👤 Nora M Aborehab

Despite their effectiveness in agriculture to control a variety of pests, organophosphorus compounds (OPC) such as malathion were linked with neurological dysfunctions and possibly death. The present study aimed to investigate the impact of OPC exposure on neuroinflammation via disrupting the equilibrium between pro-inflammatory (RORγt/STAT3/IL-17/IL-22) and anti-inflammatory (FOXP3/STAT5/IL-10) pathways. The study extended to evaluate the potential of BCG vaccination in alleviating neuroinflammation. Rats were distributed into four groups: control, malathion-intoxicated group, BCG-treated group, and scopolamine-treated group. Behavioral tests and histopathological investigations of the cerebral cortex were done. FOXP3, RORγt, STAT3, and STAT5 were estimated using qRT-PCR. Acetylcholine (Ach), BDNF, IL-10, IL-17, IL-22, BCL2, and BAX were estimated using ELISA, whereas GFAP and IL-1β were estimated via immunohistochemical analysis. The malathion-intoxicated group revealed higher gene expression of RORγt and STAT3, along with lower gene expression of FOXP3 and STAT5, compared with the control group. Moreover, the concentrations of IL-17, IL-22, and BAX were higher, along with lower concentrations of BDNF, IL-10, and BCL2, compared with the control group. Furthermore, GFAP and IL-1β showed marked positive cytoplasmic expression. However, the BCG-treated group reversed all the abovementioned findings. Collectively, the study highlights that malathion induces neuroinflammation via skewing the balance between the proinflammatory (RORγt/STAT3/IL-17/IL-22) and the antiinflammatory (FOXP3/STAT5/IL-10), leading to behavioral fluctations and brain's histological disruption. This imbalance resulted in cytokine production, neuronal apoptosis, and neurodegeneration. BCG administration alleviates these effects owing to its anti-inflammatory and neuroprotective effects. Show less

various extracts of Moringa oleifera Lam. leaves, were reported to possess antiobesity effect in experimental animals models, yet its active doses and mechanism of action are still unclear. The metabolic profiling of 70% ethanol extract of M. oleifera (MO) leaves was performed using HPLC-MS/MS analysis. The antiobesity activity of MO was tested in high fat diet induced obesity in rats at 200 and 400 mg/kg body weight orally for 1 month. Total cholesterol (TC), high density lipoproteins (HDL-C), low density lipoprotein-cholesterol (LDL-C), triglycerides (TGs), insulin resistance, insulin sensitivity, and adipose tissue index were monitored. In addition, fatty acid synthase (FAS) and HMG-CoA reductase mRNA from liver tissue, Peroxisome Proliferator-Activated Receptor alpha (PPARα) and Melanocortin-4 receptor (MC4R) RNA from adipose tissue were quantified using qRT-PCR. MO hard gelatin capsules (400 mg/capsule) were formulated and standardized using HPLC-RP analysis and tested on fifteen female participants, aged 45-55 with a BMI of 29-34 kg/m Thirteen metabolites were tentatively identified using HPLC-MS/MS analysis including flavonols, flavones and a phenolic acid. MO 400 showed a prominent effect on reducing the rats' final weights, % weight increase and adiposity index (P < 0.05). Glucose, insulin and HOMA-IR were significantly reduced and R-QUICKI was significantly increased by MO 400 (P < 0.001). Mean tissue level of leptin and vaspin were significantly reduced, adiponectin, omentin and GLUT-4 expression were increased significantly by MO 400 (P < 0.01). MO 400 significantly suppressed FAS and HMG-CoA reductase and increased mRNA expression of MC4R and PPAR-α (P < 0.01). Eight weeks administration of MO hard gelatin capsules to obese patients showed significant reduction of the average BMI, TC and LDL compared to the baseline values (p < 0.05). Our results presented a scientific evidence for the traditional use of M. oleifera leaves as antiobesity herbal medicine. Show less