Ampelopsin facilitates diabetic wound healing and keratinocyte cell progression by inhibiting the NLRP3 inflammasome pathway in macrophages.

IF 16.4 1区化学 Q1 CHEMISTRY, MULTIDISCIPLINARY Accounts of Chemical Research Pub Date : 2024-05-01 DOI:10.4149/gpb_2023039

Qiong Zhou, Geng Cheng

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Abstract

Ampelopsin (AMP) had a wound-healing effect in rat skin wounds with or without purulent infection. However, the role of AMP in diabetic wound healing remains poorly defined. Wounds were created on the dorsal skin of type 2 diabetic mouse model, and the histological features of wounds were examined by hematoxylin and eosin (HE) staining. Caspase-1 activity and the secretion of inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA). Cell viability and migration were examined through cell counting kit-8 (CCK-8) and wound healing assays, respectively. AMP facilitated wound healing in vivo. AMP notably facilitated platelet endothelial cell adhesion molecule-31 (CD31), collagen type I alpha 1 chain (COL1A1), and alpha-smooth muscle actin (α-SMA), and inhibited matrix metallopeptidase 9 (MMP9) and cyclooxygenase 2 (Cox2) expression in diabetic wounds. The inflammasome pathway was implicated in skin injury. AMP inhibited pro-inflammatory factor secretions and NLR family pyrin domain containing 3 (NLRP3) inflammasome pathway in diabetic wounds and high glucose-treated THP-1 macrophages. AMP-mediated NLRP3 inflammasome inhibition in THP-1 macrophages increased cell viability and migratory capacity in HaCaT cells. AMP facilitated diabetic wound healing and increased keratinocyte cell viability and migratory ability by inhibiting the NLRP3 inflammasome pathway in macrophages.

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安泼辣素通过抑制巨噬细胞中的 NLRP3 炎性体通路，促进糖尿病伤口愈合和角质细胞进展。

安泼辣素（AMP）对有或没有化脓感染的大鼠皮肤伤口有愈合作用。然而，AMP 在糖尿病伤口愈合中的作用仍未明确。研究人员在 2 型糖尿病小鼠模型的背部皮肤上制造伤口，并用苏木精和伊红（HE）染色法检查伤口的组织学特征。用酶联免疫吸附试验（ELISA）检测 Caspase-1 活性和炎性细胞因子的分泌。细胞活力和迁移分别通过细胞计数试剂盒-8（CCK-8）和伤口愈合试验进行检测。AMP 可促进体内伤口愈合。在糖尿病伤口中，AMP明显促进了血小板内皮细胞粘附分子-31（CD31）、胶原蛋白I型α1链（COL1A1）和α-平滑肌肌动蛋白（α-SMA）的表达，并抑制了基质金属肽酶9（MMP9）和环氧化酶2（Cox2）的表达。炎症小体通路与皮肤损伤有关。在糖尿病伤口和高糖处理的 THP-1 巨噬细胞中，AMP 可抑制促炎因子分泌和 NLR 家族含吡咯啉结构域 3（NLRP3）炎性组通路。在 THP-1 巨噬细胞中，AMP 介导的 NLRP3 炎症体抑制提高了 HaCaT 细胞的细胞活力和迁移能力。通过抑制巨噬细胞中的 NLRP3 炎性体途径，AMP 促进了糖尿病伤口的愈合，并提高了角质细胞的活力和迁移能力。

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来源期刊

Accounts of Chemical Research 化学-化学综合

CiteScore

31.40

自引率

1.10%

发文量

312

审稿时长

2 months

期刊介绍： Accounts of Chemical Research presents short, concise and critical articles offering easy-to-read overviews of basic research and applications in all areas of chemistry and biochemistry. These short reviews focus on research from the author’s own laboratory and are designed to teach the reader about a research project. In addition, Accounts of Chemical Research publishes commentaries that give an informed opinion on a current research problem. Special Issues online are devoted to a single topic of unusual activity and significance. Accounts of Chemical Research replaces the traditional article abstract with an article "Conspectus." These entries synopsize the research affording the reader a closer look at the content and significance of an article. Through this provision of a more detailed description of the article contents, the Conspectus enhances the article's discoverability by search engines and the exposure for the research.

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