Juvenile dermatomyositis (JDM) is a rare autoimmune disease primarily affecting children, characterized by muscle weakness and skin lesions. This study identifies 145 genes significantly associated with JDM through differential gene expression analysis, weighted gene coexpression network analysis (WGCNA), protein-protein interaction network analysis, and miRNA and transcription factor (TF) prediction, using blood and muscle microarray sequencing datasets. Functional enrichment analysis indicates that these genes are involved in crucial biological processes, including cytokine-mediated signaling, extracellular matrix organization, and immune response. Further analysis reveals key TFs (e.g., STAT1 and NFKB1) and miRNAs (e.g., hsa-miR-127-3p and hsa-miR-17-5p) that may regulate the expression of these critical genes in JDM. The findings provide new insights into the molecular mechanisms of JDM and offer potential targets for future diagnostic and therapeutic strategies.

Resveratrol, often referred to as 3,4′,5-trihydroxystilbene (RSV), is a compound with a variety of pharmacological benefits, such as antiaging, neuroprotective, chemopreventive, antioxidant, and anti-inflammatory qualities. To investigate neuroprotective properties of resveratrol propionate (RPE), H2O2 was added to SH-SY5Y cells (human neuroblastoma cell line) that had been pretreated with RPE. The modulation of Bcl-2 and Bax proteins, the mitochondrial membrane potential (MMP), cytochrome c release, the activation of caspase-9 and caspase-3, DNA fragmentation, and membrane catenin analysis were all measured in this study using flow cytometry. The protective effect of RPE pretreatment of SH-SY5Y cells on the H2O2-induced death process was further investigated using annexin V-fluorescein isothiocyanate (FITC). The induction of caspase-9 and caspase-3, release of cytochrome c, loss of MMP, modification of Bcl-2 and Bax, DNA fragmentation, and annexin V-FITC/PI (propidium iodide) double staining all indicate that RPEs are capable of successfully shielding SH-SY5Y cells from H2O2-induced cytotoxicity. Therefore, RPE is considered a good candidate for the prevention and treatment of neurodegeneration induced by oxidative damage.

Tobacco smoke contains toxic chemical substances that mediate the generation of reactive oxygen species and lung cancer. This study investigates the potential of essential oils (EOs) from Juniperus oxycedrus (JOX) and Juniperus phoenicea L. (JPH) in reducing the harmful effects of cigarette smoke. The EO of JOX (JOX-EO) and JPH (JPH-EO) showed good inhibition of nicotine, with IC50 values of 16.78 ± 1.04 μg/mL and 18.40 ± 0.46 μg/mL, respectively. Moreover, JOX-EO had the greatest percentage reduction of basic tar (64.45%), followed by neutral tar (53.23%), and acidic tar (25.15%). Furthermore, the evaluated JOX-EO demonstrated efficacy in inhibiting polycyclic aromatic hydrocarbons (PAHs). In vivo experiments on rats chronically exposed to cigarette smoke reveal promising results regarding oxidative stress markers. The administration of JOX-EO at 200 mg/kg for 15 days postsmoking cessation shows significant improvements in hematological variables (red blood cells [RBC], platelets [PLT], hemoglobin [HB], hematocrit [HCT], and mean corpuscular volume [MCV]). The oxidative stress markers, including glutathione (GSH), malondialdehyde (MDA), glutathione S-transferase (GST), glutathione peroxidase (GPx), and catalase (CAT), were significantly reduced, indicating powerful antioxidant potential. The EOs exhibited concentration-dependent percentage inhibition of human lung carcinoma (A549) cell viability, with IC50 values indicating greater potential than etoposide, the standard used for comparison. Both EOs demonstrate the capacity to mitigate the lingering effects of smoking, such as oxidative stress and lung cancer, providing reassurance and comfort to those affected.

