The Johnson & Johnson Skin Research Center, Consumer & Personal Products Worldwide, A Division of Johnson & Johnson Family of Consumer Companies, Inc., 199 Grandview Road, Skillman, NJ 08558, USA.
J Dermatol Sci. 2013 Jul;71(1):58-66. doi: 10.1016/j.jdermsci.2013.03.009. Epub 2013 Apr 10.
The loss of subcutaneous (sc) fat is associated with aging. Inflammatory cytokines, such as interleukin-1 α (IL-1α), interleukin-11 (IL-11) and tumor necrosis factor-α (TNF-α), are known to inhibit the differentiation of preadipocytes.
This study investigated the potential role of inflammatory cytokines in solar-radiation-induced facial fat loss.
Cultured fibroblasts, keratinocytes, and skin equivalents were exposed to various doses of radiation from a solar simulator. Inflammatory cytokines' mRNA production and protein secretion were examined by qRT-PCR and ELISA, respectively. In some experiments, epidermal-dermal equivalents were pretreated topically with a broad-spectrum sunscreen prior to solar simulated radiation (SSR). Human facial preadipocytes treated with recombinant IL-11 or with conditioned media from solar-irradiated equivalents were evaluated for the level of adipocyte differentiation by image analyses, Oil red O staining, and the expression of adipocyte differentiation markers.
IL-11, IL-1α, IL-6, and TNF-α protein secretion were induced from epidermal-dermal equivalents by exposure to SSR. A sunscreen prevented SSR-induced inflammatory cytokines production from such equivalents. Exposure of facial preadipocytes to conditioned medium from solar-irradiated epidermal-dermal equivalents inhibited their differentiation into mature adipocytes. Consequently, conditioned medium from sunscreen-pretreated, solar-irradiated equivalents did not inhibit differentiation of preadipocytes. A cocktail of neutralizing antibodies to IL-11, IL-1α, IL-6 and TNF-α significantly reduced the SSR-induced inhibition of preadipocyte differentiation.
These results support the hypothesis that SSR-induced inflammatory cytokine may be involved in the photoaging-induced loss of facial subcutaneous fat. Inhibition of this process, e.g. by sunscreens, might slow or prevent photoaging-induced changes in facial contouring.
皮下（sc）脂肪的流失与衰老有关。已知炎性细胞因子，如白细胞介素-1α（IL-1α）、白细胞介素-11（IL-11）和肿瘤坏死因子-α（TNF-α），可抑制前脂肪细胞的分化。
本研究旨在探讨炎性细胞因子在太阳辐射引起的面部脂肪减少中的潜在作用。
将培养的成纤维细胞、角质形成细胞和皮肤等效物暴露于来自太阳模拟器的各种剂量的辐射下。通过 qRT-PCR 和 ELISA 分别检测炎性细胞因子的 mRNA 产生和蛋白分泌。在一些实验中，在进行太阳模拟辐射（SSR）之前，用广谱防晒霜对表皮-真皮等效物进行局部预处理。用重组 IL-11 或来自太阳照射等效物的条件培养基处理人面部前脂肪细胞，通过图像分析、油红 O 染色和脂肪细胞分化标志物的表达评估脂肪细胞分化水平。
SSR 暴露可诱导表皮-真皮等效物中产生 IL-11、IL-1α、IL-6 和 TNF-α 蛋白。防晒霜可防止此类等效物 SSR 诱导的炎性细胞因子产生。将来自太阳照射的表皮-真皮等效物的条件培养基暴露于面部前脂肪细胞中可抑制其分化为成熟脂肪细胞。因此，来自防晒预处理、太阳照射等效物的条件培养基不会抑制前脂肪细胞的分化。中和 IL-11、IL-1α、IL-6 和 TNF-α 的单克隆抗体混合物可显著减少 SSR 诱导的前脂肪细胞分化抑制。
这些结果支持这样一种假说，即 SSR 诱导的炎性细胞因子可能参与光老化引起的面部皮下脂肪减少。抑制该过程，例如通过防晒霜，可能会减缓或预防光老化对面部轮廓的影响。
