Polygonatum sibiricum has long been a popular functional food in Asia, known for its anti-inflammatory properties. However, its efficacy in alleviating colitis has yet to be investigated. This study aimed to explore the therapeutic potential of P. sibiricum polysaccharides (PSP) in dextran sulfate sodium (DSS)-induced colitis, focusing on the related pyroptosis mechanisms. Scanning electron microscopy (SEM) analysis showed that PSP possesses a smooth surface with no pore structure and a dense, lamellar structure adorned with numerous spherical entities. PSP treatment significantly reduced colitis symptoms and decreased pro-inflammatory cytokines, likely through suppression of the Toll like receptor 4 (TLR4)/nuclear factor κB (NF-κB) signaling pathway. Additionally, PSP attenuated NOD-like receptor protein 3 (NLRP3)/apoptosis-associated speck-like protein containing a CARD (ASC)/Caspase-1/Gasdermin D (GSDMD)-mediated pyroptosis and mitochondria damage in the colon, while enhanced the expression of tight junction and adherens junction proteins. Microbiota sequencing showed that PSP increased the abundance of phylum Bacteroidota and genus such as g_unclassified_f_Muribaculaceae, Lactobacillus, Clostridia_UCG-014, and Lachnospiraceae_NK4A136_group, while decreased the phylum Proteobacteria and the genus Enterobacter, Escherichia-Shigella, and Blautia. In conclusion, this study demonstrates that PSP exerts the potential therapeutic role against colitis, which was mediated by the regulation of gut microbiota and the inhibition of colonic NLRP3/ASC/Caspase-1/GSDMD signaling pathway.

Objective: To explore the effect of astaxanthin on immune function and myocardial injury in mice with chronic sleep deprivation (CSD). Methods: A modified multi-platform water environment method was used to establish an CSD mouse model for two weeks. At the same time, mice were intragastrically administered with astaxanthin at different doses. Immune function and myocardial injury were evaluated by measuring organ coefficients as well as using the carbon clearance test and commercial enzyme-linked immunosorbent assay (ELISA) kits. The targets of astaxanthin and related biological processes and pathways were analyzed by network pharmacology. Results: Compared with the model group, body mass, phagocytic index and clearance index significantly increased in the treatment groups, and heart, spleen and pancreas coefficients decreased. Moreover, the levels of serum creatine kinase (CK), superoxide dismutase (SOD), tumor necrosis factor-α (TNF-α), glutathione peroxidase (GSH-Px), interleukin (IL)-1β, IL-6, nitric oxide synthase (NOS) and γ-glutamyl transpeptidase (γ-GT) rose markedly in each treatment group, and the level of malondialdehyde (MDA) significantly declined. Conclusion: Astaxanthin greatly ameliorates immune dysfunction and myocardial injury caused by CSD, perhaps by regulating the neurotrophic factors, Toll-like receptor, nuclear factor-κB (NF-κB), T cell receptor and apoptosis signaling pathways and inhibiting inflammatory response.

The aim of this study was to elucidate the mechanism of action of astaxanthin in reversing insulin resistance in mice with type 2 diabetes mellitus (T2DM). In this study, a T2DM model was established by feeding a high-calorie diet, and the effect of astaxanthin on glucose tolerance and insulin resistance in T2DM mice was evaluated by oral glucose tolerance test (OGTT) and insulin tolerance test (ITT). The contents of tumor necrosis factor-α (TNF-α) and fructosamine (FRA) were determined by enzyme-linked immunosorbent assay (ELISA). Furthermore, the expressions of Janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3) and nuclear factor κB (NF-κB) in mouse liver were detected by Western blot, and the role of inflammatory signaling in reversing insulin resistance by astaxanthin was explored under the guidance of network pharmacology analysis. It was found that astaxanthin significantly reduced blood glucose, TNF-α, and FRA levels, and enhanced islet function and alleviate insulin resistance in T2DM mice. Western blot results showed that astaxanthin significantly inhibited the phosphorylation of JAK2, STAT3 and NF-κB proteins. In summary, astaxanthin lowers blood glucose and reverses insulin resistance by inhibiting the JAK2/STAT3 and NF-κB signaling pathways.