Department of Biomedical Sciences, Seoul National University Graduate School, Seoul 110‑744, Republic of Korea.
Department of Dermatology, Seoul National University College of Medicine, Seoul 110‑744, Republic of Korea.
Int J Mol Med. 2018 May;41(5):3073-3080. doi: 10.3892/ijmm.2018.3508. Epub 2018 Feb 22.
Exposure of the skin to ultraviolet (UV) radiation causes extracellular matrix (ECM) collapse in the dermis, owing to an increase in matrix metalloproteinase (MMP) production in both the epidermis and dermis, and a decrease in type I collagen expression in the dermis. Recently, black rice (Oryza sativa L.) was reported to have a wide range of pharmacological effects in various settings. However, the effects of black rice extract (BRE) on UV‑irradiated skin cells have not yet been characterized. BRE treatment did not affect cell morphology and viability of HaCaT and human dermal fibroblasts (HDF). We demonstrated that BRE downregulated basal and UV‑induced MMP‑1 expression in HaCaT cells. Furthermore, BRE significantly increased type I procollagen expression, and decreased MMP‑1 and MMP‑3 expression in UV‑irradiated HDF. The underlying mechanisms of these results involve a decrease in p38 and c‑Jun N‑terminal kinase activity, and suppression of UV‑induced activation of activator protein‑1 (AP‑1). BRE reduced UV‑induced reactive oxygen species production in HaCaT cells in a dose‑dependent manner. Indeed, mass spectrometry revealed that BRE contained antioxidative flavonoid components such as cyanidin‑3‑O‑β‑D‑glycoside and taxifolin‑7‑O‑glucoside. These findings suggest that BRE attenuates UV‑induced ECM damage by modulating mitogen‑activated protein kinase and AP‑1 signaling, and could be used as an active ingredient for preventing photoaging of the skin.
皮肤暴露于紫外线(UV)辐射会导致真皮细胞外基质(ECM)崩溃,这是由于表皮和真皮中基质金属蛋白酶(MMP)的产生增加,以及真皮中 I 型胶原蛋白表达减少所致。最近,黑米(Oryza sativa L.)在各种环境中被报道具有广泛的药理作用。然而,黑米提取物(BRE)对 UV 照射的皮肤细胞的影响尚未得到表征。BRE 处理不影响 HaCaT 和人真皮成纤维细胞(HDF)的细胞形态和活力。我们证明 BRE 下调了 HaCaT 细胞中基础和 UV 诱导的 MMP-1 表达。此外,BRE 显著增加了 UV 照射的 HDF 中 I 型原胶原的表达,降低了 MMP-1 和 MMP-3 的表达。这些结果的潜在机制涉及 p38 和 c-Jun N-末端激酶活性的降低,以及抑制 UV 诱导的激活蛋白-1(AP-1)的激活。BRE 以剂量依赖的方式减少了 HaCaT 细胞中 UV 诱导的活性氧的产生。事实上,质谱分析表明 BRE 含有抗氧化黄酮类成分,如矢车菊素-3-O-β-D-葡萄糖苷和杨梅素-7-O-葡萄糖苷。这些发现表明,BRE 通过调节丝裂原活化蛋白激酶和 AP-1 信号通路来减轻 UV 诱导的 ECM 损伤,可作为预防皮肤光老化的活性成分。