitis virus infection-induced neuroinflammation and pharmacological intervention

Proceedings for Annual Meeting of The Japanese Pharmacological Society (2018)

Chun‐Jung Chen Su‐Lan Liao Cheng-Yi Chang Yu‐Ting Hung

Background: Neuroinflammation has a central role in common pathologies of brain diseases. Japanese encephalitis, which is caused by infection with mosquito-transmitted Japanese encephalitis virus (JEV), is an example of an immunopathological disease closely associated with pathological disruption of the BBB and severe neuroinflammation. Those immunopathological changes correlate well with the onset and disease progression of Japanese encephalitis and represent promising targets for therapeutic control.

Viral encephalitis

10.1254/jpssuppl.wcp2018.0_po3-4-5

Cite

Citations (0)

TNF-α and IL-1β mediate Japanese encephalitis virus-induced RANTES gene expression in astrocytes

Neurochemistry International (2010)

Chun‐Jung Chen Yen‐Chuan Ou Cheng-Yi Chang Hung-Chuan Pan Su‐Lan Liao

Viral encephalitis

Astrogliosis

10.1016/j.neuint.2010.12.009

Cite

Citations (40)

Quercetin protects against cerebral ischemia/reperfusion and oxygen glucose deprivation/reoxygenation neurotoxicity

The Journal of Nutritional Biochemistry (2020)

Yayu Wang Cheng-Yi Chang Shih‐Yi Lin Jiaan‐Der Wang Chih-Cheng Wu

Neurotoxicity

10.1016/j.jnutbio.2020.108436

Cite

Citations (65)

Aspirin restores ABT-737-mediated apoptosis in human renal carcinoma cells

Biochemical and Biophysical Research Communications (2018)

Yen‐Chuan Ou Jian‐Ri Li Jiaan‐Der Wang Wen‐Ying Chen Yu‐Hsiang Kuan

XIAP

10.1016/j.bbrc.2018.05.142

Cite

Citations (14)

Fabrication and characterization of Co(11~00)/Mo(211) and Co(112~0)/Mo(100) bilayered films on MgO

IEEE Transactions on Magnetics (1996)

Y. D. Yao Y. Liou J. C. A. Huang Su‐Lan Liao I. Klik

Co/Mo bilayered films have been successfully grown on MgO(100) and MgO(110) substrates by molecular beam epitaxy. According to the reflection high energy electron diffraction and X-ray diffraction measurements the crystal structure of the film depends on the orientation of the buffer and substrate. The growth of biaxial Co(112~0)/Mo(100) on MgO(100) and of uniaxial Co(11~00)/Mo(211) on MgO(110) substrates has been confirmed. The anisotropic magnetoresistance (AMR) is strongly influenced by the Co orientation which is altered by growth on Mo/MgO(100) and MgO(110). In Co(112~0)/Mo(100) on MgO(110) AMR is isotropic for all in-plane fields. However, for Co(11~00)/Mo(211) on MgO(110) we observed enhancement of AMR along the easy axis at 10 K.

Characterization

10.1109/20.539113

Cite

Citations (7)

Detrimental effects of post-treatment with fatty acids on brain injury in ischemic rats

NeuroToxicology (2007)

Dan Yang Hui Pan Yu-Ju Yen Chuang Wang Ya‐Wen Chuang

Malondialdehyde

Cerebral edema

10.1016/j.neuro.2007.08.003

Cite

Citations (40)

Glechoma hederacea extracts attenuate cholestatic liver injury in a bile duct-ligated rat model

Journal of Ethnopharmacology (2017)

Yayu Wang Shih‐Yi Lin Wen‐Ying Chen Su‐Lan Liao Chih-Cheng Wu

10.1016/j.jep.2017.04.011

Cite

Citations (40)

Magnetoresistance Study in Co-Cr Superlattices and Films

Chinese Journal of Physics (1994)

Y. D. Yao Y. Liou J. C. A. Huang Su‐Lan Liao C. H. Lee

Source

Cite

Citations (5)

Zinc toxicity on neonatal cortical neurons: involvement of glutathione chelation

Journal of Neurochemistry (2003)

Chun‐Jung Chen Su‐Lan Liao

Abstract Several mechanisms have been implicated in pathological neuronal death including zinc neurotoxicity, calcium excitotoxicity and oxidative injury. Glutathione (GSH) serves to provide reducing equivalents for the maintenance of oxidant homeostasis, and also plays roles in intracellular and intercellular signaling in the brain. We investigated the role of GSH homeostasis in the neurotoxic action of zinc using both mixed cortical cultures containing neurons and glia, and cortical neurons prepared from 1‐day‐old rats. Zinc caused neuronal cell death in a concentration‐dependent manner. In parallel, a high concentration of zinc depleted GSH, in a time‐dependent manner, preceding the onset of neuronal damage. Depletion of GSH by diethylmaleate injured neurons and exacerbated zinc‐induced death. In contrast, replenishment of GSH attenuated zinc neurotoxicity. The thiol‐containing compounds N ‐acetylcysteine and GSH chemically chelated zinc leading to decreases in the influx of zinc, the fall in GSH level and neuronal death. Interestingly, the glycolytic substrate pyruvate, but not lactate, chelated zinc concentration dependently and prevented its toxicity. On the other hand, pyrrolidine dithiocarbamate, serving as a zinc chaperon, enhanced its entry and toxicity. The results suggest that zinc non‐enzymatically depleted GSH, an intrinsic factor for neuron survival, leading to activation of the cellular death signal and eventually neuronal death.

Neurotoxicity

Zinc toxicity

Homeostasis

Excitotoxicity

10.1046/j.1471-4159.2003.01691.x

Cite

Citations (79)

Gliotoxic Action of Glutamate on Cultured Astrocytes

Journal of Neurochemistry (2000)

Chun‐Jung Chen Su‐Lan Liao Jon‐Son Kuo

Abstract: Because of the well‐documented importance of glutamate clearance by astrocytes in protecting neurons against excitotoxicity, it was interesting to examine whether L‐glutamate exerts a toxic action on cultured astrocytes. Cell damage was evaluated by measuring activity of lactate dehydrogenase (LDH) released into the culture medium. Exposure of astrocyte cultures of the neonatal rat cerebral cortex to L‐glutamate resulted in a concentration‐ and time‐dependent increase in the release of LDH. L‐Glutamate‐induced gliotoxicity appeared to be mediated predominantly by the increase of oxidative stress because the reduced glutathione content and its effects were almost completely blocked by vitamin E and pyrrolidinedithiocarbamate. To support this notion further, the supplementation or depletion of intracellular reduced glutathione content attenuated or worsened L‐glutamate toxicity, respectively. Activation of the glutamate transporter mimicked the action of L‐glutamate on astrocytes. In addition, degrees of cell damage were not directly correlated to the levels of glutamate uptake. Moreover, the mechanism of this toxicity required energy and macromolecular synthesis. Taken together, brief exposure to L‐glutamate resulted in glutamate uptake and cell swelling, whereas sustained exposure injured astrocytes via oxidative stress instead of the excitatory mechanism.

Excitotoxicity

Mechanism of Action

Neurotoxicity

Glutamic acid

10.1046/j.1471-4159.2000.0751557.x

Cite

Citations (166)