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基于Homogalacturonan丰富的丁基水凝通过NF-κB/NLRP3轴增强了6-生醇通过NF-κB/NLRP3轴的结肠炎缓解作用

Qun Wang¹, Zhaomei Wang², Jun Song³

¹Guangdong Provincial Key Laboratory of Functional Food Active Substances, College of Food Sciences, South China Agricultural University, Guangzhou, Guangdong Province 510642, China.

International journal of biological macromolecules

|June 18, 2023

概括

一种新改性pectin水凝装载着纳米脂质载体,将6-醇输送到结肠炎症部位. 这个系统通过向炎症途径和增强药物释放来协同缓解结肠炎.

科学领域:

生物材料科学生物材料科学
药物输送系统药物输送系统
胃肠病学胃肠病学

背景情况:

炎症性肠道疾病,特别是结肠炎,是一个重大的治疗挑战.
有针对性的药物输送系统对于提高治疗疗效和减少副作用至关重要.
6-生 (6G) 具有抗炎性质,但需要有效地输送到结肠.

研究的目的:

开发一个结肠炎症部位特定的口服输送系统为6-gingerol (6G).
为了研究纳米脂质载体 (NLC) 载荷的homogalacturonan丰富的pectin (MCP4) 水凝 (6G-NLC/MCP4水凝) 的结肠炎缓解作用.

主要方法:

制造具有"形"超结构的6G-NLC/MCP4水凝.
使用冷扫描电子显微镜进行结构分析.
通过在炎症区域的加勒-3相互作用来评估向能力.
评估持续药物释放的特征.
通过NF-κB/NLRP3信号通路研究协同作用的抗结肠炎效应.

主要成果:

6G-NLC/MCP4水凝表现出一种"类似子"的结构,嵌入了6G-NLCs.
在MCP4中的homogalacturonan (HG) 域特别准在炎症的结肠区域过度表达的galactin-3.
在严重炎症区域实现了6G的持续释放.
观察到结肠炎的协同缓解,涉及NF-κB/NLRP3轴的调节.

结论:

6G-NLC/MCP4水凝作为有效的结肠炎症部位特定的传递系统为6-gingerol.
6-醇向NF-κB通路,并抑制NLRP3的活性.
MCP4调节了Galectin-3和Rev-Erbα/β,防止了炎症酶激活,从而缓解了协同性结肠炎.

关键词:

6 - 生醇的使用情况荷莫加拉克图罗纳丰富的点.水凝是一种水凝.在NF-κB/NLRP3轴上协同作用的抗结肠炎药物

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