Vol 18, No 4 (2024)

Background:Fusarium oxysporum f. sp. Albedinis a telluric fungal pathogen commonly found in soils, is the causal agent of fungal vascular wilt of date palms in Moroccan oases. The infection by the pathogen leads to the death of the date palm after six months to two years, which causes enormous economic and environmental damage.

Objective:The framework of this paper is to determine the chemical composition of six essential oils using GC-MS and their antifungal activity on the mycelial growth of Fusarium oxysporum f. sp. Albedinis, as well as the molecular docking study to evaluate the inhibitory potential of fungal trypsin.

Methods:The essential oils were extracted from different parts of the plants (whole plant, flowers, and leaves) by steam distillation, and were identified using gas chromatography-mass spectrometry (GC/MS). The antifungal assay of the extracted essential oils and their main components was assessed using the direct contact method with the fungus at different concentrations; the obtained results were evaluated by calculating the minimum inhibitory concentration (MIC) of each essential oil, followed by an in-silico study of the major identified compounds for better understanding of the inhibitory potential against fungal trypsin activity.

Results:The identification of the different bioactive compounds using GC-MS revealed that Rosmarinus officinalis Eo was characterized by eucalyptol 46.26%, camphor 10.03%, and β-pinene 6.63%; while Lavandula officinalis Eo was endowed by the presence of linalool 14.93%, camphor 14.11%, and linalyl acetate 11.17%. Furthermore, Artemisia herba alba was rich in 1,3,5-cycloheptatriene, 1,6- dimethyl- 36.44%, camphor 22.50%, and α-thujone 7.21%. While Eucalyptus globulus was rich in eucalyptol 74.32%, β-Cymene 11.41%, α-Pinene 6.96%. Finally, Mentha pepirita and Mentha pulegium were both characterized by the presence of D-limonene 20.15%, trans-carveol 19.59%, D-Carvone 14.96%, and pulegone (42.40%), 3-cyclopentene-1-ethanol, 2,2,4-trimethyl- (11.28%), 1,3,4- trimethyl-3-cyclohexenyl-1-carboxaldehyde (9.68%), respectively. Regarding the in vitro, all Eos from different plants exhibited pronounced antifungal effect. The MIC values recorded for E. globulus were MIC= 1.75 mg/L, M. pulegium and L. officinalis (MIC= 1.80 mg/L), and M. piperita (MIC= 1.90 mg/L). The strongest inhibition potential was associated with R. officinalis EO (MIC= 1.15 mg/L) and A. herba alba EO (MIC= 1.60 mg/L). As for the computational study performed camphor one of the bioactive compounds showed its ability to act against trypsin which could be considered a potential candidate against Fusarium oxysporum f. sp. Albedinis.

Conclusion:The studied essential oils from different medicinal and aromatic plants showed significant antifungal activity, probably due to the Camphor which could have an inhibitory effect on the Fusarium oxysporum f. sp. Albedinis trypsin. Further research should be conducted in vivo for a better understanding of the mechanism of action of these essential oils.

Background:The most common Inflammatory Bowel Diseases (IBD) affecting the gastrointestinal system are Crohn's disease and ulcerative colitis. However, the usual therapies for them are associated with a multitude of side effects. The blue-green microalgae Arthrospira platensis is known for its safety profile, nutritional, and medicinal properties in the treatment of different inflammatory and gastrointestinal disorders.

Objective:The objective of this study was to investigate the potential intestinal anti-inflammatory effects of the aqueous extract derived from Arthrospira platensis (AAP) in a mouse model of DNBS-induced colitis.

Methods:GC-MS and FTIR-ATR were used to determine the different types of chemical compounds found in the AAP extract. BALB/c mice that received DNBS intrarectally were treated with three doses (50, 100 and 200 mg/kg) of AAP for three days. The inflammatory status was assessed daily using a Disease Activity Index (DAI). Mice were sacrificed on the third day, and the extent of colonic damage was evaluated through both macroscopic and histological examinations. Finally, biochemical assays of different markers (MDA, NO, and GSH) were performed.

Results:The GC-MS analysis revealed the presence of eleven bioactive compounds, including 2- thiophenecarboxylic acid, 2-biphenyl ester, palmitic acid, 2-linoleoyl glycerol, ethyl isoallocholate, and methyl palmitate. In addition, FTIR spectroscopy revealed the presence of amino, hydroxyl, and glucosidic groups. The treatment of colitic mice with AAP decreased the severity of colitis, as demonstrated by the improvement in the clinical score and the reduction of colonic tissue damage, as well as the modulation of the local biochemical marker levels.

Conclusion:The AAP effectively improves DNBS-induced colitis, but its short treatment duration and focus on acute colitis highlight the need for further research on long-term and chronic effects.

Introduction:Gallic acid (GA), a natural phenolic acid, has been reported as an antitumor agent in various cancer cells. Although some mechanisms, such as apoptosis, are well known, the details of other mechanisms, such as their pro-oxidant and autophagy activity, are still considerable.

Methods:The pro-oxidative activity and anti-proliferative activity of GA on HEK 293 and HepG2 cells were measured in the absence and presence of exogenous Cu (II) and Fe (II). Furthermore, colony forming, ROS generation, apoptosis induction, autophagy and mitochondrial membrane potential (MMP) were examined.

Results:HepG2 cells treated with GA + Cu (II) significantly reduced cell viability (p (<0.001). GA +Cu (II) induced morphological changes in HepG2 cells and stimulated apoptotic cell death. Moreover, GA +Cu (II) triggered the mitochondrial-dependent apoptotic pathway by increasing intracellular ROS levels and disrupting MMP. Furthermore, GA+ Cu (II) significantly reduced the Plating Efficiency and Surviving Fraction while increasing autophagic vacuoles in the HepG2 cells.

Conclusion:According to our results, GA played a pro-oxidant role in the presence of Cu (II), triggered apoptosis by increased ROS and disruption of MMP. This combination also induced autophagy in HepG2. These effects hold promise for future anticancer research.