Kyushu University Academic Staff Educational and Research Activities Database
List of Presentations
Sachiko Take Last modified date:2018.05.16

Research Associate / Science for Biological Information / Department of Basic Medicine / Faculty of Medical Sciences

1. Md. Youssef Saleh Ahmed, HOSSAIN MD. SHAMIM, Masataka Ifuku, Sachiko Take, Toshihiko Katafuchi, Plasmalogens attenuate IL-1β-mediated iNOS induction by inhibiting p38MAPK activation in mouse astrocytes, 第64回西日本生理学会, 2013.10, Glial cells in the brain produce reactive nitrogen species like nitric oxide (NO) that affect badly the surrounding neurons upon various inflammations. However, how do glia regulate the synthesis of NO is mostly unknown. We found that plasmalogens (Pls, one type of glycerophospholipids) can reduce the cytokine IL-1β-mediated induction of NO synthetic enzyme (iNOS) in astrocytes. We further found that Pls reduced phosphorylation of the kinase p38MAPK, which might be a mechanism of Pls-induced iNOS suppression in the astrocytes. It is therefore possible that Pls may play important defensive role in neuroinflammation and further studies could reveal new therapeutic drugs to combat neurodegenerative diseases..
2. HOSSAIN MD. SHAMIM, Md. Youssef Saleh Ahmed, Masataka Ifuku, Sachiko Take, Toshihiko Katafuchi, Plasmalogens rescue neuronal cell death through an activation of AKT and ERK survival signaling, 第64回西日本生理学会, 2013.10, Plasmalogens (Pls) are unique glycerophospholipids characterized by the presence of a vinyl ether linkage at the sn-1 position of the glycerol backbone. In Alzheimer diseases (AD) patients, reduced Pls levels were reported in blood and affected brain tissues. In the present study, we found that Pls enhance the survival signals of AKT and ERK in neuronal cell culture models. Pls inhibited serum starvation-induced neuronal cell death by inhibiting activation of caspase-9 and caspase-3. Future study could reveal new therapeutic approach to cure neurodegenerative diseases due to neuron cell death..
3. Selective serotonin reuptake inhibitors recovered immunologically induced fatigue in rats: in vivo microdialysis and behavioral study..
4. Central mechanisms of immunologically induced fatigue: involvement of IFN-α and 5-HT system in the brain..