以肺部界面活性劑抑制樹技體轉染巨噬細胞過程中產生之腫瘤壞死因子-α

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Title:	以肺部界面活性劑抑制樹技體轉染巨噬細胞過程中產生之腫瘤壞死因子-α
Authors:	郭榮華
Contributors:	藥物科技研究所
Date:	2006
Issue Date:	2008-05-19 15:22:43 (UTC+8)
Publisher:	台南縣：嘉南藥理科技大學藥物科技研究所
Abstract:	The immunomodulation of pro-inflammatory cytokines such as tumor necrosis factor-α(TNF-α) from macrophages, stimulated by plasmid DNA with CpG motifs, is a critical process for the success of gene therapy. These proinflammatory cytokines have been reported to inhibit transgene expression and induce acute toxicity in lipid-based systemic gene delivery systems. However, very little is known about inflammatory toxicity using non-lipid based gene delivery systems such as dendrimers. In the present study, pulmonary surfactant was proposed to modulate TNF-α secretion in cultured RAW 264.7 murine macrophage-like cells activated by pDNA and dendrimer-mediated transfection. We found that pulmonary surfactant suppressed TNF-α release in macrophages activated by plasmid DNA and dendrimer-mediated transfection. Also, the inhibitory effect of pulmonary surfactant followed a dose-dependent manner. Simultaneously, pulmonary surfactant enhanced transfection efficiencies mediated by dendrimers in macrophage cells. The immunologic properties of some of the individual components of naturally or synthetically pulmonary surfactant have also been investigated. 1,2-Dipalmitoyl-sn-Glycero-3-Phosphocholine (DPPC), 1,2-Dioleoyl-sn-Glycero-3-[Phospho-rac-(1-glycerol)] (Sodium Salt) (DOPG), and tyloxapol have minimally inhibitory effects of TNF-α release in macrophages activated by pDNA and dendrimer-mediated transfection. These findings suggest that incorporation of pulmonary surfactant into dendrimer-based gene delivery systems can offer synergistically advantage effects in anti-inflammation and transfection efficiencies.
Relation:	計畫編號 : CNIP9502
Appears in Collections:	[Dept. of Pharmacy] CNU Project

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