A greenhouse experiment was conducted to determine the potential of arbuscular mycorrhizal fungi (AMF) to mitigate the allelopathic effects of invasive Nicotiana glauca on the growth of Acacia gerrardii seedlings. Aqueous extracts from N. glauca leaves and flowers (at concentrations of 20, 60, and 100 g/L) and AMF treatment (±AMF) were applied to A. gerrardii seedlings arranged in a factorial experiment with four replicates. After 6 months, vegetative (plant fresh and dry weight, height, leaf number area), physiological (photosynthesis, stomatal conductance, transpiration rate), chlorophyll a and b, proline, and root (length, surface area, diameter, volume, tip number) parameters as well as root distribution in five root diameter classes (0–5 mm, in 1 mm increments) were examined. The presence of AMF increased the seedling growth parameters. The 20 g/L treatment stimulated most of the vegetative growth, root, chlorophyll, and photosynthesis parameters at both inoculant levels for all extract types and concentrations, and the 100 g/L treatment inhibited seedling growth whether inoculated with AMF or not. This decline was alleviated in AMF-treated seedlings. For both extract sources, root length decreased as extract concentration increased, and roots <1 mm accounted for the greatest proportion of total root length, surface area, and tip number, with higher values observed in AMF-treated seedlings compared to their untreated counterparts. Further research is required at the field level to identify AMF strains and their interaction effects in alleviating the allelopathic impact of N. glauca on A. gerrardii seedling growth.

Chronic Obstructive Pulmonary Disease (COPD) is a complex inflammatory lung condition characterized by oxidative stress, changes in airway structure, and gradually worsening airflow blockage. Existing treatments offer only symptomatic management, emphasizing the need for multi-target therapeutic interventions. This study employed a combined approach of network pharmacology and molecular docking to investigate the therapeutic effects of bioactive compounds derived from Cladophora glomerata on COPD. Disease-associated genes were collected from GeneCards, Online Mendelian Inheritance in Man (OMIM), and National Center for Biotechnology Information (NCBI), while compounds from C. glomerata and their predicted molecular targets were obtained from SwissTargetPrediction. A cross-comparison of targets related to compounds and diseases revealed nine common genes, among which three central genes TP53, CASP8, and EGFR were identified using protein–protein interaction (PPI) network analysis. Analysis of gene–disease interactions highlighted Tumor Protein p53 (TP53) and Epidermal Growth Factor Receptor (EGFR) as major regulatory targets. GeneMANIA-based functional and co-expression analysis revealed predominant physical interactions (77.64%) and co-expression relationships (8.01%), highlighting strong functional connectivity among the identified genes. Molecular docking further confirmed that C. glomerata derived compounds, particularly Quinoline, 1,2,3,4-tetrahydro-1-((2-phenylcyclopropyl)sulfonyl)-, trans- (Pubchem ID: 91709903) (−7.5 kcal/mol) and1,2,4-Oxadiazole, 3-(1,3-benzodioxol-5-yl)-5-[(4-iodo-1H-pyrazol-1-yl)methyl]- (Pubchem ID: 5301194) (−7.3 kcal/mol), exhibit favorable predicted binding affinities toward EGFR and TP53 in molecular docking analysis. Overall, these insights suggest that Cladophora glomerata compounds may modulate key COPD-related pathways through multi-target interactions, providing a scientific basis for future experimental studies and the development of marine-derived therapeutic agents for COPD management.