Ozone (O3) and polystyrene nanoparticles (PNPs) display diffusive behavior that leads to toxicity in many tissues of the adult organism. In this study, we evaluated the interactions between atmospheric pollutants and human muscle, using human myogenic progenitor cells (huMPCs) derived from vastus lateralis skeletal muscle. To achieve this goal, O3 and PNPs were first tested individually to understand the impact of the single pollutant on huMPCs. Subsequently, pollutants were tested in combination to examine their potential synergistic effects, given the simultaneous presence of multiple pollutants in the atmosphere. Cell viability was assessed after treatment with O3 and PNPs, and it seems to be significantly affected in huMPCs exposed to the pollutants, tested both alone and in combination. Similarly, the differentiation capability of treated huMPCs was evaluated, and it was found to be significantly reduced compared to controls, especially when O3 and PNPs are tested in combination. Furthermore, an alteration in the expression of microRNAs involved in myogenic cells' proliferation and differentiation pathways was found. In light of the correlation between pollutants and increased oxidant levels, and O3's ability to produce the superoxide anion, superoxide anion levels in huMPCs exposed to pollutants were also assessed, and an increase in this oxidant was recorded. Thus, this preliminary study suggests that exposure to O3 and PNPs affects human muscle, as it alters all the analyzed parameters in huMPCs, filling a gap in the current literature.

Piper betle is an edible plant known for its potent antioxidant activity. Among its phenolic constituents, cinnamic acid has been identified as a key compound contributing to this bioactivity. Although cinnamic acid is a well-known molecule, this study is the first to report its isolation from P. betle leaves, contributing valuable insights into the chemotaxonomy and phytochemical profile of the species. The aim of this research is to isolate cinnamic acid from the methanol extract of betel leaves and evaluate its antioxidant activity using DPPH and nonenzymatic mimic superoxide dismutase (mSOD) assays. Furthermore, computational analyses were performed using density functional theory (DFT) to assess the antioxidant properties, and molecular docking studies were conducted to investigate the interaction mechanisms of cinnamic acid and its derivatives with several enzymes. The results obtained that cinnamic acid had a strong antioxidant activity with IC50 value using the DPPH and mSOD methods of 76.46 and 36 μg/mL, respectively. The analysis used DFT studies of reactive cinnamic acid as seen from the values of several global descriptive parameters. The deviation in the energy gap from EHOMO and ELUMO is quite small, which is 0.0205 eV. Based on the molecular docking results, cinnamic acid ligands and its derivatives act on the amino acid active sites against xanthine oxidase (XO), NADPH oxidase (NO), cytochrome P450 (CP450), and lipoxygenase (LO) receptors although the binding affinity values are not stronger than the positive control for these four receptors. Therefore, cinnamic acid and its derivatives can be used as a compound to counteract free radicals or as an antioxidant.

Background and AimsThe more severe forms of sickle cell disease (SCD) are highly inflammatory genetic disorders that cause significant oxidative stress. To fight against the free radicals produced, the body has an antioxidant system. In addition, haptoglobin has been reported in several studies as possessing oxidant and inflammatory properties depending on the nature of the genotype. This study hypothesizes that the HP2 allele of haptoglobin may exacerbate oxidative stress in sickle cell patients with inflammation.MethodsAn analytical cross‐sectional study was conducted for 6 months. The patients recruited were those with severe forms of sickle cell anemia, regularly followed at the hematology department of the Yaoundé Central Hospital and the Bafoussam Regional Hospital. The Public Health Research Biotechnology Laboratory (LAPHER‐Biotech) in Yaoundé provided a framework for genotyping haptoglobin by allele‐specific PCR. Next, iron, oxidative stress, and inflammatory parameters were assessed by standard methods, and the statistical software R Version 4.1.1. allowed for the data analysis.ResultsSamples from 149 participants were analyzed. Patients with Hp phenotypes 2‐2 had a considerable elevation of reduced glutathione (14.3 μmol/L) compared to those of phenotype Hp 2‐1 (11.2 μmol/L) and genotype Hp 1‐1 (11.8 μmol/L) (p = 0.075). Malondialdehyde was significantly higher in patients with Hp phenotypes 2‐2 compared to those with Hp phenotype 2‐1 and Hp phenotype 1‐1 (p = 0.008). The oxidative stress index (OSI) was higher in patients with the Hp 2‐2 phenotype than those with the Hp 2‐1 and Hp 1‐1 phenotypes (p = 0.008) suggesting that they are more affected by oxidative stress.ConclusionThis study supports the hypothesis that the Hp 2‐2 phenotype of haptoglobin is associated with an imbalance in the oxidative balance in favor of oxidants, suggesting that the latter is a major contributor to the worsening pathophysiology of SCD.

