Text Mining Protocol to Retrieve Significant Drug-Gene Interactions from PubMed Abstracts.

Genes and proteins form the basis of all cellular processes and ensure a smooth functioning of the human system. The diseases caused in humans can be either genetic in nature or may be caused due to external factors. Genetic diseases are mainly the result of any anomaly in gene/protein structure or function. This disruption interferes with the normal expression of cellular components. Against external factors, even though the immunogenicity of every individual protects them to a certain extent from infections, they are still susceptible to other disease-causing agents. Understanding the biological pathway/entities that could be targeted by specific drugs is an essential component of drug discovery. The traditional drug target discovery process is time-consuming and practically not feasible. A computational approach could provide speed and efficiency to the method. With the presence of vast biomedical literature, text mining also seems to be an obvious choice which could efficiently aid with other computational methods in identifying drug-gene targets. These could aid in initial stages of reviewing the disease components or can even aid parallel in extracting drug-disease-gene/protein relationships from literature. The present chapter aims at finding drug-gene interactions and how the information could be explored for drug interaction.

Chemopreventive effect of montelukast in n-nitroso n-methyl urea induced mammary carcinogenesis in female Sprague-Dawley rats.

OBJECTIVE: The objective of the study was to evaluate the chemopreventive effect of montelukast sodium; selective reversible cysteinyl leukotriene D4-receptor antagonist in N-nitroso N-methyl urea (NMU) induced mammary carcinogenesis in virgin female Sprague-Dawley rats. MATERIALS AND METHODS: Thirty rats were divided into five groups (normal control, disease control, montelukast1 mg/kg, montelukast10 mg/kg, tamoxifen10 mg/kg) of six animals each. The drug was administered in two doses,1 mg/kg,and 10 mg/kg orally and compared with the standard drug tamoxifen (10 mg/kg)p.o. RESULTS: Montelukast sodium 1 mg/kg,10 mg/kg, and tamoxifen10 mg/kg decreased the tumor incidences by 50%,66.67%, and 83.33% and the total number of tumors in group by 41.67%, 58.33% and 91.67% respectively, when compared to the disease control. Montelukast sodium 1 mg/kg,10 mg/kg,and tamoxifen10 mg/kg decreased the average tumor burden by 86.41%,94.8% and 95.97%and average tumor volume by 89.52%, 95.84%, and 95.4%respectively, when compared to disease control group. CONCLUSION: The results revealed that montelukast sodium prevent the mammary carcinogenesis and confirms the role of cysteinyl leukotriene D4-receptor in mammary gland neoplasia.

Effect of silymarin on streptozotocin-nicotinamide-induced type 2 diabetic nephropathy in rats.

INTRODUCTION: Diabetic nephropathy is the major cause of end-stage renal disease worldwide. Silymarin is a flavonoid mixture obtained from Silybum marianum. Various preclinical and clinical studies have revealed that it has antidiabetic activity. The objective of this study was to evaluate the effect of silymarin on type 2 diabetic nephropathy in rats. MATERIALS AND METHODS: Non-insulin-dependent diabetes mellitus was induced in overnight-fasted male albino Wistar rats by an intramuscular injection of streptozotocin and nicotinamide. Eighteen rats with diabetic nephropathy and 6 rats without induced nephropathy were divided into 4 groups, each containing 6 animals. Group 1 was the normal control and group 2 was the DM control. Groups 3 and 4 were rats with diabetic nephropathy that received 60 mg/kg and 120 mg/kg of silymarin for 60 days. RESULTS: At the end of the study period, the diabetic control group had significantly higher blood glucose, glycosylated hemoglobin, urine volume, serum uric acid, and urine albumin levels when compared to the normal control group. Silymarin-treated groups showed significantly lower levels of blood glucose, glycosylated hemoglobin, urine volume, serum creatinine, serum uric acid, and urine albumin, when compared to the diabetic control group. Histopathological studies reports strongly supported the protective effect of silymarin. CONCLUSIONS: These findings suggest that silymarin has protective effects for kidneys affected by type 2 diabetes mellitus. If the safety and efficacy is confirmed in humans, silymarin will be a good medication to prevent nephropathy-induced premature death in diabetic patients.