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BACKGROUND: Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by pruritus and eczema lesions and psychiatric comorbidities. The gut–brain–skin axis plays a pivotal role during AD development, which might suggest a novel therapeutic strategy for AD. The present study aims to uncover the protective effects and underlying mechanisms of fructo‐oligofructose (FOS), a type of prebiotic, on AD‐like skin manifestations and comorbid anxiety and depression in AD mice. RESULTS: Female Kunming mice were treated topically with 2,4‐dinitrofluorobenzene (DNFB) to induce AD‐like symptoms and FOS was administered daily for 14 days. The results showed that FOS could alleviate AD‐like skin lesions markedly as evidenced by dramatic decreases in severity score, scratching bouts, the levels of immunoglobulin E (IgE) and T helper 1(Th1)/Th2‐related cytokines, and the infiltration of inflammatory cells and mast cells to the dermal tissues. The comorbid anxiety and depressive‐like behaviors, estimated by the forced swimming test (FST), the tail‐suspension test (TST), the open‐field test (OFT), and the zero maze test (ZMT) in AD mice, were significantly attenuated by FOS. Fructo‐oligofructose significantly upregulated brain neurotransmitters levels of 5‐hydroxytryptamine (5‐HT) and dopamine (DA). Furthermore, FOS treatment increased the relative abundance of gut microbiota, such as Prevotella and Lactobacillus and the concentrations of short‐chain fatty acids (SCFAs), especially acetate and iso‐butyrate in the feces of AD mice. The correlation analysis indicated that the reshaped gut microbiome composition and enhanced SCFAs formation are associated with skin inflammation and behavioral alteration. CONCLUSION: Collectively, these data identify FOS as a promising microbiota‐targeted treatment for AD‐like skin inflammation and comorbid anxiety and depressive‐like behaviors. © 2023 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Ischemia-reperfusion (I/R) injury causes cardiac dysfunction through several mechanisms including the irregular expression of some long noncoding RNA. However, the role of SNHG12 in myocardial I/R injury remains unclear. Here, we found the increase of the SNHG12 level in hypoxia-reoxygenation (H/R)-injured-H9c2 cells. SNHG12 silencing enhanced the apoptosis of H/R-injured H9c2 cells, while SNHG12 overexpression relieved the cardiomyocyte apoptosis induced by H/R stimulation. Additionally, the suppression of SNHG12 significantly boosted the H/R-induced expression and the production of TNF-α, IL-6, and IL-1β, as well as the activation of NF-κB, which were fully reversed after overexpression of SNHG12. Mechanistically, SNHG12 adversely regulated the production of receptor for advanced glycation end products (RAGE) in H/R-stimulated H9c2 cells. Antibody blocking of RAGE alleviated the apoptosis of H/R-injured H9c2 cells. Collectively, we have determined a valuable mechanism by which the high level of SNHG12 contributes to H9c2 cells against H/R injury through the reduction of RAGE expression. [ABSTRACT FROM AUTHOR]

Vascular disease is the prime determinant to cardiovascular morbidities and mortalities, which comprises the early vascular damage and subsequent cardiovascular events. Non-alcohol Fatty Liver Disease (NAFLD) is a systemic metabolic disorder that drives the progression of vascular disease through complex interactions. Although a causal relationship between NAFLD and cardiovascular disease (CVD) has not been established, a growing number of epidemiological studies have demonstrated an independent association between NAFLD and early vascular disease and subsequent cardiovascular events. In addition, mechanistic studies suggest that NAFLD initiates and accelerates vascular injury by increasing systemic inflammation and oxidative stress, impairing insulin sensitivity and lipid metabolism, and modulating epigenetics, the intestinal flora and hepatic autonomic nervous system; thus, NAFLD is a putative driving force for CVD progression. In this review, we summarize the clinical evidence supporting the association of NAFLD with subclinical vascular disease and cardiovascular events and discuss the potential mechanisms by which NAFLD promotes the progression of vascular disease. [ABSTRACT FROM AUTHOR]