Abstract：
BACKGROUND: Ultraviolet-B (UVB) radiation is the leading environmental cause of skin damage and photoaging. The epidermis and dermis layers of the skin mainly absorb UVB. UVB stimulates apoptosis, cell cycle arrest, generation of reactive oxygen species, and degradation of collagen and elastin fibers.
OBJECTIVE: This study investigated the potential of human growth hormone (hGH) in protecting the skin fibroblasts and keratinocytes (HFFF-2 and HaCaT cell lines) from UVB-induced damage.
METHODS: The MTT assay was performed to evaluate UVB-induced mitochondrial damage via assessing the mitochondrial dehydrogenase activity, and flow cytometry was carried out to investigate the effects of UVB and hGH on the cell cycle and apoptosis of UVB-irradiated cells. In addition, the fold change mRNA expression levels of Type I collagen and elastin in HFFF-2 cells were evaluated using the qRT-PCR method following UVB exposure.
RESULTS: We observed that treatment of cells with hGH before UVB exposure inhibited UVB-induced loss of mitochondrial dehydrogenase activity, apoptosis, and sub-G1 population formation in both cell lines. We also found that hGH-treated HFFF-2 cells showed up-regulated mRNA expression of Type I collagen, elastin, and IGF-1 in response to UVB irradiation.
CONCLUSIONS: These findings suggest hGH as a potential anti-UVB compound that can protect skin cells from UVB-induced damage. Our findings merit further investigation and can be used to better understand the role of hGH in skin photoaging.
OBJECTIVE: This study investigated the potential of human growth hormone (hGH) in protecting the skin fibroblasts and keratinocytes (HFFF-2 and HaCaT cell lines) from UVB-induced damage.
METHODS: The MTT assay was performed to evaluate UVB-induced mitochondrial damage via assessing the mitochondrial dehydrogenase activity, and flow cytometry was carried out to investigate the effects of UVB and hGH on the cell cycle and apoptosis of UVB-irradiated cells. In addition, the fold change mRNA expression levels of Type I collagen and elastin in HFFF-2 cells were evaluated using the qRT-PCR method following UVB exposure.
RESULTS: We observed that treatment of cells with hGH before UVB exposure inhibited UVB-induced loss of mitochondrial dehydrogenase activity, apoptosis, and sub-G1 population formation in both cell lines. We also found that hGH-treated HFFF-2 cells showed up-regulated mRNA expression of Type I collagen, elastin, and IGF-1 in response to UVB irradiation.
CONCLUSIONS: These findings suggest hGH as a potential anti-UVB compound that can protect skin cells from UVB-induced damage. Our findings merit further investigation and can be used to better understand the role of hGH in skin photoaging.
摘要：
背景：紫外线B（UVB）辐射是皮肤损伤和光老化的主要环境原因。皮肤的表皮和真皮层主要吸收UVB。UVB刺激细胞凋亡，细胞周期停滞,产生活性氧，以及胶原蛋白和弹性蛋白纤维的降解。
目的：本研究探讨了人生长激素（hGH）保护皮肤成纤维细胞和角质形成细胞（HFFF-2和HaCaT细胞系）免受UVB诱导的损伤的潜力。
方法：MTT分析通过评估线粒体脱氢酶活性来评估UVB诱导的线粒体损伤，并采用流式细胞仪检测UVB和hGH对UVB照射细胞细胞周期和凋亡的影响。此外,在UVB暴露后,使用qRT-PCR方法评估HFFF-2细胞中I型胶原和弹性蛋白的倍数变化mRNA表达水平。
结果：我们观察到在UVB暴露前用hGH处理细胞抑制了UVB诱导的线粒体脱氢酶活性丧失，凋亡，以及两种细胞系中的亚G1群体形成。我们还发现hGH处理的HFFF-2细胞显示I型胶原的mRNA表达上调,弹性蛋白,和IGF-1对UVB照射的反应。
结论：这些发现表明hGH是一种潜在的抗UVB化合物，可以保护皮肤细胞免受UVB诱导的损伤。我们的发现值得进一步研究，可用于更好地了解hGH在皮肤光老化中的作用。
目的：本研究探讨了人生长激素（hGH）保护皮肤成纤维细胞和角质形成细胞（HFFF-2和HaCaT细胞系）免受UVB诱导的损伤的潜力。
方法：MTT分析通过评估线粒体脱氢酶活性来评估UVB诱导的线粒体损伤，并采用流式细胞仪检测UVB和hGH对UVB照射细胞细胞周期和凋亡的影响。此外,在UVB暴露后,使用qRT-PCR方法评估HFFF-2细胞中I型胶原和弹性蛋白的倍数变化mRNA表达水平。
结果：我们观察到在UVB暴露前用hGH处理细胞抑制了UVB诱导的线粒体脱氢酶活性丧失，凋亡，以及两种细胞系中的亚G1群体形成。我们还发现hGH处理的HFFF-2细胞显示I型胶原的mRNA表达上调,弹性蛋白,和IGF-1对UVB照射的反应。
结论：这些发现表明hGH是一种潜在的抗UVB化合物，可以保护皮肤细胞免受UVB诱导的损伤。我们的发现值得进一步研究，可用于更好地了解hGH在皮肤光老化中的作用。
