The anticancer properties of Laminaria japonica peptides (LJPs) have never been studied. Here, we extracted LJPs from fresh seaweed and explored their anti-liver cancer activity (in vivo and in vitro). LJPs were isolated/purified by HPLC-ESI-MS. HepG2 cell apoptosis and cell cycle were evaluated. MTT assays were used to examine the cytotoxicity of LJPs. Caspase activation of caspases 3 and 9, cleaved caspases 3 and 9, and cleaved PARP was examined by Western blotting. The PI3K/AKT pathway and the phosphorylation states of MAPKs (p38 and JNK) were examined. We found that the LJP-1 peptide had the most antiproliferative activity in H22 cells in vitro. LJP-1 blocked H22 cells in the G0/G1 phase, accompanied by inhibition of cyclin expression. LJP-1 induced apoptosis through caspase activation and regulation of the ASK1/MAPK pathway. Concurrent in vivo studies demonstrated that LJP-1 significantly inhibited tumor growth and induced tumor cell apoptosis/necrosis. In conclusion, LJPs, particularly LJP-1, exert strong inhibitory effects on liver cancer growth in vivo and in vitro. LJP-1 induces HCC cell apoptosis through the caspase-dependent pathway and G0/G1 arrest. LJP-1 induces caspase-dependent apoptosis, in part by inhibiting PI3K, MAPK signaling pathways, and cell cycle proteins. LJP-1 has the potential to be a novel candidate for human liver cancer therapeutics.

This study aims to identify the mechanism of geniposide regulating oxidative stress in colorectal cancer (CRC) through network pharmacology and bioinformatics analysis. Targets of geniposide, oxidative stress-related targets and targets related to CRC were applied from databases. The hub genes for geniposide regulating oxidative stress in CRC were identified with the protein–protein interaction (PPI) network. Furthermore, we applied Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment to analyze the hub genes from a macro perspective. We verified the hub genes by molecular docking, GEPIA, HPA and starBase database. We identified five hub genes: IL1B, GSK3B, NOS3, RELA and CDK4. GO analysis results suggested that the anti-colorectal cancer effect of geniposide by regulating oxidative stress is possibly related to the influence of multiple biological processes, including response to temperature stimulus, response to alkaloid, nitric oxide biosynthetic process, nitric oxide metabolic process, reactive nitrogen species metabolic process, cellular response to peptide, etc. KEGG enrichment analysis results indicated that the PI3K–Akt signaling pathway, IL-17 signaling pathway, p53 signaling pathway, NF-κB signaling pathway and NOD-like receptor signaling pathway are likely to be the significant pathways. Molecular docking results showed that the geniposide had a good binding activity with the hub genes. This study demonstrates that geniposide can regulate oxidative stress in CRC, and induction of oxidative stress is one of the possible mechanisms of anti-recurrence and metastasis effects of geniposide against CRC.

Obesity is a chronic and complex disease defined by the excessive deposition of fat and is highly associated with oxidative stress. Adzuki bean saponins (ABS) showed anti-obesity activity in our previous in vivo study; however, the active saponins of adzuki beans and potential mechanisms are still unclear. This research aims to elucidate the anti-obesity effects of ABS in improving lipid metabolism and oxidative stress, exploring the effective ingredients and potential molecular mechanisms through UHPLC-QE-MS analysis, network pharmacology, bioinformatics, and in vitro experiments both in the 3T3-L1 cell line and HepG2 cell line. The results indicate that ABS can improve intracellular lipid accumulation, adipogenesis, oxidative stress, and mitochondrial damage caused by lipid accumulation including ROS generation, abnormal mitochondrial membrane potential, and ATP disorder. Fifteen saponin components were identified with the UHPLC-QE-MS analysis. The network pharmacology and bioinformatics analyses indicated that the PI3K/Akt signaling pathway is associated with the bioactive effect of ABS. Through Western blotting and immunofluorescence analysis, the anti-obesity effect of ABS is achieved through regulation of the PI3K/Akt/GSK3β/β-catenin signaling pathway and activation of downstream transcription factor c-Myc in the lipid accumulation cell model, and regulation of β-catenin signaling and inhibition of downstream transcription factor C/EBPα in the adipocyte cell model. These results illustrate the biological activity of ABS in improving fat metabolism and oxidative stress by restoring mitochondrial function through β-catenin signaling, the PI3K/Akt/GSK3β/β-catenin signaling pathway, laying the foundation for its further development.

