Abstract

The combined application of clove oil in a lipid nanocarrier opens a promising avenue for bone and joints therapy. In this study, we successfully developed a tunable controlled-release lipid platform for the efficient delivery of clove oil (CO) for the treatment of rheumatoid arthritis (RA). The ultra-small nanostructured lipid carriers co-loaded with CO (CONCs) were developed through an aqueous titration method followed by microfluidization. The CONCs appeared to be spherical (particle size of 120 nm), stable (zeta potential of −27 mV), and entrapped efficiently (84.5%). In toluene:acetone:glacial acetic acid (90:9:1 percent v/v/v) solvent systems, high-performance thin layer chromatography (HPTLC) analysis revealed the primary components in CO as eugenol (RF = 0.58). The CONCs greatly increased the therapeutic impact of CO in both in vitro and in vivo biological tests, which was further supported by excellent antiarthritic action. The CONC had an antiarthritic activity that was slightly higher than neat CO and slightly lower than standard, according to our data. The improved formulation inhibited serum lysosomal enzymes and proinflammatory cytokines while also improving hind leg function. This study provides a proof of concept to treat RA with a new strategy utilizing essential oils via nanodelivery.

Highlights

  • Arthritis, or joint inflammation, is a chronic condition caused by a disruption in the production of pro-inflammatory cytokines and enzymes [1]

  • clove oil (CO) and GO in 1:1 ratio demonstrated better solubility performance (Table 1), GO was selected as a solid lipid for the study

  • The surfactant chosen for drug development must be able to (i) lower interfacial tension to a very low value to aid dispersion during nanoemulsion preparation, (ii) provide a flexible film that can deform around droplets, and (iii) have the appropriate lipophilic character to provide the correct curvature at the interfacial region for the desired nanoemulsion type (i.e., o/w, w/o, or bicontinuous) [32,38,39,40]

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Summary

Introduction

Joint inflammation, is a chronic condition caused by a disruption in the production of pro-inflammatory cytokines and enzymes [1]. Analgesics, nonsteroidal anti-inflammatory medicines (NSAIDs), immunosuppressive glucocorticoids (ISGs), anticytokines (ACs), and disease-modifying antirheumatic medications (DMARDs) are currently accessible pharmaceuticals [3]. Exceptional progress has been observed in the long-term development of DMARDs, which include (a) traditional DMARDs such as methotrexate, hydrochloroquine, and sulfadiazine, (b) targeted synthetic DMARDs, such as tofacitinib (pan-JAK) inhibitor) and baricitinib (JAK1/2-inhibitors), and (c) biologic DMARDs, such as infliximab tumor necrosis factor-α (TNF-α) inhibitor), etanercept (TNF-receptor inhibitor), siltuximab (interleukin-6 (IL-6) inhibitor), tocilizumab (IL-6R inhibitor), rituximab (B-cell depleting antibody), and abatacept (co-stimulatory molecules inhibitor) utilized for this purpose [5,6,7]. NSAIDs, ISGs, ACs, and DMARDs have been shown to have low success rates in the treatment of RA, as well as significant side effects and substantial financial expense [5,8]. Herbs are always preferred over synthetic drugs due to their myriad benefits and triumph of popular therapeutic diversity [9,10]

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