Factor TNF-α Research Articles

Role of Raf Kinase Inhibitor Protein in Modulating Echinococcal Cyst Fluid-induced Degranulation in Bone Marrow-Derived Mast Cells

Objective: This study aimed to investigate the role of Raf kinase inhibitor protein (RKIP) in degranulation induced by echinococcal cyst fluid (EgCF) in bone marrow-derived mast cells (BMMCs). Methods: Primary BMMCs were isolated and cultured from the femurs and tibias of RKIP gene knockout (KO) and wild-type (WT) C57BL/6 mice. EgCF-induced degranulation models were established for both groups. Samples of cells and supernatant were collected for analysis. Surface expression levels of CD117 and Fc-epsilon Receptor Ⅰ α (FcεRIα) were assessed. Supernatant concentrations of β-hexosaminidase, IL-4, IL-6, and tumor necrosis factor (TNF-α) were measured. Cellular mRNA levels of IL-4, IL-6, and TNF-α were quantified, and changes in RKIP protein expression during degranulation in WT BMMCs were monitored. Results: After 4 weeks of induction culture, the double-positive rates for CD117 and FcεRIα exceeded 98% in both KO and WT BMMCs. Following sensitization, BMMCs from the KO group demonstrated significantly higher degranulation rates compared to the WT group (p < 0.05). In WT BMMCs, surface RKIP protein expression progressively decreased at 1 hour, 2 hours, and 3 hours post-sensitization, corresponding with degranulation progression (p < 0.05). The KO group exhibited elevated release of BMMC-related cytokines, including IL-4, IL-6, and TNF-α, compared to the WT group after sensitization (p < 0.05). Similarly, transcription levels of cytokines IL-4, IL-6, and TNF-α were higher in the KO group than in the WT group following sensitization (p < 0.05). Conclusion: RKIP gene knockout resulted in an increased EgCF-induced release of cytokines and bioactive substances by BMMCs, indicating that RKIP may suppress EgCF-induced BMMC degranulation. These findings suggest that RKIP could serve as a potential therapeutic target for managing allergic reactions associated with cystic echinococcosis.

The preventive effect of probiotic Lactobacillus plantarum X86 isolated from raw milk on Staphylococcus aureus-induced mastitis in rats

Mastitis is the most common and challenging disease that affects dairy animal welfare and causes huge economic loss in dairy industry globally. Conventional antibiotic treatment of mastitis raised the drug resistance and unsuccessful therapy. As an alternative approach, probiotic lactobacilli had shown multifunctional effects against diseases. Lactobacillus strains against mastitis are worth screening and evaluating. In this study, milk-derived Lactobacillus spp. from Ningxia, China were screened in vitro and the anti-mastitis effect of a candidate strain was evaluated through a Staphylococcus aureus-induced rat mastitis model. The results showed that Lactobacillus plantarum X86 exhibited a high adhesion rate of MAC-T cells, presented the best probiotic properties, and demonstrated anti-S. aureus effects in vitro through comprehensive assessment. Furthermore, L. plantarum X86 alleviated pathological damage to the mammary gland, liver, and colon, inhibited the mRNA expression of pro-inflammatory cytokines factors IL-1β, IL-6, and TNF-α in mammary gland tissue; and increased the content of intestine SCFAs in a rat mastitis model induced by S. aureus. In conclusion, our results suggested that L. plantarum X86 could be a promising probiotic for the prevention and treatment of S. aureus-induced mastitis.

GLI3 is Inhibited by miR-143-3p and Attenuates Septic-induced Lung Injury and Inflammation by Targeting SFRP1.

Transcription factors (TF) are the central regulatory hubs of signaling pathways in eukaryotic cells. Here, we explored the abnormal expression of TF in septic-induced lung injury by sequencing. The levels of target proteins were detected using Western Blot and Elisa. Cell function was evaluated using CCK8 and transwell assays. A double luciferase reporter assay was performed to detect interactions between target molecules. We found that TF glioma-associated oncogene (GLI) family zinc finger 3 (GLI3) was abnormally low expressed in a lipopolysaccharide (LPS) induced acute lung injury (ALI) cell model. In an in vitro model, GLI3 overexpression promoted the proliferation and migration and inhibited apoptosis of lung epithelial cells in LPS-induced inflammatory environment. Importantly, GLI3 overexpression inhibited the secretion of inflammatory factors IL-1β, IL-6, and TNF-α. Additionally, miR-143-3p inhibited the expression of GLI3. MiR-143-3p inhibitor alleviated the cell damage caused by LPS, while knocking down GLI3 counteracted this effect, indicating that miR-143-3p downregulated GLI3 and inhibited its anti-inflammatory effect. Secreted frizzled related protein-1 (SFRP1) was upregulated in LPS-treated cells and SFRP1 promoter interacted with GLI3, suggesting that SFRP1 was a target of TF GLI3. Co-transfection with GLI3 knockdown and SFRP1 overexpression plasmids attenuated the secretion of inflammatory factors IL- 1β, IL-6, and TNF-α caused by GLI3 knockdown in LPS-treated cells, indicating that SFRP1 plays an anti-inflammatory role as a GLI3 target in the ALI cell model. miR-143-3p caused degradation of GLI3 mRNA and thus inhibited the transcription of SFRP1, leading to decreased proliferation and increased levels of inflammatory factors, providing new potential targets for the clinical diagnosis and treatment of ALI.

