Anti-inflammatory Research Articles

New and future heart failure drugs.

In the past decade, our understanding of heart failure pathophysiology has advanced significantly, resulting in the development of new medications such as angiotensin-neprilysin inhibitors, sodium-glucose cotransporter-2 inhibitors and oral soluble guanylate cyclase stimulators. Backed by positive findings from large randomized controlled trials, recommendations for their use were recently included in the 2022 AHA/ACC/HFSA guidelines and 2023 ESC guidelines for management of heart failure. Promising drugs for future heart failure treatment include agents that modulate the neurohormonal system, vasodilators, anti-inflammatory drugs, mitotropes, which improve deranged energy metabolism of the failing heart, and myotropes, which increase cardiac contractility by affecting cardiac sarcomere function. Here, we discuss these new and future heart failure drugs. We explain their mechanisms of action, critically evaluate their performance in clinical trials and summarize the clinical scenarios in which the latest guidelines recommend their use. This Review aims to offer clinicians and researchers a comprehensive overview of novel therapeutic classes in heart failure treatment.

ROS Responsive Cerium Oxide Biomimetic Nanoparticles Alleviates Calcium Oxalate Crystals Induced Kidney Injury via Suppressing Oxidative Stress and M1 Macrophage Polarization.

Emerging studies have demonstrated that M1 macrophage polarization and oxidative stress play important roles in calcium oxalate (CaOx) induced kidney injury, which leads to increased crystals deposition. ROS scavenging nanozymes and kidney-targeted nanoparticles for antioxidant drugs delivery have emerged as an arisen methodology for kidney injury therapy. However, cell membrane biomimetic-modified nanozymes as anti-inflammatory drug delivery systems for the treatment of kidney injury is rarely reported. Herein, the ROS responsive red blood cell-membrane-coated resatorvid-loaded cerium oxide nanoparticles (RBCM@CeO2/TAK-242) are constructed to suppress CaOx induced kidney injury and crystals deposition. In vitro, RBCM@CeO2/TAK-242 shows effective internalization by renal tubular epithelial cells, along with demonstrated antioxidative, anti-inflammatory, and macrophage reprogramming effects. Glyoxalate(Gly)-induced renal CaOx crystals mouse model is established, RBCM@CeO2/TAK-242 shows excellent injured kidney targeting and biosafety, and could effectively suppress CaOx induced kidney injury and crystals deposition. RBCM@CeO2/TAK-242 has a dual protective effect by both inhibiting oxidative stress and modulating macrophage polarization in vivo. In addition, RNA seq analysis reveals that RBCM@CeO2/TAK-242 protects against CaOx induced kidney injury via suppressing the TLR4/NF-κB pathway. This study provides an innovative strategy for RBCM@CeO2/TAK-242 as injured kidney targeting and dual protective effects for the treatment of CaOx induced kidney injury and crystals deposition.

Elbow arthritis

Most patients with primary osteoarthritis of the elbow report a history of heavy lifting work with the affected upper limb. Conservative treatment, including activity modifications, nonsteroidal anti-inflammatory drug (NSAID) intake, and intra-articular injections can provide sufficient pain relief in the early stages when used in combination. If surgery is required, many patients experience significant pain relief from joint-preserving procedures despite existing cartilage damage. Although open debridement procedures are effective, arthroscopic osteocapsular arthroplasty has become established as the preferred surgical procedure. The ulnar nerve should be assessed during surgery and treated if necessary. Total elbow arthroplasty (TEP) is successful in terms of pain relief and function; however, it is recommended for older patients with advanced osteoarthritis or for whom joint-preserving procedures have failed.

Gold nanoparticles as innovative therapeutics for oral mucositis: A review of current evidence.

