Microglia

Publication Title: 
Neurochemical Research

The fruit of Terminalia chebula Retz has been used as a traditional medicine in Asia and contains tannic acid, chebulagic acid, chebulinic acid and corilagin. Extract from T. chebula seeds (TCE) has various biological functions. We observed the neuroprotective effects of TCE against ischemic damage in the hippocampal C1 region (CA1) of the gerbil that had received oral administrations of TCE (100 mg/kg) once a day for 7 days before the induction of transient cerebral ischemia.

Author(s): 
Park, Joon Ha
Joo, Han Seung
Yoo, Ki-Yeon
Shin, Bich Na
Kim, In Hye
Lee, Choong Hyun
Choi, Jung Hoon
Byun, Kyunghee
Lee, Bonghee
Lim, Soon Sung
Kim, Myong Jo
Won, Moo-Ho
Publication Title: 
Molecules (Basel, Switzerland)

Terminalia chebula, native to Southeast Asia, is a popular medicinal plant in Ayurveda. It has been previously reported to have strong antioxidant and anti-inflammatory efficacy. In this study, we aimed to investigate if fruit extract from T. chebula might protect neuronal cells against ischemia and related diseases by reduction of oxidative damage and inflammation in rat pheochromocytoma cells (PC12) using in vitro oxygen-glucose deprivation followed by reoxygenation (OGD-R) ischemia and hydrogen peroxide (H2O2) induced cell death.

Author(s): 
Gaire, Bhakta Prasad
Jamarkattel-Pandit, Nirmala
Lee, Donghun
Song, Jungbin
Kim, Ji Young
Park, Juyeon
Jung, Soyoung
Choi, Ho-Young
Kim, Hocheol
Publication Title: 
PloS One

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that causes progressive paralysis due to motor neuron death. Several lines of published evidence suggested that inhibition of epidermal growth factor receptor (EGFR) signaling might protect neurons from degeneration. To test this hypothesis in vivo, we treated the SOD1 transgenic mouse model of ALS with erlotinib, an EGFR inhibitor clinically approved for oncology indications.

Author(s): 
Le Pichon, Claire E.
Dominguez, Sara L.
Solanoy, Hilda
Ngu, Hai
Lewin-Koh, Nicholas
Chen, Mark
Eastham-Anderson, Jeffrey
Watts, Ryan
Scearce-Levie, Kimberly
Publication Title: 
Medical Hypotheses

Naturally occurring T regulatory cells targeting epitopes derived from various heat shock proteins escape thymic negative selection and can be activated by vaccination with heat shock proteins; hence, vaccination with such proteins has exerted favorable effects on rodent models of autoimmune disorders.

Author(s): 
McCarty, Mark F.
Al-Harbi, Saleh A.
Publication Title: 
Schizophrenia Bulletin

Schizophrenia is a highly polygenic brain disorder. The main hypothesis for disease etiology in schizophrenia primarily focuses on the role of dysfunctional synaptic transmission. Previous studies have therefore directed their investigations toward the role of neuronal dysfunction. However, recent studies have shown that apart from neurons, glial cells also play a major role in synaptic transmission. Therefore, we investigated the potential causal involvement of the 3 principle glial cell lineages in risk to schizophrenia.

Author(s): 
Goudriaan, Andrea
de Leeuw, Christiaan
Ripke, Stephan
Hultman, Christina M.
Sklar, Pamela
Sullivan, Patrick F.
Smit, August B.
Posthuma, Danielle
Verheijen, Mark H. G.
Publication Title: 
The Journal of Neuroscience: The Official Journal of the Society for Neuroscience

Aging is the predominant risk factor for neurodegenerative diseases. One key phenotype as the brain ages is an aberrant innate immune response characterized by proinflammation. However, the molecular mechanisms underlying aging-associated proinflammation are poorly defined. Whether chronic inflammation plays a causal role in cognitive decline in aging and neurodegeneration has not been established. Here we report a mechanistic link between chronic inflammation and aging microglia and a causal role of aging microglia in neurodegenerative cognitive deficits.

Author(s): 
Cho, Seo-Hyun
Chen, Jason A.
Sayed, Faten
Ward, Michael E.
Gao, Fuying
Nguyen, Thi A.
Krabbe, Grietje
Sohn, Peter Dongmin
Lo, Iris
Minami, Sakura
Devidze, Nino
Zhou, Yungui
Coppola, Giovanni
Gan, Li
Publication Title: 
PloS One

Microglial activation plays an important role in neuroinflammation, which contributes to neuronal damage, and inhibition of microglial activation may have therapeutic benefits that could alleviate the progression of neurodegeneration. Recent studies have indicated that the antimalarial agent artemisinin has the ability to inhibit NF-?B activation. In this study, the inhibitory effects of artemisinin on the production of proinflammatory mediators were investigated in lipopolysaccharide (LPS)-stimulated primary microglia.

Author(s): 
Zhu, Cansheng
Xiong, Zhaojun
Chen, Xiaohong
Peng, Fuhua
Hu, Xueqiang
Chen, Yanming
Wang, Qing
Publication Title: 
Molecules (Basel, Switzerland)

Terminalia chebula, native to Southeast Asia, is a popular medicinal plant in Ayurveda. It has been previously reported to have strong antioxidant and anti-inflammatory efficacy. In this study, we aimed to investigate if fruit extract from T. chebula might protect neuronal cells against ischemia and related diseases by reduction of oxidative damage and inflammation in rat pheochromocytoma cells (PC12) using in vitro oxygen-glucose deprivation followed by reoxygenation (OGD-R) ischemia and hydrogen peroxide (H2O2) induced cell death.

Author(s): 
Gaire, Bhakta Prasad
Jamarkattel-Pandit, Nirmala
Lee, Donghun
Song, Jungbin
Kim, Ji Young
Park, Juyeon
Jung, Soyoung
Choi, Ho-Young
Kim, Hocheol
Publication Title: 
Molecules (Basel, Switzerland)

Terminalia chebula, native to Southeast Asia, is a popular medicinal plant in Ayurveda. It has been previously reported to have strong antioxidant and anti-inflammatory efficacy. In this study, we aimed to investigate if fruit extract from T. chebula might protect neuronal cells against ischemia and related diseases by reduction of oxidative damage and inflammation in rat pheochromocytoma cells (PC12) using in vitro oxygen-glucose deprivation followed by reoxygenation (OGD-R) ischemia and hydrogen peroxide (H2O2) induced cell death.

Author(s): 
Gaire, Bhakta Prasad
Jamarkattel-Pandit, Nirmala
Lee, Donghun
Song, Jungbin
Kim, Ji Young
Park, Juyeon
Jung, Soyoung
Choi, Ho-Young
Kim, Hocheol
Publication Title: 
Proceedings of the National Academy of Sciences of the United States of America

The neuropathological sequelae of carbon monoxide (CO) poisoning cannot be explained by hypoxic stress alone. CO poisoning also causes adduct formation between myelin basic protein (MBP) and malonylaldehyde, a reactive product of lipid peroxidation, resulting in an immunological cascade. MBP loses its normal cationic characteristics, and antibody recognition of MBP is altered. Immunohistochemical evidence of degraded MBP occurs in brain over days, along with influx of macrophages and CD-4 lymphocytes.

Author(s): 
Thom, Stephen R.
Bhopale, Veena M.
Fisher, Donald
Zhang, Jie
Gimotty, Phyllis

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