Rosacea is an inflammatory disease affecting the central part of face characterized by persistent or recurrent episodes of erythema, papules, pustules and telangiectasias of unknown etiology. Helicobacter pylori (H. pylori) is a gram-negative bacillus, which is one of the main causes of chronic gastritis, gastric cancer and gastrointestinal ulcers. Recent evidences have suggested that H. pylori infection is closely related to the occurrence of diseases. In recent years, studies have found that Helicobacter pylori infection is associated with the occurrence of acne rosacea. So the treatment of Helicobacter pylori infection may be a therapeutic method of acne rosacea. But it continues to be controversial. In other studies, the treatment of Helicobacter pylori did not significantly reduce the severity of acne rosacea. To further explore the association between acne rosacea and Helicobacter pylori infection, a summarize method was used to study the relationship between acne rosacea and Helicobacter pylori, providing reference for clinical acne rosacea therapy. Systematic searches were conducted on Wanfang Data, CQVIP, Springer, Public Health Management Corporation (PHMC), CNKI, and Pubmed, from January 1,2008 to Mar. 1, 2018, using Helicobacter pylori and rosacea to retrieve the literature. Depending on the inclusion and exclusion criteria, 27 articles considered or confirmed the correlation between H. pylori and rosacea. Epidemiological investigations and experiments have confirmed that H. pylori infection is associated with the development of rosacea. The effect of anti-H. pylori therapy is better than the routine therapy for rosacea. H. pylori can stimulate the immune system to produce a large number of inflammatory mediators, leading to the occurrence and aggravation of rosacea inflammation. It is confirmed that H. pylori infection is involved in the development of rosacea. It is suggested that rosacea patients should be tested for H. pylori infection, the H. pylori-positive rosacea patients should be treated with eradication of H. pylori, so as to enhance the therapeutic effect of rosacea. This study adds that H. pylori infection is involved in the development of rosacea. Epidemiological investigations and experiments have confirmed the rationality. The effect of anti-H. pylori therapy is better than the routine therapy for rosacea. H. pylori-positive rosacea patients should be treated with the therapeutic method of eradication of H. pylori.

In recent years, the World Health Organization (WHO) has included fatigue as a major risk factor for human life and health. The incidence rate of fatigue is high. In Europe and America, nearly 1/3 of the population is suffering from fatigue. Due to the acceleration of modern people’s life rhythm and the increase of work pressure, more and more attention has been paid to central fatigue. The activation of NF-κB is related to central fatigue, which has been paid little attention by previous studies. At the same time, previous studies have mostly focused on the immune regulation function of NF-κB, while the NF-κB pathway plays an equally important role in regulating nerve function. NF-κB can participate in the occurrence and development of central fatigue by mediating immune inflammatory response, regulating central excitability and inhibitory transmitters, regulating synaptic plasticity and regulating central nervous system (CNS) functional genes. In addition to neuroprotective effects, NF-κB also has nerve damage effects, which is also closely related to the occurrence and development of central fatigue. In this review, we focus on the relationship between NF-κB pathway and central fatigue and further explore the biological mechanism of central fatigue. At the same time, the clinical application and potential of typical NF-κB inhibitors in the treatment of fatigue were analyzed to provide reference for the clinical treatment of central fatigue.

In recent years, the incidence of fatigue has been increasing, and the effective prevention and treatment of fatigue has become an urgent problem. As a result, the genetic research of fatigue has become a hot spot. Transcriptome-level regulation is the key link in the gene regulatory network. The transcriptome includes messenger RNAs (mRNAs) and noncoding RNAs (ncRNAs). MRNAs are common research targets in gene expression profiling. Noncoding RNAs, including miRNAs, lncRNAs, circRNAs and so on, have been developed rapidly. Studies have shown that miRNAs are closely related to the occurrence and development of fatigue. MiRNAs can regulate the immune inflammatory reaction in the central nervous system (CNS), regulate the transmission of nerve impulses and gene expression, regulate brain development and brain function, and participate in the occurrence and development of fatigue by regulating mitochondrial function and energy metabolism. LncRNAs can regulate dopaminergic neurons to participate in the occurrence and development of fatigue. This has certain value in the diagnosis of chronic fatigue syndrome (CFS). CircRNAs can participate in the occurrence and development of fatigue by regulating the NF-κB pathway, TNF-α and IL-1β. The ceRNA hypothesis posits that in addition to the function of miRNAs in unidirectional regulation, mRNAs, lncRNAs and circRNAs can regulate gene expression by competitive binding with miRNAs, forming a ceRNA regulatory network with miRNAs. Therefore, we suggest that the miRNA-centered ceRNA regulatory network is closely related to fatigue. At present, there are few studies on fatigue-related ncRNA genes, and most of these limited studies are on miRNAs in ncRNAs. However, there are a few studies on the relationship between lncRNAs, cirRNAs and fatigue. Less research is available on the pathogenesis of fatigue based on the ceRNA regulatory network. Therefore, exploring the complex mechanism of fatigue based on the ceRNA regulatory network is of great significance. In this review, we summarize the relationship between miRNAs, lncRNAs and circRNAs in ncRNAs and fatigue, and focus on exploring the regulatory role of the miRNA-centered ceRNA regulatory network in the occurrence and development of fatigue, in order to gain a comprehensive, in-depth and new understanding of the essence of the fatigue gene regulatory network.