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Brassica rapa has been widely reported as an anti-diabetic plant and is widely used in traditional medicine for the treatment of various disorders. However, the molecular mechanism underlying the plant's anti-diabetic activity has not been elucidated. Therefore, the present study aimed to investigate the possible molecular mechanism of B.rapa for managing diabetes mellitus through network pharmacology and molecular docking studies. The active ingredients and associated target proteins were obtained from a literature review and the Swiss Target Prediction platform and validated using the PubChem database. The disease-associated genes were retrieved from the Genecard database. The B. rapa-DM target network was analyzed using the STRING database, and the results were integrated and visualized using Cytoscape software. The molecular mechanism and therapeutic effect of B.rapa for the treatment of DM were determined by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses using the Enrichr Platform. Fifty-two active ingredients were screened from B. rapa, and 1528 putative target genes were identified from these ingredients. Four hundred and fifty-four overlapping targets matched with DM were considered potential therapeutic targets. First, ten key targets (ALB, AKT1, TNF, GAPDH, MAPK3, EGFR, VEGFA, CTNNB1, CASP3, and STAT3) were found by topological analysis. Then, the results of GO and KEGG suggested that the anti-diabetes effect of B. rapa was strongly associated with the AGE-RAGE signaling pathway in diabetic complications, Neuroactive ligand-receptor interaction, Lipid and atherosclerosis, PI3K-Akt signaling pathway, and Calcium signaling pathway. The AKT1 (Serine/Threonine Protein Kinase) enzyme is targeted by major bioactive constituents of B.rapa. Molecular Docking studies revealed that Liquiritin (docking score -6.1 Kcal/mol) showed the highest binding affinity with AKT1. These results suggest that Brassica rapa may play a role in regulating several pathways that are involved in the development of Diabetes Mellitus. Keywords: Network pharmacology, molecular mechanisms, Brassica rapa, Diabetes Mellitus (DM)

The present study demonstrates the anti-tumor effects of combined supplementations of dietary fish oil (Maxepa) and 1alpha,25-dihydroxyvitamin D(3) (vitamin D(3)) on 7,12-dimethylbenz(alpha)anthracene (DMBA)-induced rat mammary carcinogenesis. Female Sprague-Dawley rats at 50 days of age were treated with 7,12-dimethylbenz(alpha)anthracene (DMBA; 0.5mg/100g body weight) by a single tail vein injection in an oil emulsion. Both fish oil (rich in EPA and DHA) and vitamin D(3) were administered orally at a dose of 0.5 ml/day/rat and 0.3 microg/100 microL propylene glycol twice a week respectively and continued to 35 weeks after DMBA administration. Fish oil in combination with vitamin D(3) resulted in a significant reduction in incidence, multiplicity and volume of mammary tumors. These supplementation also inhibited DMBA-induced mammary 7-methylguanine DNA adducts formation, which was measured by HPLC-fluorescence assay (at four sequential time points; ANOVA, F=42.56, P

Chitosan adsorbed microspheres containing tetanus toxoid were prepared in the size range of 10 µm to 75 µm, by emulsion-cross linking technique at different speeds of agitation. The amount of tetanus toxoid incorporated into chitosan microspheres were estimated by limes flocculation test and in vivo evaluation of tetanus toxoid adsorbed chitosan microspheres were determined by toxin neutralization method using albino mice. The results of in vivo release for the batches of 10 µm and 25 µm correlates with the results of in vitro in which both the batches passes the limit of IP standard (4 Lf) where as, for the batches of 50 µm and 75 µm, the in vitro release of tetanus toxoid was 2 Lf. But our in vivo studies for the batches of 50 µm and 75 µm fail to pass the limit stated in IP. The release of tetanus toxoid from the chitosan microspheres was found to be sustained for the period of 6 months.