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肌酸和烟酰胺可预防人成纤维细胞氧化诱导的衰老。

Creatine and Nicotinamide Prevent Oxidant-Induced Senescence in Human Fibroblasts.

机构信息

Department of Pharmacology & Toxicology, Boonshoft School of Medicine at Wright State University, Dayton Ohio, OH 45435, USA.

Dayton Veterans Administration Medical Center, Dayton Ohio, OH 45428, USA.

出版信息

Nutrients. 2021 Nov 16;13(11):4102. doi: 10.3390/nu13114102.

Abstract

Dermal fibroblasts provide structural support by producing collagen and other structural/support proteins beneath the epidermis. Fibroblasts also produce insulin-like growth factor-1 (IGF-1), which binds to the IGF-1 receptors (IGF-1Rs) on keratinocytes to activate signaling pathways that regulate cell proliferation and cellular responses to genotoxic stressors like ultraviolet B radiation. Our group has determined that the lack of IGF-1 expression due to fibroblast senescence in the dermis of geriatric individuals is correlated with an increased incidence of skin cancer. The present studies tested the hypothesis that pro-energetics creatine monohydrate (Cr) and nicotinamide (NAM) can protect normal dermal human fibroblasts (DHF) against experimentally induced senescence. To that end, we used an experimental model of senescence in which primary DHF are treated with hydrogen peroxide (HO) in vitro, with senescence measured by staining for beta-galactosidase activity, p21 protein expression, and senescence associated secretory phenotype cytokine mRNA levels. We also determined the effect of HO on IGF-1 mRNA and protein expression. Our studies indicate that pretreatment with Cr or NAM protects DHF from the HO-induced cell senescence. Treatment with pro-energetics post-HO had no effect. Moreover, these agents also inhibited reactive oxygen species generation from HO treatment. These studies suggest a potential strategy for protecting fibroblasts in geriatric skin from undergoing stress-induced senescence, which may maintain IGF-1 levels and therefore limit carcinogenesis in epidermal keratinocytes.

摘要

真皮成纤维细胞通过在表皮下方产生胶原蛋白和其他结构/支持蛋白来提供结构支撑。成纤维细胞还产生胰岛素样生长因子-1(IGF-1),它与角蛋白细胞上的 IGF-1 受体(IGF-1R)结合,激活信号通路,调节细胞增殖和细胞对紫外线 B 辐射等遗传毒性应激源的反应。我们的研究小组已经确定,由于老年人真皮中成纤维细胞的衰老导致 IGF-1 表达缺失,与皮肤癌发病率增加有关。本研究检验了这样一种假设,即促能剂肌酸一水合物(Cr)和烟酰胺(NAM)可以保护正常的真皮人成纤维细胞(DHF)免受实验诱导的衰老。为此,我们使用了一种衰老的实验模型,其中原代 DHF 用体外过氧化氢(HO)处理,通过β-半乳糖苷酶活性、p21 蛋白表达和衰老相关分泌表型细胞因子 mRNA 水平染色来测量衰老。我们还确定了 HO 对 IGF-1 mRNA 和蛋白表达的影响。我们的研究表明,Cr 或 NAM 的预处理可防止 DHF 发生 HO 诱导的细胞衰老。HO 后用促能剂治疗没有效果。此外,这些药物还抑制了来自 HO 处理的活性氧的产生。这些研究表明,在老年人皮肤中保护成纤维细胞免受应激诱导衰老的潜在策略可能维持 IGF-1 水平,从而限制表皮角质形成细胞的癌变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5398/8622652/ddf8d91399f9/nutrients-13-04102-g001.jpg

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