Formononetin alleviates thermal injury-induced skin fibroblast apoptosis and promotes cell proliferation and migration

IF 3.2 3区医学 Q2 CRITICAL CARE MEDICINE

Burns Pub Date : 2024-08-29 DOI:10.1016/j.burns.2024.08.022

Meiyue Yang , Zhibo Yang , Xiangjun Huang , Xiaoping Li , Fangqin Chou , Shuiqing Zeng

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引用次数: 0

Abstract

The aim of this study was to explore the effect and mechanism of formononetin (FMNT) in thermal-injured fibroblast proliferation, apoptosis, and oxidative stress. After thermal injury, human skin fibroblast (HSF) cells showed inhibited proliferation, migration, extracellular matrix (ECM) synthesis; and increased apoptosis, reactive oxygen species (ROS) production, and inflammation. Specifically, after thermal injury, cell viability, migration distance, and protein levels of collagen I, collagen III, α-SMA, MMP1, and MMP3 were reduced; cell apoptosis rate and TUNEL-positive cell numbers were increased; the levels of Bax and cleaved caspase-3 were elevated, while Bcl-2 level was reduced. Moreover, the thermally injured HSF cells showed increased levels of ROS, MDA, LDH, TNF-α, and IL-1β, and decreased GSH, SOD, GSH-Px, and CAT. FMNT levels can partially eliminate the effects of thermal injury on HSF cells, as shown by promoting thermally injured HSF cell proliferation and migration, and inhibiting cell apoptosis, ROS production, and inflammation. FMNT exerted no significant effect on normal HSF cells. Additionally, the levels of the P13K/AKT/mTOR signaling-related proteins (p-P13K, p-AKT, and p-mTOR) were reduced in thermally injured HSF cells, whereas FMNT could promote p-P13K, p-AKT, and p-mTOR levels. FMNT can partially alleviate the thermal injury-induced inhibition of fibroblast proliferation and migration; FMNT also inhibited the apoptosis, ROS level, and inflammation in thermal-injured cells. The effects of FMNT may be mediated by regulating the P13K/AKT/mTOR pathway.

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福莫西汀能缓解热损伤引起的皮肤成纤维细胞凋亡，促进细胞增殖和迁移。

本研究旨在探讨福莫西汀（FMNT）对热损伤成纤维细胞增殖、凋亡和氧化应激的影响及其机制。热损伤后，人皮肤成纤维细胞（HSF）的增殖、迁移和细胞外基质（ECM）合成受到抑制，细胞凋亡、活性氧（ROS）生成和炎症反应增加。具体来说，热损伤后，细胞存活率、迁移距离以及胶原蛋白 I、胶原蛋白 III、α-SMA、MMP1 和 MMP3 蛋白水平降低；细胞凋亡率和 TUNEL 阳性细胞数量增加；Bax 和裂解的 caspase-3 水平升高，而 Bcl-2 水平降低。此外，热损伤 HSF 细胞的 ROS、MDA、LDH、TNF-α 和 IL-1β 水平升高，GSH、SOD、GSH-Px 和 CAT 水平降低。FMNT 水平可部分消除热损伤对 HSF 细胞的影响，具体表现为促进热损伤 HSF 细胞的增殖和迁移，抑制细胞凋亡、ROS 生成和炎症反应。FMNT 对正常 HSF 细胞无明显影响。此外，在热损伤的 HSF 细胞中，P13K/AKT/mTOR 信号相关蛋白（p-P13K、p-AKT 和 p-mTOR）的水平降低，而 FMNT 可促进 p-P13K、p-AKT 和 p-mTOR 的水平。FMNT 可部分缓解热损伤引起的成纤维细胞增殖和迁移抑制；FMNT 还可抑制热损伤细胞的凋亡、ROS 水平和炎症反应。FMNT的作用可能是通过调节P13K/AKT/mTOR通路介导的。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Burns 医学-皮肤病学

CiteScore

4.50

自引率

18.50%

发文量

304

审稿时长

72 days

期刊介绍： Burns aims to foster the exchange of information among all engaged in preventing and treating the effects of burns. The journal focuses on clinical, scientific and social aspects of these injuries and covers the prevention of the injury, the epidemiology of such injuries and all aspects of treatment including development of new techniques and technologies and verification of existing ones. Regular features include clinical and scientific papers, state of the art reviews and descriptions of burn-care in practice. Topics covered by Burns include: the effects of smoke on man and animals, their tissues and cells; the responses to and treatment of patients and animals with chemical injuries to the skin; the biological and clinical effects of cold injuries; surgical techniques which are, or may be relevant to the treatment of burned patients during the acute or reconstructive phase following injury; well controlled laboratory studies of the effectiveness of anti-microbial agents on infection and new materials on scarring and healing; inflammatory responses to injury, effectiveness of related agents and other compounds used to modify the physiological and cellular responses to the injury; experimental studies of burns and the outcome of burn wound healing; regenerative medicine concerning the skin.