Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by progressive cognitive decline. Tetrahydroxy stilbene glucoside (TSG) has been demonstrated to improve learning and memory in aged mice; however, its underlying mechanisms remain incompletely understood. This study aimed to elucidate the effects of TSG on cognitive impairment in APP/PS1 mice through analysis of gut microbiota and associated metabolites. Behavioral tests, immunohistochemistry, and 16S rDNA sequencing revealed that TSG treatment improved cognitive function and alleviated neuroinflammation. Furthermore, TSG restored gut microbiota homeostasis and normalized aberrant metabolite profiles, accompanied by elevated levels of short-chain fatty acids (SCFAs). Correlation analysis indicated associations between alterations in gut microbiota, metabolites, and SCFAs. Notably, TSG promoted the production and content of SCFAs, especially acetic acid, propionic acid, and hexanoic acid. These findings suggest that TSG mitigates AD-related pathology possibly via modulation of specific gut microbial communities and their metabolic outputs, providing a basis for further therapeutic exploration.

Alcoholic liver disease (ALD) covers including but not limited to oxidative stress. Alcohol, as the primary stroke, promote the second stroke of liver cells via action of oxidative stress-related lipid peroxidation and inflammatory cytokines, resulting into inflammatory response. Inflammation is essential to pathogenesis of hepatic diseases. Therefore, inflammasomes are multi-protein complexes which realize the risk and gather to regulate caspase-1 activation, activating cytokines such as interleukin-1β (IL-1β) and interleukin-18 (IL-18). Unlike inflammatory responses, the inflammasome activation particularly needs two signals in other to enlarge inflammation. It has been discovered in several human hepatic diseases and realized to be a major contributor to organic damage. Especially, we mainly pay close attention to the activation and function of inflammasome in ALD. Additionally, gut microbes are involved in the regulation of inflammation by constructing a gut specific immune system rather than reusing the infectious pathogens. Fungal flora has an auxiliary effect on inflammatory response, metabolic disorders, and bacterial microbial regulation and host defense, while alcohol abuse causes an imbalance in the microflora of human gut as the feed-back. After alcohol stimulation, the metabolites of gut microbiota will change, and then create a vicious cycle to liver. In brief, the application and translation of the current review promises new approaches in the treatment of ALD, especially from inflammasomes and gut microbiota.