Oral mucositis (OM) remains a debilitating side effect in patients undergoing cancer therapy. DNA damage and oxidative stress generated by radiation and/or chemotherapy activate key inflammatory pathways, ultimately resulting in the destruction of the epithelial barrier, leading to microbial colonization, and ulceration. These ulcerative lesions are often extremely painful, compromising nutrition and oral hygiene, requiring intravenous nutritional support, resulting in longer periods of hospitalization and increased cost. Ulcers often increase the risk of secondary infection, disrupting cancer therapy and patient prognosis. Despite these issues, there is no approved therapy to mitigate OM. Ultrasmall (< 10nm) spherical gold nanoparticles (AuNPs) with low toxicity offer unique size- and surface chemistry-dependent anti-inflammatory and antioxidant properties. However, physicochemical design of AuNPs, including size, capping agent, and surface charge critically influence their colloidal stability, toxicity, and therapeutic efficacy. AuNP below 10nm demonstrate increased therapeutic efficacy due to the high surface area-to-volume ratio, however, particles smaller than 2nm also show increased potential for inducing cellular death. Furthermore, anionic capping agents make AuNPs less toxic with increased anti-inflammatory response, while cationic particles are potent antimicrobials but toxic. Thus, surface chemistry modulation is a promising strategy to design AuNPs (< 10nm) as potential therapeutic agents for OM. This review provides a comprehensive overview of the OM pathophysiology, discusses current interventional concepts, critically analyses the existing literature on AuNP as an anti-inflammatory, antioxidant, and antimicrobial agent and highlights the benefits and challenges associated with using AuNPs as a therapeutic agent against OM.

Improving dexamethasone drug loading and efficacy in treating rheumatoid arthritis via liposome: Focusing on inflammation and molecular mechanisms.

Rheumatoid arthritis (RA) is a chronic autoimmune disease that affects approximately 0.46% of the global population. Conventional therapeutics for RA, including disease-modifying antirheumatic drugs (DMARDs), nonsteroidal anti-inflammatory drugs (NSAIDs), and corticosteroids, frequently result in unintended adverse effects. Dexamethasone (DEX) is a potent glucocorticoid used to treat RA due to its anti-inflammatory and immunosuppressive properties. Liposomal delivery of DEX, particularly when liposomes are surface-modified with targeting ligands like peptides or sialic acid, can improve drug efficacy by enhancing its distribution to inflamed joints and minimizing toxicity. This study investigates the potential of liposomal drug delivery systems to enhance the efficacy and targeting of DEX in the treatment of RA. Results from various studies demonstrate that liposomal DEX significantly inhibits arthritis progression in animal models, reduces joint inflammation and damage, and alleviates cartilage destruction compared to free DEX. The liposomal formulation also shows better hemocompatibility, fewer adverse effects on body weight and immune organ index, and a longer circulation time with higher bioavailability. The anti-inflammatory mechanism is associated with the downregulation of pro-inflammatory cytokines like tumor necrosis factor-α (TNF-α) and B-cell-activating factor (BAFF), which are key players in the pathogenesis of RA. Additionally, liposomal DEX can induce the expression of anti-inflammatory cytokines like interleukin-10 (IL-10), which has significant anti-inflammatory and immunoregulatory properties. The findings suggest that liposomal DEX represents a promising candidate for effective and safe RA therapy, with the potential to improve the management of this debilitating disease by providing targeted delivery and sustained release of the drug.

Role of Podoplanin (PDPN) in Advancing the Progression and Metastasis of Glioblastoma Multiforme (GBM)

Glioblastoma multiforme (GBM) is a malignant primary brain tumor categorized as a Grade 4 astrocytic glioma by the World Health Organization (WHO). Some of the established risk factors of GBM include inherited genetic syndromes, body mass index, alcohol consumption, use of non-steroidal anti-inflammatory drugs (NSAIDs), and therapeutic ionizing radiation. Vascular anomalies, including local and peripheral thrombosis, are common features of GBM. Podoplanin (PDPN), a ligand of the C-type lectin receptor (CLEC-2), promotes platelet activation, aggregation, venous thromboembolism (VTE), lymphatic vessel formation, and tumor metastasis in GBM patients. It is regulated by Prox1 and is expressed in developing and adult mammalian brains. It was initially identified on lymphatic endothelial cells (LECs) as the E11 antigen and on fibroblastic reticular cells (FRCs) of lymphoid organs and thymic epithelial cells as gp38. In recent research studies, its expression has been linked with prognosis in GBM. PDPN-expressing cancer cells are highly pernicious, with a mutant aptitude to form stem cells. Such cells, on colocalization to the surrounding tissues, transition from epithelial to mesenchymal cells, contributing to the malignant carcinogenesis of GBM. PDPN can be used as an independent prognostic factor in GBM, and this review provides strong preclinical and clinical evidence supporting these claims.

