The gut microbiome acts as an integral part of the gastrointestinal tract (GIT) that has the largest and vulnerable surface with desirable features to observe foods, nutrients, and environmental factors, as well as to differentiate commensals, invading pathogens, and others. It is well-known that the gut has a strong connection with the central nervous system (CNS) in the context of health and disease. A healthy gut with diverse microbes is vital for normal brain functions and emotional behaviors. In addition, the CNS controls most aspects of the GI physiology. The molecular interaction between the gut/microbiome and CNS is complex and bidirectional, ensuring the maintenance of gut homeostasis and proper digestion. Besides this, several mechanisms have been proposed, including endocrine, neuronal, toll-like receptor, and metabolites-dependent pathways. Changes in the bidirectional relationship between the GIT and CNS are linked with the pathogenesis of gastrointestinal and neurological disorders; therefore, the microbiota/gut-and-brain axis is an emerging and widely accepted concept. In this review, we summarize the recent findings supporting the role of the gut microbiota and immune system on the maintenance of brain functions and the development of neurological disorders. In addition, we highlight the recent advances in improving of neurological diseases by probiotics/prebiotics/synbiotics and fecal microbiota transplantation via the concept of the gut–brain axis.
The gut–liver axis plays important roles in both the maintenance of a healthy liver and the pathogenesis of liver diseases, where the gut microbiota acts as a major determinant of this relationship. Gut bacteria-derived metabolites and cellular components are key molecules that affect the function of the liver and modulate the pathology of liver diseases. Accumulating evidence showed that gut microbiota produces a myriad of molecules, including lipopolysaccharide, lipoteichoic acid, peptidoglycan, and DNA, as well as short-chain fatty acids, bile acids, trimethylamine, and indole derivatives. The translocation of these components to the liver exerts beneficial or pathogenic effects by interacting with liver immune cells. This is a bidirectional relationship. Therefore, the existence of crosstalk between the gut and liver and its implications on host health and diseases are essential for the etiology and treatment of diseases. Several mechanisms have been proposed for the pathogenesis of liver diseases, but still, the mechanisms behind the pathogenic role of gut-derived components on liver pathogenesis remain elusive and not understandable. This review discusses the current progress on the gut microbiota and its components in terms of the progression of liver diseases, and in turn, how liver diseases indirectly affect the intestinal function and induce intestinal inflammation. Moreover, this paper highlights the current therapeutic and preventive strategies used to restore the gut microbiota composition and improve host health.
Background: Alzheimer’s disease (AD) is a lethal progressive neurodegenerative disorder. Currently, many acetylcholinesterase inhibitors, such as donepezil, is widely used for the treatment of AD. However, the efficacy of long-term donepezil use is limited. SIP3, a mixture of Santalum album, Illicium verum, and Polygala tenuifolia, a new formula derived from traditional Korean herbal medicine. In this study, SIP3 were assessed the survival of Drosophila AD model and synergistic effect of SIP3, donepezil co-treatment of AD using APP/PS1 transgenic mice. Methods: In Drosophila AD models, we analyzed the survival, climbing ability and acridine orange (AO) staining. In APP/PS1 mice, at six months of age were randomized into four groups. Then, these groups were orally administered vehicle (for the control), donepezil, low and high doses SIP3 plus Donepezil respectively for six months. The passive avoidance test (PAT) and the Morris water maze (MWM) were analyzed cognitive behavioral changes. In addition, the forced swimming test (FST) and the tail suspension test (TST) were assessed depression-like behavior. To investigate the molecular and cellular mechanisms underlying positive effects of SIP3 on AD, the cerebral cortex transcriptomes were analyzed by RNA sequencing.Results: Using the passive avoidance test (PAT), we analyzed the combination of SIP3 and donepezil improved the learning capabilities and memory of APP/PS1 mice, compared with the group treated with donepezil only, in late stage of AD. In addition, using the Morris water maze (MWM) test, co-treatment with donepezil and a low concentration of SIP3 significantly ameliorated cognitive impairment. Co-administration of SIP3 and donepezil effectively reduced depression-like behavior in the forced swimming and tail suspension tests. Furthermore, RNA sequencing of cerebral cortex transcriptome revealed that gene expression profiles after low dose of SIP3 co-treatment are slightly similar to those of normal phenotype mice than those obtained after donepezil treatment alone. Gene ontology (GO) along with Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway have demonstrated that differentially expressed genes were involved in locomotor behavior and neuroactive ligand-receptor interactions. Collectively: our results suggest that co-treatment of low dose of SIP3 and donepezil improves impaired learning, memory, and depression in late stage of AD in mice.
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