In recent years, the incidence rate of cancer has been on the rise all over the world, and the age of cancer patients has shown a younger trend, which seriously endangers patients’ health. Edible/medicinal mushrooms have not only become a new source of nutritional supplements but have also emerged as a promising adjunct to conventional medicine, either by directly or indirectly killing tumor cells and enhancing immunity, or through their use in conjunction with modern cancer therapies to enhance their efficacy or reduce their side-effects, improving patients’ quality of life. Although the anti-cancer potential of edible and medicinal mushrooms has been widely studied in the past, this review focuses on the most recent literature from the last five years, providing an up-to-date and comprehensive summary of the current findings. In this review, we aim to analyze the anti-cancer effects of edible/medicinal mushrooms, including Schizophyllum commune, Trametes versicolor, Grifola frondosa, Ganoderma lucidum, Lentinula edodes, Laetiporus sulphureus, Boletus edulis, and Phellinus igniarius, as well as their potential anti-cancer mechanisms, providing strong theoretical support for the further development of edible/medicinal mushroom anti-cancer products.

Diabetes mellitus is characterized by insulin resistance, impaired glucose homeostasis, and dysregulated glucose metabolism, leading to complications. Inonotus obliquus (Chaga) has shown potential anti-diabetic effects, but the bioactive compounds and molecular targets remain unclear. This study aimed to identify the bioactive components of Chaga and elucidate their anti-diabetic mechanisms using LC-MS compound screening, network pharmacology, molecular docking, and bioinformatics analyses. Chaga extract was prepared using 95% ethanol, and bioactive compounds were identified through UHPLC-QE-MS analysis. Target prediction was conducted using Swiss Target Prediction and SEA databases, while diabetes-related targets were retrieved from GeneCards. A PPI network was constructed using STRING and analyzed for GO and KEGG enrichment. Molecular docking was performed using AutoDock Vina, and gene expression was validated using the GSE7014 dataset and GEPIA database, with immune cell infiltration analyzed through CIBERSORT. UHPLC-QE-MS identified 30 bioactive compounds from Chaga, including 21 triterpenoids, four flavonoids, and two diterpenoids. Network pharmacology predicted 432 anti-diabetic targets, with 167 core targets enriched in key pathways, primarily the PI3K/Akt signaling pathway. Molecular docking revealed strong binding affinities of five key compounds with seven core targets. Bioinformatics analysis validated significant expression changes in ESR1, IL6, and SRC, while immune cell infiltration analysis showed correlations between core targets and immune cell subtypes. This study highlights the anti-diabetic potential of Chaga by identifying key bioactive compounds and their interactions with central diabetic targets. Further in vitro and in vivo studies are needed to validate these findings.

This study aimed to explore the molecular mechanisms of phytochemicals from Chaga mushroom (Inonotus obliquus) against colorectal cancer (CRC) using a combination of network pharmacology, molecular docking, and bioinformatics. Active components and targets of Chaga mushroom and CRC were collected from databases. A drug-compound-target-disease network was constructed, and protein–protein interaction (PPI) analysis was performed to identify core targets. KEGG and GO enrichment analyses were conducted to elucidate the involved pathways. Molecular docking estimated the binding affinities of key compounds to their targets, and bioinformatics analysis assessed differential gene expression and immune infiltration. The study identified 26 bioactive compounds and 244 potential targets. Core targets included AKT1, IFNG, and MMP9. Molecular docking showed strong binding affinities, and bioinformatics analysis revealed significant differential expression and immune infiltration patterns. These findings suggest that Chaga mushroom phytochemicals may exert anticancer effects through multiple pathways, highlighting their potential as novel CRC treatments. This study provides a comprehensive understanding of the molecular mechanisms underlying the anticancer effects of Chaga mushroom phytochemicals on CRC. Future research should focus on experimental validation and further exploration of their therapeutic potential.