Ginger has been reported to potentially treat Alzheimer’s disease (AD), but the specific compounds responsible for this biological function and their mechanisms are still unknown. In this study, a combination of network pharmacology, molecular docking, and dynamic simulation technology was used to screen active substances that regulate AD and explore their mechanisms. The TCMSP, GeneCards, OMIM, and DisGeNET databases were utilized to obtain 95 cross-targets related to ginger’s active ingredients and AD as key targets. A functional enrichment analysis revealed that the pathways in which ginger’s active substances may be involved in regulating AD include response to exogenous stimuli, response to oxidative stress, response to toxic substances, and lipid metabolism, among others. Furthermore, a drug-active ingredient–key target interaction network diagram was constructed, highlighting that 6-Gingerol is associated with 16 key targets. Additionally, a protein–protein interaction (PPI) network was mapped for the key targets, and HUB genes (ALB, ACTB, GAPDH, CASP3, and CAT) were identified. Based on the results of network pharmacology and cell experiments, 6-Gingerol was selected as the active ingredient for further investigation. Molecular docking was performed between 6-Gingerol and its 16 key targets, and the top three proteins with the strongest binding affinities (ACHE, MMP2, and PTGS2) were chosen for molecular dynamics analysis together with the CASP3 protein as the HUB gene. The findings indicate that 6-Gingerol exhibits strong binding ability to these disease targets, suggesting its potential role in regulating AD at the molecular level, as well as in abnormal cholinesterase metabolism and cell apoptosis, among other related regulatory pathways. These results provide a solid theoretical foundation for future in vitro experiments using actual cells and animal experiments to further investigate the application of 6-Gingerol.

Glomerella leaf spot (GLS), mainly caused by Colletotrichum fructicola, is a destructive disease of apple. However, the underlying pathogenesis mechanisms of GLS are still largely obscure. Previous infection transcriptome analysis showed that transcription factor CfGti1 was induced during leaf infection. The present study confirms that the CfGti1 gene is strongly expressed in conidia and early infection. To identify functions performed, we generated gene deletion mutant ΔCfGti1 by homologous recombination. Phenotypic analysis revealed that ΔCfGti1 lost pathogenicity to apple leaves by blocking appressorium-mediated host penetration, although penetration pegs still developed on cellophane. In addition, ΔCfGti1 colonization and hyphal extension in wounded apple fruit were dramatically decreased. The ΔCfGti1 mutant exhibited defects in growth and development of hyphae, which may be partly responsible for its inability to colonize apple. Comparative transcriptome and qRT-PCR analyses suggested that CfGti1 regulated appressorium-mediated host penetration by modulating genes related to metabolism of appressorial lipid droplets. Interestingly, CfGti1 also regulated the expression of ybtS and AKT1 or AFT1-1 related to biosynthesis of AK and AF host-specific toxins. This study demonstrated that CfGti1 is a pivotal regulator for apple GLS pathogenesis in C. fructicola.

Parkinson’s disease (PD) is a neurodegenerative disease that is closely related to genetic and environmental factors, among which pesticide exposure is considered an important risk factor. Fresh jujube and hawthorn, as widely consumed fruits, may contain pesticide residues, but the potential effects of long-term low-dose intake on PD are not yet clear. This study combines network toxicology and molecular docking technology to elucidate the molecular mechanism of PD induced by residual pesticides in fresh jujube and hawthorn. Firstly, common risk pesticides (such as organophosphates and pyrethroids) in fresh jujube and hawthorn were screened through the database. Subsequently, a “pesticide target—PD” interactive network was constructed using network toxicology to predict key targets and related pathways. Finally, molecular docking technology was used to verify the binding ability of pesticide molecules to PD-related proteins. The results indicate that some pesticides (such as chlorpyrifos and cypermethrin) may increase the risk of PD by affecting lipid metabolism and oxidative stress response. This study provides a new approach for assessing the neurotoxicity of pesticide residues and suggests the need to pay attention to the potential impact of dietary pesticide exposure on PD, providing a scientific basis for food safety regulation and PD prevention strategies.