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高氯酸血竭素通过β-连环蛋白、ERK/p38和AKT信号通路促进人HaCaT角质形成细胞的伤口愈合。

Dracorhodin perchlorate enhances wound healing via β-catenin, ERK/p38, and AKT signaling in human HaCaT keratinocytes.

作者信息

Lu Chi-Cheng, Yang Jai-Sing, Chiu Yu-Jen, Tsai Fuu-Jen, Hsu Yuan-Man, Yin Mei-Chin, Juan Yu-Ning, Ho Tsung-Jung, Chen Hao-Ping

机构信息

Department of Sport Performance, National Taiwan University of Sport, Taichung 40404, Taiwan, R.O.C.

Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 40447, Taiwan, R.O.C.

出版信息

Exp Ther Med. 2021 Aug;22(2):822. doi: 10.3892/etm.2021.10254. Epub 2021 Jun 2.

Abstract

Dracorhodin can be isolated from the exudates of the fruit of . Previous studies suggested that dracorhodin perchlorate can promote fibroblast proliferation and enhance angiogenesis during wound healing. In the present study, the potential bioactivity of dracorhodin perchlorate in human HaCaT keratinocytes, were investigated , with specific focus on HaCaT wound healing. The results of scratch assay demonstrated the progressive closure of the wound after treatment with dracorhodin perchlorate in a time-dependent manner. An MTT assay and propidium iodide exclusion detected using flow cytometry were used to detect cell viability of HaCaT cells. Potential signaling pathways underlying the effects mediated by dracorhodin perchlorate in HaCaT cells were clarified by western blot analysis and kinase activity assays. Dracorhodin perchlorate significantly increased the protein expression levels of β-catenin and activation of AKT, ERK and p38 in HaCaT cells. In addition, dracorhodin perchlorate did not induce HaCaT cell proliferation but promoted cell migration. Other mechanisms may yet be involved in the dracorhodin perchlorate-induced wound healing process of human keratinocytes. In summary, dracorhodin perchlorate may serve to be a potential molecularly-targeted phytochemical that can improve skin wound healing.

摘要

血竭红素可从[植物名称]果实的渗出物中分离得到。先前的研究表明,高氯血竭红素在伤口愈合过程中可促进成纤维细胞增殖并增强血管生成。在本研究中,我们研究了高氯血竭红素在人HaCaT角质形成细胞中的潜在生物活性,特别关注其对HaCaT细胞伤口愈合的影响。划痕试验结果表明,用高氯血竭红素处理后,伤口呈时间依赖性逐渐闭合。采用MTT法和流式细胞术检测碘化丙啶排除法来检测HaCaT细胞的活力。通过蛋白质印迹分析和激酶活性测定,阐明了高氯血竭红素在HaCaT细胞中介导的效应所潜在的信号通路。高氯血竭红素显著提高了HaCaT细胞中β-连环蛋白的蛋白表达水平以及AKT、ERK和p38的激活。此外,高氯血竭红素并未诱导HaCaT细胞增殖,但促进了细胞迁移。高氯血竭红素诱导人角质形成细胞伤口愈合的过程可能还涉及其他机制。总之,高氯血竭红素可能是一种潜在的分子靶向植物化学物质,可促进皮肤伤口愈合。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d2/8193218/f83f32a4cede/etm-22-02-10254-g00.jpg

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