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1.
Food Funct ; 15(8): 4246-4261, 2024 Apr 22.
Artigo em Inglês | MEDLINE | ID: mdl-38526064

RESUMO

The gut and skin microbiota are microbial barriers, resisting harmful foreign microorganisms and maintaining internal homeostasis. Dysbiosis of the gut and skin microbiota is involved in aging progression. However, interventions targeting facial skin wellness taking into account the gut-skin axis are scarce. In this study, the impact of an eight-week intervention with oral (O), topical (T), and both oral and topical (OT) xylo-oligosaccharides (XOS) by regulating gut and skin microbiota on facial cutaneous aging was investigated in a double-blind placebo-controlled trial in females. An increase in the proportion of participants with skin rejuvenation was observed, along with a significant reduction in facial pores after OT intervention. The reduction of cutaneous Cutibacterium by OT intervention was greater than that in the O and T groups. These interventions can change the skin microbial structure. Intestinal Bifidobacterium was enriched only by dual treatment with oral and topical XOS. Function prediction analysis revealed a decrease in K02770 encoding fructose-1-phosphate kinase involved in de novo lipid synthesis from fructose with dual intervention, suggesting that inhibition of lipophilic Cutibacterium may contribute to reducing facial pores. Overall, the dual XOS intervention approach is most effective for improving both gut and skin microbiota, as well as facial skin aging.


Assuntos
Microbioma Gastrointestinal , Envelhecimento da Pele , Pele , Humanos , Feminino , Envelhecimento da Pele/efeitos dos fármacos , Microbioma Gastrointestinal/efeitos dos fármacos , Pele/microbiologia , Adulto , Método Duplo-Cego , Pessoa de Meia-Idade , Face , Microbiota/efeitos dos fármacos , Oligossacarídeos/farmacologia , Bactérias/classificação , Bactérias/efeitos dos fármacos
2.
Mol Med Rep ; 20(4): 3388-3394, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31432140

RESUMO

Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease. MicroRNAs (miRNAs) are a group of endogenous small non­coding RNAs that regulate target genes, and play a critical role in many biological processes. However, the underlying mechanism of specific miRNA, miR­130a­3p, in AS remains largely unknown. Therefore, the present study aimed to explore the underlying mechanism of miR­130a­3p in the development of AS. In the present study, it was revealed that miR­130a­3p was downregulated in T cells from HLA­B27­positive AS patients compared with the HLA­B27­negative healthy controls. Next, bioinformatics software TargetScan 7.2 was used to predict the target genes of miR­130a­3p, and a luciferase reporter assay indicated that HOXB1 was the direct target gene of miR­130a­3p. Furthermore, it was determined that HOXB1 expression was upregulated in T cells from HLA­B27­positive AS patients. In addition, the results of the present study indicated that miR­130a­3p inhibitor significantly inhibited cell proliferation ability and induced cell apoptosis of Jurkat T cells, while the miR­130a­3p mimic promoted proliferation ability and inhibited cell apoptosis of Jurkat T cells. Notably, all the effects of the miR­130a­3p mimic on Jurkat T cells were reversed by HOXB1­plasmid. Collectively, our data indicated that miR­130a­3p was decreased in T cells from AS patients and it could regulate T­cell survival by targeting HOXB1.


Assuntos
Apoptose/imunologia , Regulação para Baixo/imunologia , MicroRNAs/imunologia , Espondilite Anquilosante/imunologia , Linfócitos T/imunologia , Adulto , Sobrevivência Celular/imunologia , Feminino , Antígeno HLA-B27/imunologia , Proteínas de Homeodomínio/imunologia , Humanos , Células Jurkat , Masculino , Pessoa de Meia-Idade , Espondilite Anquilosante/patologia , Linfócitos T/patologia
3.
Food Funct ; 10(4): 1928-1939, 2019 Apr 17.
Artigo em Inglês | MEDLINE | ID: mdl-30869676

RESUMO

Glucomannans (GMs) from diverse natural plants have great potentiality in enhancing the host immune system. The protective effects of three GMs on the intestinal mucosal immunity in colitis mice were investigated and compared in this study. The three GMs (KGM, AGP, and DOP) were obtained from Amorphophallus rivieri, Aloe vera, and Dendrobium officinale, respectively, having different weight-averaged molecular weights (Mw), acetyl group content, and molar ratios of mannose to glucose (M/G). The three fractions were administered with or without dextran sodium sulfate (DSS) containing drinking water. Macroscopic observations (health state, crypt depth, and bowel thickness of colon tissue) were conducted. Furthermore, related cytokines and mRNA expressions of TLRs were measured by ELISA and RT-qPCR, respectively. Results showed that the administration of the three GMs improved the health state of colitis mice, such as the recovery of body weight, and the increase of the immune organ index, crypt depth, bowel wall thickness, and total number of immune cells. The integrity of intestinal mucosa was maintained by the increased number of goblet cells and mucin protein production. Further studies showed that GMs kept the balance between pro- and anti-inflammatory cytokines and also regulated the expressions of TLR-2, TLR-4, TLR-6, and TLR-9. The above results suggested that GMs could attenuate the intestinal epithelial injury and regulate the intestinal mucosal immunity. Structural features including the M/G ratio, Mw, and the content of acetyl groups jointly influence the protective effects of GMs on the colitis mice.


Assuntos
Aloe/química , Amorphophallus/química , Colite/prevenção & controle , Dendrobium/química , Mananas/administração & dosagem , Extratos Vegetais/administração & dosagem , Substâncias Protetoras/administração & dosagem , Animais , Colite/induzido quimicamente , Colite/genética , Colite/imunologia , Citocinas/genética , Citocinas/imunologia , Sulfato de Dextrana/efeitos adversos , Feminino , Humanos , Mucosa Intestinal/efeitos dos fármacos , Mucosa Intestinal/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Receptor 2 Toll-Like/genética , Receptor 2 Toll-Like/imunologia , Receptor 4 Toll-Like/genética , Receptor 4 Toll-Like/imunologia , Receptor 6 Toll-Like/genética , Receptor 6 Toll-Like/imunologia
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