Natural products play important roles in the pathogenesis of many human malignancies, including colorectal cancer, and can act as a gene regulator in many cancers. They regulate malignant cell growth through many cellular signal pathways, including Rac family small GTPase 1 (RAC1)/PI3K/AKT (α-serine/threonine-protein kinase), mitogen-activated protein kinase (MAPK), Wnt/β-catenin pathway, transforming growth factor-β (TGF-β), Janus kinase and signal transducer and activator of transcription (JAK-STAT), nuclear factor kappa-B (NF-κB), the Notch pathway, Hippo pathway, and Hedgehog pathway. In this review, we describe the epigenetic roles of several natural products, e.g., platycodin D (PD), ginsenoside Rd, tretinoin, Rutin, curcumin, clove extract, betulinic acid, resveratrol, and curcumin, in colorectal cancer, including their impact on colorectal cancer cell proliferation, apoptosis, invasion, migration, and anti-chemotherapeutic resistance. The aim is to illustrate the epigenetic mechanisms of action of natural products in cancer prevention and treatment, and to provide (1) a theoretical basis for the study of the role of epigenetics in influencing colorectal cancer; (2) new directions for studying the occurrence, development, and prognosis of colorectal cancer; and (3) new targets for treating and preventing colorectal cancer.

Regeneration is a complex process influenced by many independent or combined factors, including inflammation, proliferation, and tissue remodeling. The ocean, the most extensive resource on Earth, is rich in Seaweed. With increasing research in recent years, researchers have discovered that seaweed polysaccharides have various pharmacological effects, including a particular efficacy in promoting bone tissue regeneration. However, the application of this material in the field of bone tissue engineering is very limited. However, there are few studies on the polysaccharide at home and abroad, and little is known about its potential application value in bone repair. In addition, the bioavailability of the seaweed polysaccharide is also low, and there are still many problems to be solved. For example, the ease of solubility of fucoidan in water is a key issue that restricts its practical application. In this review, we summarize the applications and mechanisms of seaweed polysaccharides in bone healing. We also propose to combine seaweed polysaccharides with novel technologies through different types of preparations, hydrogels, scaffolds, and 3D printing to improve their use in tissue healing and regeneration.

This review examines the multifaceted roles of medicinal plant natural products in influencing gut microbiota and their subsequent impact on various organ systems through established gut axes, including the gut-brain, gut-liver, gut-heart, gut-lung, and gut-kidney axes. Medicinal plant natural products have exhibited diverse pharmacological activities, including modulation of microbiota composition, enhancement of metabolic processes, and alleviation of inflammation and oxidative stress. Evidence suggests that these components can ameliorate conditions such as neurological disorders, metabolic syndrome, and chronic kidney disease by restoring microbial balance and improving gut barrier integrity. Furthermore, the review highlights the potential of medicinal plant natural products to foster beneficial microbial communities and improve gut health, which may lead to reduced disease severity and inflammation. By comprehensively analyzing current literature, this review provides a foundation for future research aim at exploring the therapeutic applications of medicinal plant natural products in disease prevention and treatment. The findings underscore the need for further studies to elucidate the underlying mechanisms of action and validate the clinical efficacy of medicinal plant natural products in managing chronic conditions through gut microbiota modulation.

Epilepsy treatment with antiepileptic drugs (AEDs) is usually requires for many years. Q808 is an innovative antiepileptic chemical. It exerts effective antiepileptic effect against various epilepsy models. Exploring the gene transcriptomic profile of long-term treatment of Q808 is necessary. In the present study, hippocampus RNA-sequencing was performed to reveal the transcriptome profile of rats before and after treatment of Q808 for 28 days. Results confirmed 51 differentially expressed genes (DEGs) between Q808 and healthy control groups. Gene cluster analysis showed that most upregulated DEGs linked to response to drug and nucleus, most downregulated DEGs linked to locomotory, neuronal cell body, and drug binding. Most of DEGs were enriched in the signaling transduction, substance dependence, nervous system, and neurodegenerative disease pathways. Furthermore, quantitative real-time PCR analysis confirmed that Q808 significantly increased the expression of neuroprotective genes, such as Mdk, and decreased the mRNA levels of Penk, Drd1, and Adora2a, which are highly expressed in epilepsy models. In addition, Q808 decreased the mRNA expression of Pde10A and Drd2, which are known to be closely associated with schizophrenia. Our study may provide a theoretical basis to explore the effect of Q808 on the susceptibility to epilepsy and other neurological diseases.

Disruption of neuronal excitation–inhibition balance and mitochondrial quality control may contribute importantly to lead (Pb)-induced neurotoxicity, but nutritional modulators targeting these processes remain poorly characterized. This study investigated the protective effects and underlying mechanisms of ginsenoside Rh1, a ginseng-derived bioactive compound, in Pb-exposed mice and Pb-treated HT22 hippocampal cells. Chronic Pb exposure caused spatial recognition deficits, reduced exploratory activity, anxiety-like behaviors, and marked neuronal injury, accompanied by Pb accumulation in blood and brain tissues, elevated IL-1β, TNF-α, and IL-6 levels, oxidative stress, reduced Gama-aminobutyric acid (GABA) content, and dysregulated NKCC1/KCC2 expression. In HT22 cells, Pb increased intracellular ROS generation and disrupted mitophagy-related signaling, as indicated by alterations in PINK1, Parkin, LC3, P62, and GABARAP. Rh1 treatment alleviated Pb-induced behavioral abnormalities and neuronal pathology, reduced Pb burden, suppressed neuroinflammatory responses, enhanced antioxidant defenses, improved Pb-associated alterations in GABAergic regulation, and modulated mitochondrial quality-control signaling in vivo and in vitro. These findings suggest that Rh1 may represent a promising nutritional intervention strategy for mitigating Pb-associated neurotoxicity.

Panax ginseng C.A. Meyer, a renowned medicinal herb, exerts many of its systemic effects through intricate interactions with the gut microbiota, a relationship that also addresses the challenge of its own limited oral bioavailability. This review comprehensively examines the role of ginseng and its bioactive constituents in modulating gut microbiota and their subsequent influence on host health through key gut-organ axes. Based on an in-depth analysis of literature, we summarize how ginseng intervention is associated with a modulated gut microbial ecology-characterized by enriched beneficial taxa and suppressed pathogens-and is further linked to enhanced barrier integrity, regulated microbial metabolites, and reduced inflammation and oxidative stress. These mechanisms underlie its protective effects across multiple organ systems, including the gut-brain, gut-liver, gut-lung, gut-heart, and gut-kidney axes, ameliorating conditions such as cognitive decline, hepatic inflammation, pulmonary fibrosis, atherosclerosis, and renal injury. Clinical evidence further associates ginseng with improved metabolic and cognitive parameters correlated to microbial changes. We conclude that the therapeutic activity of ginseng appears to involve, and is likely modulated by, its prebiotic-like influence on the gut microbiota. However, the degree to which its efficacy is microbiota-dependent varies across different organ systems, as established by current evidence. Further mechanistic and clinical studies, particularly those employing causal models, are essential to definitively validate its potential in treating chronic diseases via microbiota-based strategies.