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低水平激光疗法对过氧化氢诱导的 prematurely-senescent 真皮成纤维细胞的增殖、凋亡调节和氧化炎症标志物的体外影响。

In vitro effect of low-level laser therapy on the proliferative, apoptosis modulation, and oxi-inflammatory markers of premature-senescent hydrogen peroxide-induced dermal fibroblasts.

机构信息

Postgraduate Program of Pharmacology, Federal University of Santa Maria (UFSM), Av. Roraima, 1000, Santa Maria, 97105-900, Brazil.

Postgraduate Program of Gerontology, Federal University of Santa Maria (UFSM), Av. Roraima, 1000, Santa Maria, 97105-900, Brazil.

出版信息

Lasers Med Sci. 2019 Sep;34(7):1333-1343. doi: 10.1007/s10103-019-02728-1. Epub 2019 Feb 2.

Abstract

Skin aging is a complex biological process induced by intrinsic and extrinsic factors which is characterized by clinical and cellular changes, especially dermal fibroblasts. It is possible that, some procedures, such as low-level laser therapy (LLLT), could decelerate this process. To test this hypothesis, this study evaluated the in vitro LLLT on dermal fibroblast cell line (HFF-1) with premature senescence HO-induced. HFF-1 cells were cultured in standardized conditions, and initially HO exposed at different concentrations. Fibroblasts were also just exposed at different LLLT (660 nm) doses. From these curves, the lowest HO concentration that induced indicators of premature senescence and the lowest LLLT doses that triggered fibroblast proliferation were used in all assays. Cellular mortality, proliferation, and the levels of oxidative, inflammatory cytokines, apoptotic markers, and of two growth signaling molecules (FGF-1 and KGF) were compared among treatments. The HO at 50 μM concentration induced some fibroblast senescence markers and for LLLT, the best dose for treatment was 4 J (p < 0.001). The interaction between HO at 50 μM and LLLT at 4 J showed partially reversion of the higher levels of DNA oxidation, CASP 3, CASP 8, IL-1B, IL-6, and INFy induced by HO exposure. LLLT also trigger increase of IL-10 anti-inflammatory cytokine, FGF-1 and KGF levels. Cellular proliferation was also improved when fibroblasts treated with HO were exposed to LLLT (p < 0.001). These results suggest that in fibroblast with some senescence characteristics HO-induced, the LLLT presented an important protective and proliferative action, reverting partially or totally negative effects triggering by HO.

摘要

皮肤衰老 是一个由内在和外在因素引起的复杂的生物学过程,其特征是临床和细胞变化,尤其是真皮成纤维细胞。某些程序,如低水平激光疗法(LLLT),可能会减缓这个过程。为了验证这一假设,本研究评估了体外 LLLT 对诱导过早衰老的人皮肤成纤维细胞系(HFF-1)的影响。HFF-1 细胞在标准化条件下培养,并最初以不同浓度的 HO 暴露。还以不同的 LLLT(660nm)剂量仅暴露于成纤维细胞。从这些曲线中,选择诱导过早衰老的最低 HO 浓度和触发成纤维细胞增殖的最低 LLLT 剂量,用于所有检测。在所有处理中比较细胞死亡率、增殖、氧化、炎症细胞因子、凋亡标志物水平以及两种生长信号分子(FGF-1 和 KGF)。50μM 浓度的 HO 诱导了一些成纤维细胞衰老标志物,而对于 LLLT,最佳治疗剂量为 4J(p<0.001)。50μM 的 HO 与 4J 的 LLLT 之间的相互作用显示出部分逆转了 HO 暴露引起的更高水平的 DNA 氧化、CASP 3、CASP 8、IL-1B、IL-6 和 INFy。LLLT 还触发了抗炎细胞因子 IL-10、FGF-1 和 KGF 水平的增加。当用 HO 处理的成纤维细胞暴露于 LLLT 时,细胞增殖也得到改善(p<0.001)。这些结果表明,在 HO 诱导的具有某些衰老特征的成纤维细胞中,LLLT 表现出重要的保护和增殖作用,部分或完全逆转了 HO 触发的负面效应。

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