Antitubercular potential and pH-driven mode of action of salicylic acid derivatives.

In the search for new antituberculosis drugs with novel mechanisms of action, we evaluated the antimycobacterial activity of a panel of eight phenolic acids against four pathogenic mycobacterial model species, including Mycobacterium tuberculosis. We demonstrated that salicylic acid (SA), as well as the iodinated derivatives 5-iodo-salicylic acid (5ISA) and 3,5-diiodo-salicylic acid (3,5diISA), displayed promising antitubercular activities. Remarkably, using a genetically encoded mycobacterial intrabacterial pH reporter, we describe for the first time that SA, 5ISA, 3,5diISA, and the anti-inflammatory drug aspirin (ASP) act by disrupting the intrabacterial pH homeostasis of M. tuberculosis in a dose-dependent manner under in vitro conditions mimicking the endolysosomal pH of macrophages. In contrast, the structurally related second-line anti-TB drug 4-aminosalicylic acid (PAS) had no pH-dependent activity and was strongly antagonized by l-methionine supplementation, thereby suggesting distinct modes of action. Finally, we propose that SA, ASP, and its two iodinated derivatives could restrict M. tuberculosis growth in a pH-dependent manner by acidifying the cytosol of the bacilli, therefore making such compounds very attractive for further development of antibacterial agents.

Comprehensive analysis of the first complete mitogenome and plastome of a traditional Chinese medicine Viola diffusa

BackgroundViola diffusa is used in the formulation of various Traditional Chinese Medicines (TCMs), including antiviral, antimicrobial, antitussive, and anti-inflammatory drugs, due to its richness in flavonoids and triterpenoids. The biosynthesis of these compounds is largely mediated by cytochrome P450 enzymes, which are primarily located in the membranes of mitochondria and the endoplasmic reticulum.ResultsThis study presents the complete assembly of the mitogenome and plastome of Viola diffusa. The circular mitogenome spans 474,721 bp with a GC content of 44.17% and encodes 36 unique protein-coding genes, 21 tRNA, and 3 rRNA. Except for the RSCU values of 1 observed for the start codon (AUG) and tryptophan (UGG), the mitochondrial protein-coding genes exhibited a codon usage bias, with most estimates deviating from 1, similar to patterns observed in closely related species. Analysis of repetitive sequences in the mitogenome demonstrated potential homologous recombination mediated by these repeats. Sequence transfer analysis revealed 24 homologous sequences shared between the mitogenome and plastome, including nine full-length genes. Collinearity was observed among Viola diffusa species within the other members of Malpighiales order, indicated by the presence of homologous fragments. The length and arrangement of collinear blocks varied, and the mitogenome exhibited a high frequency of gene rearrangement.ConclusionsWe present the first complete assembly of the mitogenome and plastome of Viola diffusa, highlighting its implications for pharmacological, evolutionary, and taxonomic studies. Our research underscores the multifaceted importance of comprehensive mitogenome analysis.

Colon-Targeted Poly(ADP-ribose) Polymerase Inhibitors Synergize Therapeutic Effects of Mesalazine Against Rat Colitis Induced by 2,4-Dinitrobenzenesulfonic Acid

