Food and medicine homology (FMH) substances possess the dual capability of being used as both food and medicine. In recent years, the concept of FMH has been emphasized and developed in unprecedented ways. Triterpenoids, as key bioactive constituents within FMH substances, exhibit remarkable structural diversity and multi-target pharmacological activities, including anti-tumor, anti-inflammatory, antioxidant, hypoglycemic, and immunomodulatory effects. This review systematically summarizes the structural classification, spatiotemporal distribution patterns, and pharmacological mechanisms of FMH triterpenoids, with a particular focus on their dual role in disease prevention and functional foods. Addressing the challenge of low extraction efficiency from plants, synthetic biology approaches have elucidated the biosynthetic pathways regulated by rate-limiting enzymes, including oxidosqualene cyclases, cytochrome P450 monooxygenases, and UDP-glycosyltransferases. Synthetic biology strategies for the heterologous production of these triterpenoids in plant and microbial cell factories are critically evaluated. Despite advances in pathway reconstruction and enzyme engineering, challenges such as low yield, poor catalytic specificity, and scalability for industrial production persist. Emerging technologies, such as artificial intelligence-driven protein design and biosensor-based high-throughput screening, offer transformative solutions for optimizing triterpenoid biosynthesis. This work lays the groundwork for harnessing FMH triterpenoids as sustainable resources for pharmaceuticals and functional foods.

β-Amyloid (1-42) (Aβ₄₂) can induce excessive activation of microglia, resulting in exacerbated neuroinflammation and neuronal damage. Milk fat globule-epidermal growth factor-8 (MFG-E8) is known to regulate Aβ₄₂-induced neurotoxicity and inflammatory responses via multiple signaling pathways. However, insufficient secretion of endogenous MFG-E8 may lead to autoimmunity in the central nervous system and the accumulation of apoptotic cells. In this study, we systematically investigated the inhibitory effects and potential mechanisms of exogenously administered milk-derived MFG-E8 (M-MFG-E8) on Aβ₄₂-induced inflammation in BV-2 microglia using various techniques, including cell morphology analysis, immunofluorescence staining, ELISA, qRT-PCR, and Western blot assays. The results demonstrated that Aβ₄₂ significantly increased the expression levels of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in BV-2 microglia, whereas treatment with M-MFG-E8 effectively reversed these inflammatory responses. Furthermore, Aβ₄₂ stimulation increased the secretion of pro-inflammatory cytokines (TNF-α, IL-1β) and the expression of the M1 marker cluster of differentiation 86 (CD86), while suppressing the anti-inflammatory factors (arginase-1 (Arg-1), interleukin-10 (IL-10)) and the M2 marker cluster of differentiation 206 (CD206) in microglia. In contrast, M-MFG-E8 treatment promoted the polarization of microglia from the M1 to the M2 phenotype. Notably, M-MFG-E8 also inhibited the Aβ₄₂-induced upregulation of CD68, whereas M-MFG-E8 alone did not elicit this effect. Finally, our findings suggest that exogenous M-MFG-E8 may exert anti-inflammatory actions through the modulation of the NF-κB and PI3K/Akt pathways, providing new insights into neuronal cell repair and the development of functional foods.

Cardiovascular disease (CVD) remains a leading cause of global health burden, with conventional therapeutic strategies often constrained by inherent limitations. The emerging concept of the gut-heart axis, highlighting the intricate crosstalk between the gut microbiota and the cardiovascular system, has opened novel avenues for CVD prevention and treatment. This review comprehensively elucidates the therapeutic mechanisms and translational potential of polysaccharides as pivotal mediators of the gut-heart axis in the context of CVD management. Characterized by distinct physicochemical properties, polysaccharides exhibit significant capacity to reshape gut microbial communities and metabolic profiles, enhancing the production of beneficial metabolites like short-chain fatty acids (SCFAs), while suppressing pathogenic compounds such as trimethylamine N-oxide (TMAO). These effects underlie their pleiotropic cardioprotective effects, including antioxidant capacity, immune modulation, endothelial function improvement, and lipid metabolism regulation. Moreover, polysaccharides reinforce intestinal barrier integrity, remodel microbiota-host metabolic networks, and activate critical signaling pathways such as Nrf2 and TLR4/NF-κB, thereby attenuating atherosclerosis, hypertension, and myocardial injury. Clinical evidence further supports that polysaccharide-probiotic synbiotic interventions synergistically improve lipid profiles and vascular function. Despite promising prospects, the structure-activity relationships and personalized application of polysaccharides require further investigation. Their biocompatibility, multi-target mechanisms, and drug delivery potential make polysaccharide compelling candidates for innovative CVD therapeutics. Future research should leverage multi-omics technologies to decipher the complex interplay among polysaccharide, gut microbiota, and host, ultimately advancing precision nutrition and microbiome-targeted therapies.

A new polysaccharide fragment HTP-60a was isolated from Hawk tea and protected against colitis in mice. Its molecular weight is 24.1KDa, and its basic skeleton is →4)-β-D-Manp-1→3-β-D-Glcp-1→6-β-Galp-1→4-β-D-Xylp-1→4-β-D-Xylp-(1→. The biological activities of HTP-60a were separately explored through in vivo experiments. In vitro experiments show that HTP-60 can alleviate LPS-induced cellular inflammation by reducing the levels of intracellular inflammatory factors. In vivo experiments confirmed that HTP-60a can reduce the level of cellular inflammation, increase the content of short-chain fatty acids, and regulate the intestinal microbiota in mice with colitis to alleviate the development of colitis. HTP-60a improves colitis in mice by inhibiting the activation of key signaling pathways such as PI3K-Akt、NF-κB, HIF-1 etc. and restoring the expression of connexins (Tjp1, Tjp3, Nectin1, Nectin2, Nectin3, Nectin4, Cldn1, Cldn7, Cldn15, Cx43). These results suggest that HTP-60a exhibits promising attributes as a natural compound, characterized by its interactions with various targets and pathways, as well as its lack of toxicity laying a theoretical foundation for it to become a functional food that can improve colitis symptoms for further research and development.

Inflammatory bowel disease (IBD) is characterized by recurrent attacks and long courses, and the number of patients has expanded rapidly year by year. Additionally, current conventional strategies exist serious adverse effects. In this case, it is an urgent issue to find out an effective and safe treatment. Functional oligosaccharides possess safe and excellent physiological activities, and have attracted enormous attention due to their great therapeutic potential for IBD. This review emphasizes the attenuating effects of distinct functional oligosaccharides on IBD and their structure, and summarizes the main mechanisms from the aspects of regulating intestinal flora structure, repairing intestinal barrier, modulating immune function and mediating related signaling pathways in order to reveal the relationship between functional oligosaccharides, immune regulation, intestinal epithelial cells, gut flora and IBD treatment. Oligosaccharides possess excellent protective effects on IBD, and can be considered as safe and functional ingredients in the health food and pharmaceutical industry.