目的:肥胖不仅是生活方式相关疾病的危险因素,而且会导致皮肤屏障功能紊乱,由于干燥导致生活质量下降,瘙痒,和抓挠,因此需要适当的治疗。然而,没有关于这个问题的研究。因此,本研究旨在研究口服亚麻油对肥胖患者的皮肤屏障功能是否有效,并证实其效果如何。
方法:TSOD小鼠接受无菌蒸馏水(对照组)或亚麻子油(Omega组),含有高水平的omega-3脂肪酸,包括α-亚麻酸,口服八周。然后用紫外线B(UVB)照射小鼠,三天后,经皮水分流失(TEWL),这是皮肤屏障功能的主要结果,测量并观察总体皮肤外观。对皮肤样品进行苏木精和伊红(HE)染色和Ki-67免疫染色。炎症标志物Tnfα的mRNA表达水平,通过实时逆转录酶聚合酶链反应(RT-PCR)测量Cox2,Mcp1和Hmox1。我们还通过气相色谱法对皮肤和红细胞进行了脂肪酸分析。使用非配对Student'st检验和Pearson's相关性分析进行统计学分析。
结果:与对照组相比,Omega组TEWL值较低,皮肤红斑少。组织学分析显示表皮较薄,Ki-67阳性细胞较少。此外,在欧米茄集团,四个炎症相关基因的mRNA水平较低,皮肤和红细胞中的α-亚麻酸水平较高,并且观察到较低的n-6/n-3比率。皮肤中α-亚麻酸水平与炎症相关基因的表达水平呈负相关。
结论:发现口服亚麻油可以抑制肥胖患者的皮肤屏障功能障碍。这种作用是由α-亚麻酸介导的,具有抗炎特性的亚麻籽油的主要成分,被红细胞吸收并提供给皮肤。因此,口服亚麻油有望成为治疗肥胖皮肤屏障功能障碍的有效方法。
OBJECTIVE: Obesity is not only a risk factor for lifestyle-related diseases but also causes skin barrier dysfunction, which leads to a reduced quality of life due to dryness, itching, and scratching, and thus requires appropriate treatment. However, there are no studies on this issue. Therefore, this study aimed to examine whether oral intake of linseed oil is effective for skin barrier function in obesity and to confirm how the effect is demonstrated.
METHODS: TSOD mice received either sterile distilled water (Control group) or linseed oil (Omega group), containing a high level of omega-3 fatty acids, including α-linolenic acid, orally for eight weeks. Mice were then irradiated with ultraviolet B (UVB) and three days later, transepidermal water loss (TEWL), which is the primary outcome of skin barrier function, was measured and gross skin appearance was observed. Hematoxylin and eosin (HE) staining and Ki-67 immunostaining were performed on skin samples. mRNA expression levels of the inflammatory markers Tnfα, Cox2, Mcp1, and Hmox1 were measured by real-time reverse transcriptase-polymerase chain reaction (RT-PCR). We also performed fatty acid analysis of skin and erythrocytes by gas chromatography. Statistical analysis was performed using unpaired Student\'s t-test and Pearson\'s correlation analysis.
RESULTS: Compared with the Control group, the Omega group exhibited lower TEWL values and little skin erythema. Histological analysis revealed thinner epidermis and fewer Ki-67 positive cells. Additionally, in the Omega group, mRNA levels of four inflammation-related genes were lower, α-linolenic acid levels in both skin and erythrocytes were higher, and a lower n-6/n-3 ratio was observed. And α-linolenic acid levels in the skin were negatively correlated with the expression levels of inflammation-related genes.
CONCLUSIONS: Oral intake of linseed oil was found to inhibit skin barrier dysfunction in obesity. This effect was mediated by α-linolenic acid, a major component of linseed oil with anti-inflammatory properties, which was taken up by erythrocytes and supplied to the skin. Therefore, oral intake of linseed oil is expected to be a useful therapeutic method for skin barrier dysfunction in obesity.