RESUMEN

Objectives:We aimed to explore the potential role of omega-3 (ω-3) fatty acids on acne vulgaris by modulating gut microbiota.Materials and Methods:We randomly divided the untreated acne patients into two groups with or without ω-3 fatty acids intervention for 12 weeks. The Sprague Dawley (SD) rats with acne model were given isotretinoin, ω-3 fatty acids or their combination respectively. Then the colonic contents samples of the drug intervention SD rats were transferred to the pseudo sterile rats with acne model. The severity of the disease was assessed by the Global Acne Grading System (GAGS) score of the patients, and the swelling rate of auricle and the pathological section of the rat with acne model. The 16S rDNA gene sequencing was performed to detect the alteration of the gut microbiota.Results:ω-3 fatty acids could increase the diversity of the gut microbiota and regulate the flora structure positively both in the patients and rats, increase the abundance of butyric acid producing bacteria and GAGS score in the patients, and alleviate the inflammation and comedones of rats.Conclusion:Supplementation of ω-3 fatty acids could alleviate the inflammation of acne vulgaris by increasing the abundance of butyric acid producing bacteria.

Asunto(s)

Acné Vulgar , Ácidos Grasos Omega-3 , Microbioma Gastrointestinal , Animales , Humanos , Ratas , Acné Vulgar/microbiología , Adyuvantes Inmunológicos , Butiratos/uso terapéutico , Ácidos Grasos Omega-3/farmacología , Ácidos Grasos Omega-3/uso terapéutico , Inflamación/tratamiento farmacológico , Ratas Sprague-Dawley

RESUMEN

BACKGROUND: Melanoma is an extremely aggressive malignant skin tumor with high mortality. Many types of long noncoding RNAs and microRNAs have been reported to be associated with the oncogenesis of melanoma. However, a novel lncRNA-NEAT has not been thoroughly investigated in melanoma cancer. The purposes of this study were to investigate the underlying molecular mechanism in a novel couple of lnc-NEAT1 and miR-23a-3p, as well as the function role of KLF3 in the regulation of melanoma cancer. METHODS: 28 groups of tumor tissues and normal tissues were obtained from melanoma cancer patients. We performed a series of experiments and analysis, including RT-qPCR, western blots, CCK-8 assay, and migration/invasion assay, to investigate the expressions of NEAT1, miR-23a-5p and KLF3, cell viabilities, and tumor growth in vivo. RESULTS: In this study, we observed that the expression of NEAT1 was significantly upregulated in melanoma tissues, which remarkedly promoted the cells' proliferation, cell migration, and invasion in melanoma cell lines. Besides, NEAT1 could directly bind to miR-23a-3p, which was found to reverse the effect caused by NEAT1. MiR-23a-3p was discovered to bind to 3'UTR of KLF3, which reduced KLF3 expression. In addition, the overexpression of KLF3 could lower the effects of miR-23a-3p caused on melanoma cancer cell development. CONCLUSION: Our results demonstrated that NEAT1 could sponge miR-23a-3p and functions via the expression of KLF3. This axis of NEAT1/miR-23a-5p/KLF3 could together regulate melanoma cancer proliferation. This might provide a new therapeutic strategy for melanoma skin cancer.Trial registration HBTCM38574839, registered 12 October 2012.