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学科主题临床医学
Minocycline and sulforaphane inhibited lipopolysaccharide-mediated retinal microglial activation
Yang, Li-Ping; Zhu, Xiu-An; Tso, Mark O. M.
刊名MOLECULAR VISION
2007-07-09
13期:117-18页:1083-1093
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Ophthalmology
研究领域[WOS]Biochemistry & Molecular Biology ; Ophthalmology
关键词[WOS]NF-KAPPA-B ; MULTIPLE-SCLEROSIS ; NEURITE OUTGROWTH ; NERVOUS-SYSTEM ; PROTEIN-KINASE ; TARGET GENES ; NITRIC-OXIDE ; MOUSE MODEL ; MAP KINASE ; CELL-DEATH
英文摘要

PURPOSE: To elucidate the inhibitory effect of minocycline and sulforaphane on lipopolysaccharide (LPS)-induced retinal microglial activation and the mechanisms through which they exerted their inhibitory effects.

METHODS: Primary retinal microglial cultures were exposed to LPS with or without minocycline and sulforaphane. The mRNA expression of monocyte chemotactic protein (MCP)-1, MCP-3, macrophage inflammatory protein (MIP)-1 alpha, MIP-1 beta, eotaxin, regulated upon activation normal T-cell expressed and secreted (RANTES) protein, and interleukin (IL)-10 were examined by reverse transcription polymerase chain reaction (RT-PCR) assay. The mRNA expression of inducible nitric oxide synthase (iNOS) and subsequent nitric oxide (NO) production were examined by RT-PCR assay and Griess reagent assay. Protein expression of the p65 subunit of nuclear factor-kappa B (NF-kappa B) and p-p38, p-p44/42 and p-JNK mitogen-activated protein kinases (MAPKs) were examined by Western blot and immunofluorescent analysis.

RESULTS: Cultured retinal microglial cells were activated following exposure to LPS. The mRNA expression and protein production of eotaxin, RANTES, and IL-10 and the mRNA expression of iNOS and subsequent NO production were upregulated. The protein expression of p-p38, p-JNK, and the p65 subunit of NF-kappa B were also upregulated. However, the protein expression of p-p44/42 was not significantly changed. Pretreatment with minocycline or sulforaphane for 1 h before LPS administration inhibited LPS-induced microglial morphological change and inhibited LPS-induced upregulation of p-p38, but had no effect on the expression of p-p44/42, p-JNK, and the p65 subunit of NF-kappa B.

CONCLUSIONS: Minocycline and sulforaphane inhibited LPS-induced retinal microglial activation, Western blot and immunofluorescent studies showed decreased p-p38 MAPK expression. We suggested that the inhibitory effect of minocycline and sulforaphane was partly through a p38 MAPK-dependent mechanism.

语种英语
WOS记录号WOS:000248314000002
引用统计
被引频次:25[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/55182
专题北京大学第三临床医学院_眼科
作者单位1.Johns Hopkins Univ, Sch Med, Wilmer Eye Inst, Baltimore, MD 21205 USA
2.Peking Univ, Third Hosp, Ctr Eye, Beijing 100871, Peoples R China
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GB/T 7714
Yang, Li-Ping,Zhu, Xiu-An,Tso, Mark O. M.. Minocycline and sulforaphane inhibited lipopolysaccharide-mediated retinal microglial activation[J]. MOLECULAR VISION,2007,13(117-18):1083-1093.
APA Yang, Li-Ping,Zhu, Xiu-An,&Tso, Mark O. M..(2007).Minocycline and sulforaphane inhibited lipopolysaccharide-mediated retinal microglial activation.MOLECULAR VISION,13(117-18),1083-1093.
MLA Yang, Li-Ping,et al."Minocycline and sulforaphane inhibited lipopolysaccharide-mediated retinal microglial activation".MOLECULAR VISION 13.117-18(2007):1083-1093.
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