Background/Objectives: In addition to oncological applications, poly(ADP-ribose) polymerase (PARP) inhibitors have potential as anti-inflammatory agents. Colon-targeted delivery of PARP inhibitors has been evaluated as a pharmaceutical strategy to enhance their safety and therapeutic efficacy against gut inflammation. Methods: Colon-targeted PARP inhibitors 5-aminoisoquinoline (5-AIQ) and 3-aminobenzamide (3-AB) were designed and synthesized by azo coupling with salicylic acid (SA), yielding 5-AIQ azo-linked with SA (AQSA) and 3-AB azo-linked with SA (ABSA). Additional conjugation of AQSA with acidic amino acids yielded glutamic acid-conjugated AQSA (AQSA-Glu) and aspartic acid-conjugated AQSA, which further increased the hydrophilicity of AQSA. Results: The distribution coefficients of PARP inhibitors were lowered by chemical modifications, which correlated well with drug permeability via the Caco-2 cell monolayer. All derivatives were effectively converted to their corresponding PARP inhibitors in the cecal contents. Compared with observations in the oral administration of PARP inhibitors, AQSA-Glu and ABSA resulted in the accumulation of much greater amounts of each PARP inhibitor in the cecum. ABSA accumulated mesalazine (5-ASA) in the cecum to a similar extent as sulfasalazine (SSZ), a colon-targeted 5-ASA prodrug. In the DNBS-induced rat colitis model, AQSA-Glu enhanced the anticolitic potency of 5-AIQ. Furthermore, ABSA was more effective against rat colitis than SSZ or AQSA-Glu, and the anticolitic effects of AQSA-Glu were augmented by combined treatment with a colon-targeted 5-ASA prodrug. In addition, the colon-targeted delivery of PARP inhibitors substantially reduced their systemic absorption. Conclusions: Colon-targeted PARP inhibitors may improve the therapeutic and toxicological properties of inhibitors and synergize the anticolitic effects of 5-ASA.

Physiologically Based Biopharmaceutics Modeling Coupled with Biopredictive Dissolution in Development of Bioequivalent Formulation for Mesalamine Enteric Coated Tablet: A Tough Nut to Crack.

Mesalamine is a locally acting anti-inflammatory drug used to treat mild to moderate ulcerative colitis. Because of complex formulation principle and high in vivo variability, development of bioequivalent formulation for mesalamine is challenging. Further, fed state possess significant challenges for bioequivalence (BE) due to interplay of multiple factors. In the work, we have developed a novel biopredictive media for mesalamine enteric coated tablets and integrated into physiologically based biopharmaceutics model (PBBM) to predict in vivo fed behavior. USP III based gradient media was developed to mimic in vivo fed condition. The developed PBBM was initially validated with literature data and subsequently re-optimized with pilot BE study data. Further, virtual bioequivalence (VBE) was performed to evaluate model predictability for pilot BE data. Later, the model was applied for prospective BE predictions with increased subjects and parametric sensitivity analysis was performed to identify physiological factors that can impact in vivo performance. Further, the model was used to predict luminal and enterocyte concentrations in colon to demonstrate equivalent efficacy. Additionally, a novel dissolution/permeation tool (Dissoflux) was employed to compare permeability behavior of formulations. Overall, this work enabled BE prediction for complex mesalamine enteric coated tablets and helped to understand parameters that can impact in vivo performance.

Differential modulation of inflammatory cytokines by recombinant IL-10 in IL-1β and TNF-α ̶ stimulated equine chondrocytes and synoviocytes: impact of washing and timing on cytokine responses

Osteoarthritis (OA) remains a challenging joint disorder necessitating effective anti-inflammatory interventions. In this study, our primary objective was to establish an in vitro protocol that replicates the clinical investigation of anti-inflammatory drugs intended for OA management. Focusing on recombinant IL-10 (r.IL-10) as a potential anti-inflammatory treatment, we designed and implemented two distinct protocols to evaluate the efficacy of r.IL-10 in modulating chondrocyte and synoviocyte inflammation.The experimental design involved sequential stimulation with IL-1β and TNF-α for 24 h, followed by washing (model 1) or not washing (model 2) the cells before r.IL-10 treatment. Samples were collected after 6–24 h of treatment. Cellular responses were evaluated by quantifying gene expression and synthesis of key inflammatory cytokines and proteases.The expression and synthesis of inflammatory cytokines and proteases was significantly affected by washing and treatment time. The expression of IL-1β, TNF-α, IL-8, MMP-13, and ADAMTS5 were effectively reduced in r.IL-10-treated chondrocytes and synoviocytes in model 2 after 24 h, particularly at concentrations of 10 and 20 ng/mL. r.IL-10 treatment significantly increased IL-6 gene expression in chondrocytes at all time points. However, in synoviocytes, IL-6 expression was significantly lower in model 2 after 24 h of r.IL-10 treatment. r.IL-10 treatment significantly decreased IL-1β and TNF-α content in synoviocyte supernatants, particularly in model 2 at concentrations of 10 and 20 ng/mL after 6 and 24 h. r.IL-10 treatment in chondrocytes led to a significant decrease in IL-1β supernatant concentrations in model 2 after 24 h only.This study demonstrated that r.IL-10 treatment effectively reduces key inflammatory markers and matrix metalloproteinase activity in both chondrocytes and synoviocytes, particularly in model 2 where cells were not washed prior to treatment. These findings highlight r.IL-10’s potential as a robust anti-inflammatory agent for OA management and suggest its critical role in developing effective therapeutic strategies for OA.

