In order to improve the synergistic effect of unripe apple polyphenols (APP) and chitooligosaccharides (COS), apple polyphenols-chitooligosaccharides microcapsule (APCM) were prepared by spray-drying method. The effects of APCM on the release of polyphenols in simulated gastrointestinal digestion model, as well as the anti-inflammatory effect against LPS-induced RAW264.7 cells were also evaluated. Scanning electron microscope (SEM) and HPLC analysis of APP and APCM showed that during the spray-drying process, most of the polyphenols are successfully encapsulated in COS. The simulated gastrointestinal digestion model results showed that about 98% of polyphenols released from APCM within 60 min. Anti-inflammatory effect of APCM on LPS induced RAW 264.7 cells showed that although APP showed a strong inhibitory effect on cell viability at 0.6 mg/mL, the effect of APCM on cell viability was less and could maintain a high level at the same concentration. In addition, APCM significantly inhibited nitric oxide (NO) and TNF-α production via the elevation of cytokine IL-10 as the concentration increases, respectively. The results suggest that APCM alleviate the intensity of inflammatory processes by inhibiting the production of pro-inflammatory cytokines TNF-α, as well as additionally by promoting the production of anti-inflammatory cytokines IL-10. These findings provide scientific and theoretical support for the claim that traditional medicine treats inflammation-related diseases.

中文翻译：

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未成熟的苹果多酚-壳寡糖微胶囊对LPS诱导的RAW 264.7细胞的抗炎作用

为了提高未成熟苹果多酚（APP）和壳寡糖（COS）的协同作用，通过喷雾干燥法制备了苹果多酚-壳寡糖微胶囊（APCM）。还评估了APCM对模拟胃肠消化模型中多酚释放的影响，以及对LPS诱导的RAW264.7细胞的抗炎作用。扫描电镜（SEM）和APP和APCM的HPLC分析表明，在喷雾干燥过程中，大多数多酚被成功地包封在COS中；模拟胃肠消化模型结果表明，在60年代内，约有98％的APCM释放了多酚。分钟 APCM对LPS诱导的RAW 264.7细胞的抗炎作用表明，尽管APP在0.6 mg / mL的条件下对细胞生存力具有强烈的抑制作用，APCM对细胞活力的影响较小，并且在相同浓度下可以维持高水平。另外，随着浓度的升高，APCM通过细胞因子IL-10的升高显着抑制一氧化氮（NO）和TNF-α的产生。结果表明，APCM通过抑制促炎细胞因子TNF-α的产生以及另外通过促进抗炎细胞因子IL-10的产生来减轻炎性过程的强度。这些发现为传统医学治疗炎症相关疾病的说法提供了科学和理论支持。随着浓度的升高，APCM通过细胞因子IL-10的升高显着抑制一氧化氮（NO）和TNF-α的产生。结果表明，APCM通过抑制促炎细胞因子TNF-α的产生以及另外通过促进抗炎细胞因子IL-10的产生来减轻炎症过程的强度。这些发现为传统医学治疗炎症相关疾病的说法提供了科学和理论支持。随着浓度的升高，APCM通过细胞因子IL-10的升高显着抑制一氧化氮（NO）和TNF-α的产生。结果表明，APCM通过抑制促炎细胞因子TNF-α的产生以及另外通过促进抗炎细胞因子IL-10的产生来减轻炎性过程的强度。这些发现为传统医学治疗炎症相关疾病的说法提供了科学和理论支持。