Shen Tao, Duan Chao, Chen Beidong, Li Meng, Ruan Yang, Xu Danni, Shi Doudou, Yu Dan, Li Jian, Wang Changtao
The MOH Key Laboratory of Geriatrics, Beijing Hospital, National Center of Gerontology, Beijing 100730, P.R. China.
Beijing Key Laboratory of Plant Resources Research and Development, Beijing Technology and Business Unversity, Beijing 100048, P.R. China.
Mol Med Rep. 2017 Aug;16(2):1340-1346. doi: 10.3892/mmr.2017.6754. Epub 2017 Jun 12.
Tremella fuciformis polysaccharide (TFPS), which is the extract of Tremella fuciformis Berk, has previously been demonstrated to exhibit potent anti‑oxidative, anti‑inflammatory and anti‑aging effects. However, the mechanisms underlying these protective and therapeutic effects remain to be elucidated. The aim of the present study was to investigate the protective effects of TFPS on hydrogen peroxide‑induced injury of human skin fibroblasts and to elucidate the aforementioned underlying mechanisms. A hydrogen peroxide‑induced human skin fibroblast injury model was firstly established. MTT and reactive oxygen species (ROS) production assays, in addition to terminal deoxynucleotidyl transferase dUTP nick end labeling, reverse transcription‑quantitative polymerase chain reaction and western blotting, were performed to investigate the protective effects of TFPS. Hydrogen peroxide decreased human skin fibroblast viability with a concurrent increase in ROS generation and cell apoptosis. Treatment with 0‑400 µg/ml TFPS alone for up to 48 h did not result in alteration in cell viability. Notably, TFPS pre‑treatment reduced oxidative stress and cell apoptosis in hydrogen peroxide‑treated skin fibroblasts. In addition, there was profound inhibition of p16, p21, p53 and caspase‑3 expression, and activation of extracellular‑signal regulated kinase and Akt serine/threonine kinase 1, following TFPS pre‑treatment. Furthermore, it was revealed that TFPS additionally protected fibroblasts via the upregulation of SIRT1 expression, and this was abrogated by the SIRT1 inhibitor niacinamide. These results indicated that TFPS alleviated hydrogen peroxide‑induced oxidative stress and apoptosis in skin fibroblasts via upregulation of SIRT1 expression, indicating that TFPS may act as a potential therapeutic agent for oxidative‑stress‑associated skin diseases and aging.
银耳多糖（TFPS）是从银耳中提取的物质，此前已证明其具有强大的抗氧化、抗炎和抗衰老作用。然而，这些保护和治疗作用的潜在机制仍有待阐明。本研究的目的是探讨TFPS对过氧化氢诱导的人皮肤成纤维细胞损伤的保护作用，并阐明上述潜在机制。首先建立了过氧化氢诱导的人皮肤成纤维细胞损伤模型。进行MTT和活性氧（ROS）生成测定，以及末端脱氧核苷酸转移酶dUTP缺口末端标记、逆转录-定量聚合酶链反应和蛋白质印迹，以研究TFPS的保护作用。过氧化氢降低了人皮肤成纤维细胞的活力，同时增加了ROS的生成和细胞凋亡。单独用0-400μg/ml TFPS处理长达48小时不会导致细胞活力改变。值得注意的是，TFPS预处理降低了过氧化氢处理的皮肤成纤维细胞中的氧化应激和细胞凋亡。此外，TFPS预处理后，p16、p21、p53和半胱天冬酶-3的表达受到显著抑制，细胞外信号调节激酶和Akt丝氨酸/苏氨酸激酶1被激活。此外，研究发现TFPS还通过上调SIRT1表达来保护成纤维细胞，而SIRT1抑制剂烟酰胺可消除这种保护作用。这些结果表明，TFPS通过上调SIRT1表达减轻了过氧化氢诱导的皮肤成纤维细胞氧化应激和凋亡，表明TFPS可能作为一种潜在的治疗剂用于治疗与氧化应激相关的皮肤疾病和衰老。