Nuclear receptor subfamily 4 group A member 1 (NR4A1), which is also known as nuclear receptor 77 (NUR77), NGFI-B, or testicular receptor 3 (TR3), is a member of the NR4A subfamily of the nuclear receptor superfamily. NR4A1 has both nuclear localization and nuclear export signals, and NR4A1 is present in the cytoplasm as well as the nucleus. NR4A1 alters its subcellular localization through phosphorylation or SUMOylation. In the nucleus, NR4A1 plays an important role in regulating gene expression by directly binding to genomic DNA or indirectly influencing other transcription factors. In the cytoplasm, NR4A1 affects the stabilization of β-catenin, which is involved in various tumorigenesis. Furthermore, NR4A1 is involved in LPS-induced inflammasome activation. In mitochondria and endoplasmic reticulum, NR4A1 plays an important role in the induction of autophagy and apoptosis. In this review, we focused on the current knowledge of subcellular localization and molecular function of NR4A1.

The study aimed to investigate the chemical composition and antimicrobial and antioxidant activities of the essential oil from dried seeds of Xylopia aethiopica. The essential oil was obtained by hydrodistillation and analyzed by GC/FID and GC/MS. The essential oil yield was 1.35%. Forty-nine compounds were identified in the essential oil with 1,8-cineole (16.3%), β-pinene (14.8%), trans-pinocarveol (9.1%), myrtenol (8.3%), α-pinene (5.9%), and terpinen-4-ol (5.6%) as major components. The antimicrobial activity of this essential oil was studied using disk diffusion and broth microdilution methods on four bacteria (Staphylococcus aureus, Enterococcus faecalis, Escherichia coli, and Pseudomonas aeruginosa) and one fungus (Candida albicans). The essential oil exhibited excellent activity against S. aureus, E. faecalis, and C. albicans and moderate activity against E. coli. Among all strains tested, C. albicans showed the best sensitivity with a MIC of 50 mg/mL. The antioxidant activity was examined using a DPPH-free radical scavenging assay. The essential oil of X. aethiopica showed low antioxidant activity (IC50 = 784.604 ± 0.320 mg/mL) compared to that of ascorbic acid and the reference compound (IC50 = 0.163 ± 0.003 mg/mL). The results indicate that consumption of X. aethiopica seeds can reduce the virulence of food-borne pathogens and their resistance to antibiotics.

