頁籤選單縮合
題 名 | Anti-inflammatory and Neuroprotective Effects of Magnolol in Chemical Hypoxia in Rat Cultured Cortical Cells in Hypoglycemic Media |
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作 者 | Lee,Min-min; Huang,Hsueh-meei; Hsieh,Ming-tsuen; Chen,Chung-shong; Yeh,Feng-tsgh; Kuo,Jon-son; | 書刊名 | 中國生理學雜誌 |
卷 期 | 43:2 2000.06[民89.06] |
頁 次 | 頁61-67 |
分類號 | 416.29 |
關鍵詞 | Hypoxia; Magnolol; Lactate dehydrogenase; Cortical mixed culture; Lipopolysaccharide; Nitric oxide; Prostaglandin E[feaf]; |
語 文 | 英文(English) |
英文摘要 | Our previous studies demonstrated that magnolol protects neurons against chemical hypoxia by KCN in cortical neuron-astrocyte mixed cultures (14). In the present study, we examined whether the neuroprotective effect of magnolol involve modulating inflammatory mediators, prostaglandin E2 (PGE2) and nitric oxide (NO), induced by KCN (hypoxia) or KCN plus lipopolysaccharide (LPS). In glucose-absent (hypoglycemia) media, KCN or KCN plus LPS induced increases in lactate dehydrogenase (LDH) activity by 32% and 34%, and PGE2 production by 12% and 32%, respectively. Both LDH and PGE2 increases were suppressed by 100μM magnolol. In addition, although KCN or LPS alone did not increase NO generation, KCN plus LPS increased NO generation. This increase was reduced by 100μM magnolol or 10μM L-NAME, but the LDH increase and PGE2 production were not reduced by L-NAME. These findings suggest that the protective effects of magnolol against brain damage by KCN or KCN plus LPS in hypoglycemic media may involve inhibition of PGE2 production, but inhibition of NO generation may not be important. |
本系統中英文摘要資訊取自各篇刊載內容。