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50%原代人成纤维细胞死亡的致死热剂量为 48°C。

The lethal heat dose for 50% primary human fibroblast cell death is 48 °C.

机构信息

Centre for Children's Burns and Trauma Research, Centre for Children's Health Research, School of Biomedical Sciences, Queensland University of Technology, 62 Graham St, South Brisbane, QLD, 4101, Australia.

Faculty of Medicine and Children's Health Research Centre, Centre for Children's Burns and Trauma Research, Centre for Children's Health Research, The University of Queensland, 62 Graham St, South Brisbane, QLD, 4101, Australia.

出版信息

Arch Dermatol Res. 2022 Oct;314(8):809-814. doi: 10.1007/s00403-021-02217-y. Epub 2021 Mar 27.

DOI:10.1007/s00403-021-02217-y
PMID:33774732
Abstract

Understanding the effect of heat on skin cells is important for the prevention of burn injury. Knowledge of the heat dose required to kill cells can be used to study the cellular mechanisms involved in thermal injury cell death, to assist with the development of novel burn treatments. In this study, primary human skin dermal fibroblasts were exposed to temperatures from 37 to 54 °C for 1 h and the relative cell viability of heat-treated and control cells was assessed. Cell damage and viability were assessed by light microscopy, MTT assay and live/dead staining. The LD50 for 1 h of heat exposure was 48 °C for primary fibroblasts; and there was evidence that thermal damage to cells begins to occur at 43 °C. This study presents a reproducible method for examining the effect of heat on primary human cells grown in culture on a cellular level and can be used in the future to study the mechanisms behind heat-induced cell death, to inform burn injury prevention efforts and effective post-burn treatment.

摘要

了解热量对皮肤细胞的影响对于预防烧伤至关重要。了解杀死细胞所需的热量剂量可用于研究热损伤细胞死亡涉及的细胞机制,以协助开发新型烧伤治疗方法。在这项研究中,将原代人皮肤真皮成纤维细胞暴露于 37 至 54°C 的温度下 1 小时,并评估热处理和对照细胞的相对细胞活力。通过光显微镜、MTT 测定和死活染色评估细胞损伤和活力。1 小时热暴露的 LD50 为 48°C 的原代成纤维细胞;并且有证据表明,细胞的热损伤始于 43°C。本研究提供了一种可重现的方法,用于在细胞水平上检查培养中的原代人细胞暴露于热的影响,并且可用于未来研究热诱导细胞死亡背后的机制,为烧伤预防工作和有效的烧伤后治疗提供信息。

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Endoplasmic reticulum stress disrupts lysosomal homeostasis and induces blockade of autophagic flux in human trophoblasts.内质网应激破坏溶酶体稳态,并诱导人滋养细胞自噬流阻断。
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