Woodfordia uniflora is a medicinal plant used for the treatment of malaria, toothache, and stomach problems. The root parts of the plant are also used for healing liver disorders. Silica gel chromatography separation of CH2Cl2/MeOH (1:1) and MeOH extracts of roots of W. uniflora result in the isolation of three compounds, namely, bergenin (1), β‐sitosterol (2), and epigallocatechin 3‐gallate (3), reported herein for the first time from the plant. The structure of the isolated compounds was elucidated using NMR (1D and 2D) techniques. Disk diffusion and DPPH assay were used to evaluate the antibacterial and antioxidant activities, respectively. Molecular docking was done by the AutoDock Vina 4.2 program. The pharmacokinetics and toxicity profile of compounds were predicted by Swiss ADME and Pro Tox II online servers. GC‐MS analysis roots of W. uniflora result in the identification of five compounds, of which palmitic acid (34.9%) was the major constituent. The antibacterial activity result indicated that the oil extract had promising activity against P. aeruginosa, E. coli, S. pyogenes, and S. aureus with IZ of 14.3 ± 0.81, 15.0 ± 0.0, 15.6 ± 0.47, and 17.6 ± 0.47 mm, respectively, at 5 mg/mL, compared to ciprofloxacin (1Z 27–30.0 ± 0.0 mm) at 30 μg/mL. MeOH and CH2Cl2/MeOH (1:1) extract showed inhibition against E. coli (IZ of 13.6 ± 0.47 mm) and P. aeruginosa (IZ of 10.0 ± 0.0 mm), respectively, at 200 mg/mL. Bergenin (1) and β‐sitosterol (2) also displayed maximum inhibition of E. coil (IZ of 11.6 ± 0.47) and S. aureus (11.0 ± 0.0 mm), respectively, at 5 mg/mL. The antioxidant activity results showed that CH2Cl2/MeOH (1:1) and MeOH extracts, bergenin (1), and compound 3 displayed potent scavenging DPPH radical with a percentage of inhibition of 76.8 ± 0.12, 77.8 ± 0.08, 71.4 ± 0.08, and 91.2 ± 0.16, respectively, compared to ascorbic acid (93.2% ± 0.04%) at 100 μg/mL. The molecular docking analysis showed that all compounds (1–3) exhibited minimum binding energy toward PDB ID: 1HD2 (−5.2 to −6.3 kcal/mol), compared to ascorbic acid (−5.6 kcal/mol), and toward PDB ID: 1DNU (−8.0 to −10.7 kcal/mol) receptors, compared to ascorbic acid (−5.7 kcal/mol). Toward the PDB ID: 4FM9 receptor, β‐sitosterol (2) and compound 3 exhibited the best binding free energy of −9.1 and −9.8 kcal·mol, respectively, compared to vosaroxin (−7.8 kcal/mol). The drug‐likeness analysis result indicated that bergenin (1) and β‐sitosterol (2) obeyed four and five criteria of Lipinski’s rule, respectively, and are more likely to be administered orally. The in silico toxicity analysis showed none of the compounds would be cytotoxic, mutagenic, or hepatotoxic. The in vitro antioxidant and antibacterial results supported by in silico analysis demonstrated that the roots of W. uniflora have the potential to be therapeutic agents for bacterial infections and free radical–inducing diseases.

CC-chemokine ligand 18 also known as MIP-4 is a chemokine with roles in inflammation and immune responses. It has been shown that MIP-4 is involved in the development of several diseases including lung fibrosis and cancer. How exactly MIP-4 is regulated and exerts its role in lung fibrosis remains unclear. Therefore, in the present study, we examined how MIP-4 is regulated and whether it acts via its potential receptor Nir-1. A549 cells were grown and maintained in DMEM : F12 (1 : 1) and supplemented with 10% FBS and 1000 U of penicillin/streptomycin and maintained as recommended by the manufacturer (ATCC). Cell migration and invasion, immunohistochemistry (IHC), Western blot, qPCR, and siRNA Nir-1 were used to determine MIP-4 regulation and its role in cell migration. Cell migration was increased following stimulation of cells with recombinant (r) MIP-4 and bleomycin (BLM), whereas quenching rMIP-4 with its antibody (Ab) or addition of the Ab to BLM or H2O2 diminished rMIP-4-induced cell migration. Along with cell migration, rMIP-4, BLM, and H2O2 induced the formation of actin filaments dynamic structures whereas costimulation with MIP-4 Ab limited BLM- and H2O2-induced effects. MIP-4 mRNA and protein were increased by BLM and H2O2, and the addition of its Ab significantly reduced treatments effect. Experiments with siRNA investigating whether Nir-1 is a potential MIR-4 receptor indicated that the inhibition of Nir-1 decreased cell migration/invasion but did not totally inhibit rMIP-4-induced cell migration. Therefore, our data indicate that MIP-4 is regulated by BLM and H2O2 and costimulation with its Ab limits the effects on MIP-4 and that the Nir-1 receptor partially mediates MIP-4's effects on increased cell migration. These data also evidenced that MIP-4 is regulated by fibrotic and oxidative stimuli and that quenching MIP-4 with its Ab or therapeutically targeting the Nir-1 receptor may partially limit MIP-4 effects under fibrotic or oxidative stimulation.