Bilateral Rectus Sheath Block with Continuous Bupivacaine Infusions After Elective Open Gastrectomy: A Randomized Controlled Trial

Background and Objectives: Multimodal analgesia has been shown to be effective in facilitating early postoperative gastrointestinal function and rehabilitation in patients undergoing open gastrectomy. We conducted a clinical trial to investigate the effectiveness of bilateral rectus sheath block (RSB) with continuous bupivacaine infusion in comparison with placebo following elective open gastrectomy. Materials and Methods: Patients indicated for elective open gastrectomy were screened, enrolled, and randomised between October 2021 and September 2023. The patients were randomised to either Group A (intervention—continuous bupivacaine) or Group B (control—NaCl saline). The primary outcome measures were the quantity of an opioid analgesic administered during the initial 72 h post-surgery and the level of postoperative pain as indicated by the visual analogue scale (VAS). Mann–Whitney U test was used for quantitative analysis while Pearson Chi-square was used for categorical variables. Results: A total of 60 patients completed the trial, with 30 patients in each of the two groups. Patients in Group A reported lower median VAS pain scores at all observed time points following surgery (p &lt; 0.001). No patient in Group A required rescue opioid analgesia, although non-steroidal anti-inflammatory drugs were necessary during the initial 12 h postoperatively. Clinically, Group A patients had a significantly shorter time to first gas (p = 0.001), a shorter time to first bowel movement (p &lt; 0.001), a shorter time to first out-of-bed activity (p &lt; 0.001), and a shorter overall hospitalisation duration (p &lt; 0.001) compared to Group B patients. Conclusions: Bilateral RSB with continuous bupivacaine infusion is effective in managing pain and can reduce the use of opioid analgesics in the postoperative period. Furthermore, it promotes early recovery, and a shorter hospital stay.

Prevalence, risk factors, and severity of erectile dysfunction following renal transplantation.

Sexual dysfunction is common among dialysis and transplant patients. Our study evaluated the prevalence, risk factors, and severity of erectile dysfunction (ED) post-transplant in a single center. We conducted a single-centre, observational, non-interventional study of adult male renal graft recipients. Sociodemographic and clinical data were collected, and erectile function was assessed with the International Index of Erectile Function (IIEF) questionnaire. 179 patients transplanted between 1995 and 2021 were enrolled (170 answered the questionnaire). Mild, moderate, and severe ED was noted in 33.5%, 20.6% and 10.6% of cases, respectively. ED prevalence increased with age (42.6% of patients < 40, 47.4% of patients aged 40-60, 78.9% of patients > 60). The total mean IIEF score was 16.32 ± 6.93 (erectile function 19.22 ± 7.9, orgasmic function 6.8 ± 2.9, sexual desire 6.43 ± 2.1, intercourse satisfaction 8.96 ± 3.7, overall satisfaction 6.78 ± 2.6). Age, alcohol consumption, type, time on dialysis pre-transplant, and donor type were significantly associated with erectile dysfunction (p < 0.05). Most patients (93.5%) were treated for comorbidities in addition to immunosuppression. Severe ED was significantly more common among patients taking alpha blockers and non-steroidal anti-inflammatory drugs. Self-reported erectile dysfunction post renal transplantation seems influenced by age, alcohol intake, dialysis history, donor type and certain drugs, but not by comorbidities (hypertension, diabetes, heart disease).

