RESUMEN
BACKGROUND AND PURPOSE: Oat ß-glucan could ameliorate epidermal hyperplasia and accelerate epidermal barrier repair. Dectin-1 is one of the receptors of ß-glucan and many biological functions of ß-glucan are mediated by Dectin-1. Dectin-1 promotes wound healing through regulating the proliferation and migration of skin cells. Thus, this study aimed to investigate the role of oat ß-glucan and Dectin-1 in epidermal barrier repair. EXPERIMENTAL APPROACH: To investigate the role of Dectin-1 in the epidermal barrier, indicators associated with the recovery of a damaged epidermal barrier, including histopathological changes, keratinization, proliferation, apoptosis, differentiation, cell-cell junctions and lipid content were compared between WT and Dectin-1-/- mice. Further, the effect of oat ß-glucan on the disruption of the epidermal barrier was also compared between WT and Dectin-1-/- mice. KEY RESULTS: Dectin-1 deficiency resulted in delayed recovery and marked keratinization, as well as abnormal levels of keratinocyte differentiation, cell-cell junctions and lipid synthesis during the restoration of the epidermal barrier. Oat ß-glucan significantly reduces epidermal hyperplasia, promotes epidermal differentiation, increases cell-cell junction expression, promotes lipid synthesis and ultimately accelerates the recovery of damaged epidermal barriers via Dectin-1. Oat ß-glucan could promote CaS receptor expression and activate the PPAR-γ signalling pathway via Dectin-1. CONCLUSION AND IMPLICATIONS: Oat ß-glucan promote the recovery of damaged epidermal barriers through promoting epidermal differentiation, increasing the expression of cell-cell junctions and lipid synthesis through Dectin-1. Dectin-1 deficiency delay the recovery of epidermal barriers, which indicated that Dectin-1 may be a potential target in epidermal barrier repair.
Asunto(s)
Diferenciación Celular , Epidermis , Lectinas Tipo C , Regulación hacia Arriba , beta-Glucanos , Animales , Lectinas Tipo C/metabolismo , beta-Glucanos/farmacología , Epidermis/metabolismo , Epidermis/efectos de los fármacos , Diferenciación Celular/efectos de los fármacos , Ratones , Regulación hacia Arriba/efectos de los fármacos , Ratones Noqueados , Ratones Endogámicos C57BL , Uniones Intercelulares/efectos de los fármacos , Uniones Intercelulares/metabolismo , Masculino , Cicatrización de Heridas/efectos de los fármacos , Queratinocitos/efectos de los fármacos , Queratinocitos/metabolismo , Metabolismo de los Lípidos/efectos de los fármacosRESUMEN
BACKGROUND AND AIMS: Contrast-induced nephropathy (CIN) after percutaneous coronary intervention (PCI) is one of the major adverse outcomes affecting the prognosis of patients with acute ST-segment elevation myocardial infarction (STEMI). Ischemic postconditioning prior to PCI (pre-PCI) in patients with STEMI is hypothesized to be protective against CIN after PCI. METHODS: A total of 251 patients with STEMI were randomized into two groups: ischemic postconditioning group (n = 123, age, 61.1 ± 12.5 years) who underwent ischemic postconditioning prior to PCI; control group (n = 128; age, 64.1 ± 12.1 years) who underwent only PCI. Ischemic postconditioning was administered by three cycles of deflation and inflation of the balloon (1-min ischemia and 1-min reperfusion) starting 1 min after infarct-related artery (IRA) opening. Diagnostic criterion for CIN was: increase in serum creatinine level by ≥0.5 mg/dL or by ≥25% increase from preoperative level within 48 h of surgery. All patients were followed for 1 year for incidence of major cardiovascular events (MACE). RESULTS: The incidence of postoperative CIN in the ischemic postconditioning group was 5.69% as compared to 14.06% in the control group (p <0.05). At one year, the MACE incidence in the ischemic postconditioning group was 7.32% as compared to 15.63% in the control group (p <0.05). CONCLUSIONS: Pre-PCI ischemic postconditioning in STEMI patients significantly reduces the post-PCI incidence of CIN and improves long-term prognosis.