Background: The Mediterranean diet is linked to various health benefits, especially the consumption of olive oil as a key component. Multiple studies highlight its advantages, particularly due to its fatty acid composition and additional components like phenolic compounds. A significant antioxidant compound, oleocanthal, known for its antioxidant properties, has gained attention in the pharmaceutical industry for its anti-inflammatory and antiproliferative effects. It shows promise in addressing cardiovascular diseases, metabolic syndrome, and neuroprotection. This systematic review aims to evaluate the existing literature on oleocanthal, examining its role in biological processes and potential impact on conditions like inflammation and cancer. Methods: We performed several searches in PubMed (MEDLINE), Web of Science (WOS), and Cochrane based on the terms “Oleocanthal”, “Cancer”, and “Inflammation”. The inclusion criteria were as follows: studies whose main topics were oleocanthal and cancer or inflammation. On the other hand, the exclusion criteria were studies that were not focused on oleocanthal, reviews, or editorial material. Given that these findings are explanatory rather than derived from clinical trials, we refrained from employing methods to assess potential bias. This systematic review did not receive any external funding. Results: We found 174 records from these searches, where we discarded reviews and editorial material, duplicated articles, and 1 retracted article. Finally, we had 53 reports assessed for eligibility that were included in this review. Discussion: OC exhibits promising therapeutic potential against both inflammation and cancer. We addressed its ability to target inflammatory genes and pathways, offering potential treatments for conditions like rheumatic diseases by regulating pathways such as NF-kB and MAPK. Additionally, OC’s anticancer properties, particularly its notable inhibition of c-Met signaling across various cancers, highlight its efficacy, showcasing promise as a potential treatment.

Adipokines are a heterogeneous group of signalling molecules secreted prevalently by adipose tissue. Initially considered as regulators of energy metabolism and appetite, adipokines have been recognized for their substantial involvement in musculoskeletal disorders, including osteoarthritis, rheumatoid arthritis, and many others. Understanding the role of adipokines in rheumatic inflammatory and autoimmune diseases, as well as in other musculoskeletal diseases such as intervertebral disc degeneration, is crucial for the development of novel therapeutic strategies. Targeting adipokines, or their signalling pathways, may offer new opportunities for the treatment and management of these conditions. By modulating adipokines levels or activity, it may be possible to regulate inflammation, to maintain bone health, and preserve muscle mass, thereby improving the outcomes and quality of life for individuals affected by musculoskeletal diseases. The aim of this review article is to update the reader on the multifaceted role of adipokines in the main rheumatic diseases such as osteoarthritis and rheumatoid arthritis and to unravel the complex interplay among adipokines, cartilage metabolism, bone remodelling and muscles, which will pave the way for innovative therapeutic intervention in the future. For completeness, the role of adipokines in intervertebral disc degeneration will be also addressed.

Background. Obesity is associated with an increased risk for different chronic diseases such as osteoarthritis (OA) or rheumatoid arthritis (RA). In fact, adipose tissue is now recognized as an endocrine organ able to secrete a wide variety of factors called adipokines, which have been demonstrated to participate in the pathophysiology of RA by regulating inflammation and immunity. LCN2 is one of these adipose tissue‐derived factors. However, scarce information is available about the levels of this adipokine in different rheumatic diseases. Therefore, we aimed to analyze LCN2 serum levels in healthy, OA, and RA patients under different treatments. Methods. Serum levels of LCN2, among other proinflammatory and chemotactic factors, have been measured by ELISA or Multiplex in the following four groups of individuals: healthy, OA, and RA patients treated with conventional treatment or adalimumab. Results. We found increased serum levels of LCN2 in OA and RA patients. Interestingly, LCN2 serum levels show a similar pattern to that observed for different proinflammatory and chemotactic factors, being increased in RA conventional treated patients in comparison to RA patients treated with adalimumab. Also, RA patients under conventional treatment revealed a positive and significant correlation between LCN2 and CCL2, CCL3, IL‐8, IL‐1β, IL‐6, and CRP. In patients with RA treated with adalimumab, only IL‐6 and CRP correlated significantly with LCN2. Conclusions. Our results clearly suggest that LCN2 is modulated and associated with inflammation in rheumatic diseases. Therefore, the serum levels of this adipokine might be used as an additional biomarker of the inflammatory/disease activity.

Here, we present the synthesis of a series of chemical homopolymeric and copolymeric injectable hydrogels based on polyethylene glycol methyl ether methacrylate (PEGMEM) alone or with 2-dimethylamino ethyl methacrylate (DMAEM). The objective of this study was to investigate how the modification of hydrogel components influences the swelling, rheological attributes, and in vitro biocompatibility of the hydrogels. The hydrogels’ networks were formed via free radical polymerization, as assured by ¹H nuclear magnetic resonance spectroscopy (¹H NMR). The swelling of the hydrogels directly correlated with the monomer and the catalyst amounts, in addition to the molecular weight of the monomer. Rheological analysis revealed that most of the synthesized hydrogels had viscoelastic and shear-thinning properties. The storage modulus and the viscosity increased by increasing the monomer and the crosslinker fraction but decreased by increasing the catalyst. MTT analysis showed no potential toxicity of the homopolymeric hydrogels, whereas the copolymeric hydrogels were toxic only at high DMEAM concentrations. The crosslinker polyethylene glycol dimethacrylate (PEGDMA) induced inflammation in ATDC5 cells, as detected by the significant increase in nitric oxide synthase type II activity. The results suggest a range of highly tunable homopolymeric and copolymeric hydrogels as candidates for cartilage regeneration.

Background: Intervertebral disc degeneration (IVDD) is one of the main causes of chronic low back pain. The degenerative process is often initiated by an imbalance between catabolic and anabolic pathways. Despite the large socio‐economic impact, the initiation and progress of disc degeneration are poorly understood. Although intervertebral disc (IVD) and articular joint are not identical, their degenerative roads are remarkably similar. We, and another authors, previously demonstrated that E‐74‐like factor 3 (ELF3), a transcription factor induced by inflammatory mediators in various cell types including chondrocytes, is a central contributing factor for cartilage degradation. Thus, we aim to explore, for the first time, the expression, modulation, and the role of ELF3 in human IVD cells.Methods: The presence of ELF3 in healthy and degenerated IVD tissues was initially determined by immunohistochemistry in annulus fibrosus (AF) and nucleus pulposus (NP). mRNA and protein expression were measured, respectively, by RT‐qPCR and Western blot in AF and NP IVD cells harvested from healthy individuals and IVDD patients. Overexpression of ELF3 was performed by transfection of AF IVDD cells with pESE‐1: ELF3 expression vector or pCI: empty vector.Results: Our results unveiled, for the first time, the expression of ELF3 in IVD tissues. ELF3 is notably upregulated in degenerated tissues compared to those from healthy patients. In addition, the stimulation of IVDD AF cells with various proinflammatory stimuli, showed marked increase in both mRNA and protein expression of ELF3. ELF3 overexpression in AF IVDD cells resulted in the upregulation of proinflammatory and catabolic genes such as PTGS2, NOS2, LCN2, IL‐6, MMP13, and ADAMTS‐5; whereas, ELF3 silencing resulted in the opposite results.Conclusions: Our results support a novel role for ELF3 as a pro‐inflammatory and pro‐catabolic transcriptional mediator, whose targeting in IVD tissues might be of potential therapeutic relevance in disc degeneration.