Reactive arthritis

Reactive arthritis (ReA) is adisease caused by an extra-articular infection that manifests as asterile joint inflammation. In contrast to bacterial septic arthritis no pathogens can be cultured from the joint in ReA but pathogen components, such as antigens or DNA are more frequently detectable in the joint, suggesting an intra-articular culture-negative persistent infection or at least an intra-articular interaction between the host and pathogen components. The primary extra-articular infection in classical ReA is of bacterial origin and usually affects either the urogenital, gastrointestinal or, less frequently, the respiratory tract. Chlamydia (C.trachomatis and less frequently C.pneumoniae) and enterobacteria are among the most common pathogens causing ReA. The prevalence of ReA is estimated at 40/100,000 and the incidence at 5/100,000. Typical clinical manifestations are mostly self-limiting peripheral arthritis (monoarticular or oligoarticular), dactylitis and, more rarely, axial involvement and in half of the cases, there is an association with HLA-B27. Due to these similarities, classical ReA is categorized as aform of spondyloarthritis (SpA). The diagnosis is made on the basis of atypical clinical picture, evidence of aprevious or persistent infection and the exclusion of other causes of arthritis. Treatment includes physical measures, the use of anti-inflammatory agents such as nonsteroidal anti-inflammatory drugs (NSAID) or glucocorticoids, in the case of persistent arthritis, immunomodulating substances such as sulphasalazine, methotrexate and in individual cases biologics and Janus kinase inhibitors (JAKi) are used. In general, antibiotic treatment of ReA does not shorten the duration of the disease.

Investigating pain-related medication use and contribution to polypharmacy in adults with intellectual disabilities: a systematic review

BackgroundAdults with intellectual disability experience more pain than adults without and, despite a higher number of medications being prescribed, may be less likely to receive medication for pain. We conducted a systematic review of existing literature on medication for pain and painful conditions in adults with intellectual disability to explore if there is any association with polypharmacy, multimorbidity or demographic characteristics.MethodsThis systematic review followed PRISMA guidelines. Medline, Embase, PubMed, PsycINFO, Web of Science, CINAHL, Cochrane Library and Scopus were searched from January 2000 to 21st October 2024. We included original, peer-reviewed observational, qualitative or mixed-method studies published in English with data on medication for pain or painful conditions in adults with intellectual disability. Two independent reviewers performed study selection, data extraction, and quality assessment; disagreements were resolved by a third reviewer. Adapted Newcastle–Ottawa Scale or the Critical Appraisal Skills Programme for qualitative studies was used for quality assessment of included studies and findings were reported via narrative synthesis. PROSPERO registration: CRD42023415051.ResultsTwenty-seven of 26,170 articles met the eligibility criteria. Adults with intellectual disability were more likely to have simple analgesic medication than non-steroidal anti-inflammatory drugs, opioids or adjuvant pain medications than the general population. Psychotropic medications were more commonly prescribed in adults with intellectual disability than medication for pain or painful conditions. Adults with intellectual disability and caregivers reported under-recognition and most likely under-treatment of pain.ConclusionsAdults with intellectual disability may receive less pharmacological management of pain with analgesics and medication for painful conditions despite the high prevalence of polypharmacy, suggesting pain is under-treated. Better assessment and pharmacological treatment of pain and painful conditions is a key future research priority to address this health inequality and improve quality of life for this vulnerable group of people.

Adsorption of Ibuprofen from Water Using Banana Peel Biochar: Experimental Investigation and Machine Learning Algorithms

