@article {1101, title = {Unravelling the Approaches to Treat Osteoarthritis: A Focus on the Potential of Medicinal Plants}, journal = {Pharmacognosy Research}, volume = {15}, year = {2023}, month = {December 2022}, pages = {13-25}, type = {Review Article}, chapter = {13}, abstract = {

Background: Osteoarthritis (OA) is the most prevalent chronic rheumatic disorder, affecting more women than men. The prevalence and course of OA are increased by ageing and obesity. Numerous other risk factors for OA progression include oxidative stress, injury, mechanical stress, and metabolic problems. Interleukin{\textendash}1 is released during inflammatory responses, which destroys cartilage. Interleukin{\textendash}1 is correlated with the release of proteases, an enzyme that destroys cartilage further. Other cytokines similar to TNF{\textendash}alpha induce the enzyme matrix metalloproteinases (MMP), which causes joint injury. Collagenase is another enzyme that degrades collagen and so impacts negatively on the articular cartilage. NSAIDs, opioid analgesics, topical analgesics, and intra-articular steroids are being used to alleviate osteoarthritis pain, and symptoms. However, various adverse effects are linked with all of these medications, limiting their usage, for example, NSAIDs used to relieve OA pain. Nonetheless, they exhibit gastrointestinal, cardiovascular, and nephrotoxicity. Tramadol also has an effect on the central nervous and gastrointestinal systems. Patients were interested in herbal plants because they were worried about the safety and inadequate effectiveness of pharmaceuticals. Plants have been used to cure a variety of ailments since ancient times, and several plants have the ability to treat OA. According to several studies, the pain and progression of OA may be considerably slowed, or halted by bioactive chemicals found in plants. Conclusion: Here we analysed the current scientific literature available that revealed a rising number of research on the possible antiosteoarthritic effects of medicinal plants and their principal ingredients, indicating the possibility of a novel therapeutic use.

}, keywords = {Antiosteoarthritic, Cartilage, Chondrocytes, Collagenase., Herbal plants, Inflammation}, doi = {10.5530/097484900001}, author = {Sonali Verma and Sumeet Gupta and Rina Das and Kavita Munjal and Meenakshi Dhanawat and Dinesh Kumar Mehta and Gurudev Goyal and Anshu Gupta} } @article {490, title = {Lactoferrin from Camelus dromedarius Inhibits Nuclear Transcription Factor-kappa B Activation, Cyclooxygenase-2 Expression and Prostaglandin E2 Production in Stimulated Human Chondrocytes}, journal = {Pharmacognosy Research}, volume = {8}, year = {2016}, month = {February 2016}, pages = {135-141}, type = {Original Article}, chapter = {135}, abstract = {

Background: Osteoarthritis (OA) is a progressive joint disorder, which remains the leading cause of chronic disability in aged people. Nuclear factor-kappa B (NF)-κB is a major cellular event in OA and its activation by interleukin-1β (IL-1β) plays a critical role in cartilage breakdown in these patients. Objective: In this study, we examined the effect of lactoferrin on NF-κB activation, cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) production in stimulated human articular chondrocytes. Materials and Methods: Human chondrocytes were derived from OA articular cartilage and treated with camel lactoferrin and then stimulated with IL-1β. Gene expression was determined by TaqMan assays and protein expression was studied by Western immunoblotting. NF-κB activity and PGE2 levels were determined by ELISA based assays. NF-κB activity was also determined by treatment of chondrocytes with NF-κB specific inhibitor Bay 11{\textendash}7082. Results: Lactoferrin inhibited IL-1β-induced activation and nuclear translocation of NF-κB p65 in human OA chondrocytes. Lactoferrin also inhibited mRNA/protein expression of COX-2 and production of PGE2. Moreover, Bay 11{\textendash}7082 also inhibited IL-1β-induced expression of COX-2 and production of PGE2. The inhibitory effect of lactoferrin on the IL-1β induced expression of COX-2 or production of PGE2 was mediated at least in part via suppression of NF-κB activation. Conclusions: Our data determine camel lactoferrin as a novel inhibitor of IL-1β-induced activation of NF-κB signaling events and production of cartilage-degrading molecule PGE2 via inhibition of COX-2 expressions. These results may have important implications for the development of novel therapeutic strategies for the prevention/treatment of OA and other degenerative/inflammatory diseases.

}, keywords = {Chondrocytes, Cyclooxygenase-2, interleukin-1β, lactoferrin, nuclear factor-kappa B, osteoarthritis, Prostaglandin E2}, doi = {10.4103/0974-8490.175612}, author = {Naila Rasheed and Abdullah Alghasham and Zafar Rasheed} }