RESUMO
In recent years, gut microbiota have been linked to prevention and treatment of human diseases. Mushrooms are a source of potentially useful prebiotics because they contain polysaccharides, terpenoids, and other bioactive compounds. In the present review, we have summarized the prebiotic effects of mushrooms on gut microbiota in the context of immunological, metabolic, neurological, and cancer-related diseases in the last five years. We propose that mushrooms can not only change the composition of gut microbiota, but also promote secretion of beneficial metabolites. In addition, we point to the effects of host mRNA expression in gut microbiota as a direction of further study. Overall, these provide a background for further studies on the mechanisms of regulation of gut microbiota by mushrooms.
Assuntos
Agaricales/química , Microbioma Gastrointestinal , Extratos Vegetais/metabolismo , Prebióticos/análise , Agaricales/metabolismo , Animais , Humanos , Intestinos/imunologia , Intestinos/microbiologia , Extratos Vegetais/química , Polissacarídeos/química , Polissacarídeos/metabolismoRESUMO
To obtain Phellinus baumii strain with high flavonoids yield, ARTP was employed to generate mutants of a Ph. baumii strain, which were screened for higher flavonoids content. After five rounds of screening, four mutants were identified to produce more flavonoids than the wild type strain under optimal conditions, of which A67 was the mutant with the highest flavonoids productive capacity. When cultured in shake flasks, the maximum intracellular total flavonoids production of A67 reached 0.56 g/L, 86.67% higher than the total flavonoids in CK. Antagonistic testing, RAPD, and HPLC analysis suggested that ARTP caused changes of the genetic material and metabolites in Ph. baumii. In addition, the superiority of A67 to CK was proved by liquid fermentation using unstructured kinetic models, which was performed in a 50-L fermentor. The maximum intracellular total flavonoids production and dry mycelium weight of A67 reached 0.64 g/L and 15.24 g/L, which was an increase of 88.24% and 18.23% compared with CK, respectively. This work could provide an efficient and practical strategy to obtain high flavonoids production strains and the superiority of A67 could also provide a reference to further increase flavonoids production of Ph. baumii in large-scale production mode by submerged fermentation process.
Assuntos
Basidiomycota/isolamento & purificação , Basidiomycota/metabolismo , Fermentação , Flavonoides/biossíntese , Engenharia Metabólica/métodos , Mutagênese , Gases em Plasma , Basidiomycota/genética , Basidiomycota/crescimento & desenvolvimento , Cromatografia Líquida de Alta Pressão , Meios de Cultura/química , Testes Genéticos , Metabolômica , Técnica de Amplificação ao Acaso de DNA PolimórficoRESUMO
Background. Liver fibrosis is a significant liver disease in Asian countries. Sedum mexicanum Britt. (SM) has been claimed to have antihepatitis efficacy. In traditional folk medicine, a solution of boiling water-extracted SM (SME) is consumed to prevent and treat hepatitis. However, its efficacy has not yet been verified. The purpose of this study was to investigate the in vitro effect of SME on hepatoprotection. Methods. Hepatic stellate cells (HSCs) and hepatocytes (HCs) were isolated from the livers of the rats by enzymatic digestion and density gradient centrifugation. Results. Treating the HCs and aHSCs with SME caused a dose-dependent decrease in the viability of aHSCs but not that of HCs. In addition, treatment with SME resulted in apoptosis of aHSCs, as determined by DAPI analysis and flow cytometry. SME also increased the amount of cleaved caspase-3, cleaved caspase-9, and cleaved poly ADP-ribose polymerase (PARP) in aHSCs. Furthermore, SME treatment induced a dose-dependent reduction in Bcl-2 expression and increased the expression of Bax in aHSCs. Conclusions. SME did not cause cytotoxicity in HCs, but it induced apoptosis in aHSCs through the mitochondria-dependent caspase-3 pathway. Therefore, SME may possess therapeutic potential for liver fibrosis.