Ibuprofen is a significant nonsteroidal anti-inflammatory drug that poses environmental and health risks when present in wastewater because of its persistence and probable toxicity. This study investigates the use of banana peel biochar (BPB) made at 600 °C to 900 °C to eliminate ibuprofen from aqueous solutions. The uniqueness of this work lies in the high-temperature pyrolysis process, which has not been previously explored for the ibuprofen removal efficiency using BPB. The batch experiment was conducted considering initial concentrations, pH, and contact time. The data were compared with different algorithms, with Linear Regression (LR), Support Vector Machines (SVM), Decision Trees (DT), Random Forest (RF), and k-Nearest Neighbor (k-NN) to forecast the performance. The results revealed that banana peel biochar at 900 °C exhibited the highest ibuprofen removal efficiency (69.28 ± 0.83%) at 125 mg/L concentration with the sequence of BPB900 &gt; BPB800 &gt; BPB700 &gt; BPB600. A maximum removal efficiency of 72.67 ± 0.75% was observed at pH 9. Adsorption behavior was analyzed using isotherm and kinetic models, with the Freundlich isotherm model (R2 value 0.9620) indicating heterogeneous adsorption and the pseudo-second-order (PSO) kinetic model (R2 value 0.9969) suggesting that physicochemical interactions govern the process. FTIR analysis ensured the existence of functional groups (hydroxyl, carboxylic, carbonyl, and aromatic rings) responsible for adsorption. Machine learning algorithms, especially RF, demonstrated outstanding performance with 90.07% accuracy in predicting the experimental data. In comparison to other adsorbents, BPB demonstrated superior removal efficiency, underscoring its effectiveness. The study suggests that BPB, particularly at 900 °C, is effective in removing ibuprofen, and due to its sustainable production, it offers a potential solution for wastewater treatment.

Role of Inflammation and Cytokine Dysregulation in Depression in Patients with Inflammatory Skin Conditions.

The growing field of psychodermatology examines the interplay between dermatological and psychiatric comorbidities. While current literature recognizes that cutaneous and psychiatric conditions often coexist within patients, the relationship between dysregulated inflammation and depression in patients with inflammatory skin conditions has not been thoroughly explored. This review seeks to describe the connection between cutaneous disease and depression via shared inflammatory cytokine pathways. A review of current literature was conducted, and studies addressing the co-occurrence of depression and inflammatory skin diseases were included. This review focuses on depression in patients with psoriasis, atopic dermatitis, and hidradenitis suppurativa. Studies that focused on the prevalence of depression in these populations, shared inflammatory pathways, and co-management of cutaneous and psychiatric disorders were chosen. The literature revealed a high prevalence of depression in individuals with inflammatory skin conditions compared with those without cutaneous disease. Recent studies described how proinflammatory cytokines in inflammatory skin diseases can elicit inflammation in the brain, leading to depressive symptoms. Certain subsets of cytokines that mediate inflammatory pathways were associated with both cutaneous inflammation and depression, highlighting shared pathology. Antiinflammatory medications targeting shared cytokines found reductions in both cutaneous and depressive symptoms. Practitioners have emphasized interdisciplinary approaches to treating both conditions, including psychotherapy and pharmacological methods. There is a clear association between inflammatory cutaneous diseases and depression. Co-management of these conditions, including interdisciplinary methods, is essential for patients' well-being. Future research addressing similar links between other cutaneous and psychiatric conditions could yield new treatment opportunities as well.

Repurposing of monocyclic β-lactams as anti-inflammatory agents – The case of new ferrocene-azetidin-2-one hybrids

There is growing interest in developing monotherapy drugs that treat inflammation caused by microbial infections, focusing on dual antimicrobial and anti-inflammatory agents with minimal side effects and high safety margins. This study synthesized and characterized a library of novel cis-4-ferrocenylazetidin-2-ones, evaluating their antimicrobial and anti-inflammatory activities. These organometallic monocyclic β-lactams showed moderate in vitro antimicrobial activity against various standard microbial strains, including yeasts and Gram-negative and Gram-positive bacteria. Some compounds overcame the resistance of clinical Staphylococcus aureus isolates. Traditionally, monocyclic β-lactams target Gram-negative bacilli, but adding a ferrocene moiety and substituting the COOH group near the N-1 position with a non-ionizable ester group (COOR) extended their activity spectrum. The anti-inflammatory properties were assessed in macrophage-based models, revealing non-cytotoxicity below 10 μM. Two compounds were shown to be strong and selective arginase inhibitors, while five others effectively suppressed excessive NO formation without affecting basal NO production. The presence of a phenoxy group at C-3 of the β-lactam ring appeared to be crucial for selective NO inhibition. These hybrids did not scavenge NO but inhibited NO synthesis by suppressing iNOS expression. Overall, two novel hybrids were identified as promising hit candidates for treating infection-induced inflammatory reactions.

