Abstract
Background Osteoarthritis (OA) is a chronic and degenerative joint disease, which causes stiffness, pain, and decreased function. At the early stage of OA, nonsteroidal anti-inflammatory drugs (NSAIDs) are considered the first-line treatment. However, the efficacy and utility of available drug therapies are limited. We aim to use bioinformatics to identify potential genes and drugs associated with OA. Methods The genes related to OA and NSAIDs therapy were determined by text mining. Then, the common genes were performed for GO, KEGG pathway analysis, and protein-protein interaction (PPI) network analysis. Using the MCODE plugin-obtained hub genes, the expression levels of hub genes were verified using quantitative real-time polymerase chain reaction (qRT-PCR). The confirmed genes were queried in the Drug Gene Interaction Database to determine potential genes and drugs. Results The qRT-PCR result showed that the expression level of 15 genes was significantly increased in OA samples. Finally, eight potential genes were targetable to a total of 53 drugs, twenty-one of which have been employed to treat OA and 32 drugs have not yet been used in OA. Conclusions The 15 genes (including PTGS2, NLRP3, MMP9, IL1RN, CCL2, TNF, IL10, CD40, IL6, NGF, TP53, RELA, BCL2L1, VEGFA, and NOTCH1) and 32 drugs, which have not been used in OA but approved by the FDA for other diseases, could be potential genes and drugs, respectively, to improve OA treatment. Additionally, those methods provided tremendous opportunities to facilitate drug repositioning efforts and study novel target pharmacology in the pharmaceutical industry.
Highlights
OA is a chronic and degenerative joint disease that occurs commonly in the elderly, and the main concomitant symptoms were cartilage loss, subchondral bone sclerosis, synovitis, and pain [1, 2]. e incidence of OA is increasing around the world due to the aging population and the growing number of obese individuals [3]
nonsteroidal anti-inflammatory drugs (NSAIDs) include traditional NSAIDs and new COX-2 inhibitors; the former blocks COX-1 and COX-2 but the new one only blocks the COX-2 enzyme. e formation of prostaglandinH2 (PGH2) by the metabolic process of the COX enzyme is metabolized by prostaglandin E (PGE) synthase into PGE2, which is one of the significant inflammation mediator [9]
COX-1, found in most tissues, is Journal of Healthcare Engineering encoded by prostaglandin-endoperoxide synthase 1 (PTGS1) and COX-2, induced by various cytokines and growth factors, is encoded by prostaglandin-endoperoxide synthase 2 (PTGS2) [10]
Summary
OA is a chronic and degenerative joint disease that occurs commonly in the elderly, and the main concomitant symptoms were cartilage loss, subchondral bone sclerosis, synovitis, and pain [1, 2]. e incidence of OA is increasing around the world due to the aging population and the growing number of obese individuals [3]. E 15 genes (including PTGS2, NLRP3, MMP9, IL1RN, CCL2, TNF, IL10, CD40, IL6, NGF, TP53, RELA, BCL2L1, VEGFA, and NOTCH1) and 32 drugs, which have not been used in OA but approved by the FDA for other diseases, could be potential genes and drugs, respectively, to improve OA treatment. Those methods provided tremendous opportunities to facilitate drug repositioning efforts and study novel target pharmacology in the pharmaceutical industry
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