KMID : 1059520070510030251
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Journal of the Korean Chemical Society 2007 Volume.51 No. 3 p.251 ~ p.257
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The Inhibitory Effect of Nicotine on TNF-¥á Expression in Human Fetal Astrocytes
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Son Il-Hong
Lee Sung-Ik Yang Hyun-Duk Han Sun-Jung Suk Seung-Han Lee Jai-Kyoo Kim Jae-Hyun Park Joo-Young Moon Hyung-In Lee Seong-Soo
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Abstract
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The Tumor necrosis factor-¥á, (TNF-¥á), is involved in the pathogenesis of multiple sclerosis and contributes to the degeneration of oligodendrocytes as well as neurons. Nicotine has been found to have immunosuppressive and inflammation-suppressing effects. Astrocytes, the major glial cells in the CNS, are capable of producing TNF-¥á at both the mRNA and protein levels in response to interleukin-1 (IL-1) or TNF-¥á. Nicotine has been shown to influence glial cell functions. To order to explore the role of astrocytes in the production of TNF-¥á, astrocytes were pretreated with nicotine and are stimulated with IL-1¥â to determine their effects on TNF-¥á production. The results are as follows. Cytotoxic effects of nicotine on human fetal astrocytes were noted above 10 ¥ìg/ml of nicotine. The effect of IL-1¥â on TNF-¥á mRNA expression in primary cultured human fetal astrocytes was maximal at 2 h after IL- 1¥â(100 pg/ml) treatment. Human fetal astrocytes were pretreated with 0.1, 1, and 10 ¥ìg/ml of nicotine and then stimulated with IL-1¥â (100 pg/ml) for 2 h. The inhibitory effect of nicotine on expressions of TNF-¥á mRNA in human fetal astrocytes with pretreated 0.1 ¥ìg/ml of nicotine is first noted at 8 hr, and the inhibitory effect is maximal at 12 h. The inhibitory effect at 1 ¥ìg/ml of nicotine is inhibited maximal at 24 h. Nicotine at 0.1, 1 and 10 ¥ìg/ml concentrations significantly inhibits IL-1¥â-induced NF-¥êB activation. Collectively, this study indicates that nicotine might inhibit the expression of TNF-¥á in activated human fetal astrocytes.
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KEYWORD
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TNF-¥á, Human fetal astrocytes, nicotine, NF-¥êB
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