In-silico based Designing of benzo[d]thiazol-2-amine Derivatives as Analgesic and Anti-inflammatory Agents.

Benzo[d]thiazoles represent a significant class of heterocyclic compounds renowned for their diverse pharmacological activities, including analgesic and antiinflammatory properties. This molecular scaffold holds substantial interest among medicinal chemists owing to its structural versatility and therapeutic potential. Incorporating the benzo[d]thiazole moiety into drug molecules has been extensively investigated as a strategy to craft novel therapeutics with heightened efficacy and minimized adverse effects. The aim of the present research work was to design, synthesize and characterize the new benzo[d]thiazol-2-amine derivatives as potent analgesic and anti-inflammatory agents. The synthesis of the presented benzo[d]thiazol-2-amine derivatives was performed by condensing-(4-chlorobenzylidene) benzo[d]thiazol-2-amine with a number of substituted phenols in the presence of potassium iodide and anhydrous potassium carbonate in dry acetone. IR spectroscopy, 1HNMR spectroscopy, 13CNMR spectroscopy and Mass spectroscopy methods were used to characterize the structural properties of all 13 newly synthesized derivatives. The molecular properties of these newly synthesized derivatives were estimated to study the attributes of drug-like candidates. Benzo[d]thiazol-2-amine derivatives were molecularly docked with selective enzymes COX-1 and COX-2. Analgesic and anti-inflammatory activities of synthesized compounds were evaluated by using albino rats. Findings of the research suggested that compounds G3, G4, G6, G8 and G11 possess higher binding affinity than diclofenac sodium, when docking was performed with enzyme COX-1. Compounds G1, G3, G6, G8 and G10 showed lower binding affinity than Indomethacin when docking was performed with enzyme COX-2. In vitro evaluation of the COX-1 and COX-2 enzyme inhibitory activities was performed for synthesized compounds. Compounds G10 and G11 exhibited significant COX-1 and COX-2 enzyme inhibitory action with an IC50 value of 5.0 and 10 μM, respectively. Using the hot plate method and the carrageenan-induced rat paw edema model, the synthesized compounds were screened for their biological activities, including analgesic and anti-inflammatory activities. Highest analgesic action was exhibited by derivative G11 and the compound G10 showed the highest anti-inflammatory response. Inhibition of COX may be considered as a mechanism of action of these compounds. It was concluded that synthesized derivatives G10 and G11 exhibited significant analgesic and anti-inflammatory effect; therefore, the said compounds may be subjected to further clinical investigation for establishing these as future compounds for the treatment of pain and inflammation.

Design, Synthesis, and In-silico Evaluation of Quinazoline Derivatives as Anti-Inflammatory Agents

Researchers are now investigating quinazoline derivatives, which are a group of chemicals with diverse biological effects, in order to find powerful anti-inflammatory drugs. Developing and analysing novel quinazoline compounds that precisely target the 4JQA protein—a critical component of the inflammatory response—is the main goal of this study. The study will involve designing and synthesising these compounds, as well as evaluating their effectiveness using computer simulations. A number of quinazoline derivatives were synthesised by employing rational drug design ideas and synthetic chemistry methods many spectroscopic methods, such as NMR, were used to confirm the structures of the synthesised molecules. Afterward, the anti-inflammatory capabilities of these compounds were assessed using molecular docking experiments against the 4JQA protein. The docking investigations demonstrated that a number of the synthesized quinazoline derivatives had robust binding affinities and advantageous interactions with the active region of the 4JQA protein. Significant interactions with amino acid residues essential for the protein's activity were detected, indicating a potential mode of action for these chemicals as anti-inflammatory drugs. The encouraging findings from the computational docking studies establish a strong basis for subsequent laboratory and animal experiments, facilitating the progress toward creating innovative quinazoline-based medicines with anti-inflammatory properties. This study emphasizes the potential benefits of integrating computational and experimental approaches in developing new drugs, namely in the search for and development of innovative therapeutic drugs that target pathways linked with inflammation.