DNA Receptor Toll-Like Receptor 9 Signaling Pathway Plays a Major Immunomodulatory Role in Neonatal Acute Lung Injury by Inhibiting Inflammatory Response and Oxidative Stress.

To investigate the clinical efficacy of neonatal acute lung injury (NALI) and the mechanistic role of the DNA sensor Toll-like receptor 9 (TLR9) signaling pathway in treatment, Methods: This study enrolled 76 cases of NALI, randomly divided into 38 cases in the experimental group (intravenous injection of human immunoglobulin on the basis of nasal continuous positive airway pressure ventilation treatment) and 38 cases in the control group (nasal continuous positive airway pressure ventilation treatment). The pulmonary function parameters (forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and FEV1/FVC), TLR9 signaling pathway-related proteins and mRNA levels (TLR9, MyD88, p38), inflammatory factors (C-reactive protein (CRP), interleukin (IL)-1β, tumor necrosis factor (TNF)-α), and immune function indicators (immunoglobulin (Ig)A, IgG, IgM) were compared between the two groups. Pearson correlation analysis was conducted to examine the relationship between TLR9 signaling pathway protein expression and immune function indicators.After treatment, the pulmonary function parameters FVC, FEV1, and FEV1/FVC in neonates in the experimental group were considerably higher than those in the control group (P < 0.05). The serum levels of inflammatory factors CRP, IL-1β, and TNF-α in the experimental group of neonates following treatment were significantly lower than those in the control group (P < 0.05). After treatment, the levels of immune function indicators IgA, IgG, and IgM in neonates in the experimental group were considerably lower than those in the control group (P < 0.05). The protein expression levels of TLR9 showed a highly significant positive correlation with neonatal immune function indicators IgA, IgG, and IgM levels (P < 0.001). MyD88 protein expression exhibited a significant positive correlation with neonatal immune function indicators IgA, IgG, and IgM levels (P < 0.05). p38 protein expression demonstrated a significant positive correlation with neonatal immune function indicators IgA, IgG, and IgM levels (P < 0.05). In summary, the potential role of DNA receptor TLR9 signaling pathway-related proteins in the treatment of neonates with lung injury has been explored. The changes in the expression levels of TLR9/MyD88/p38 are associated with the production or regulation of immunoglobulins, and this association shows a certain correlation with the clinical efficacy in neonates with lung injury.

Evaluation of antioxidant, anti-inflammatory, and analgesic potentials of combined polyphenol-rich fractions from Ziziphus mauritiana and Ziziphus spina-christi leaves through modulation of inflammatory and oxidative stress markers in Sprague Dawley rats model.

The main objective of the present study was to combine the ethanol extracts of Ziziphus mauritiana and Ziziphus spina-christi (ZMZS) and fractioned with different solvents of increasing polarity for evaluation of antioxidant, anti-inflammatory and analgesic potentials. The ethanolic extracts of leaves were prepared using Soxhlet apparatus, mixed in ratio (1:1 w/w) and then fractionated into n-hexane, ethyl acetate and n-butanol. In vitro antioxidant activity of all fractions was assessed using total phenolic contents (TPC), total flavonoid contents (TFC), 2,2-dipehnyl, 1-picryl hydrazyl (DPPH) free radical scavenging ability, reducing power and bleachability of β-carotene in Linoleic acid system assays. Ethyl acetate fraction (EAF) showed the highest antioxidant activity in terms of the highest TPC (212.15mg/g) and TFC (39.54mg/g), better DPPH radical scavenging (IC50, 4.82µg/ml), reducing power and β-carotene bleachability. The reverse-phase high-performance liquid chromatography (Rp-HPLC) was performed for the characterization of polyphenols in Ziziphus mauritiana and Ziziphus spina-christi extracts individually and ethyl acetate fraction of ZMZS. Results showed that EAF was enriched with phenolic acids, notable coumarin, gallic acid, salicylic acid and chlorogenic acid, whereas quercetin and kaempferol were the most abundant flavonoids. In vivo anti-inflammatory activity of most potent ethyl acetate fraction was performed using a carrageenan-induced model and analgesic activity using hot plate method in male Sprague Dawley rats. Further, the suppression of inflammatory biomarkers and the oxidative stress parameters were evaluated. Results indicate that EAF possesses significant anti-inflammatory and anti-analgesic properties at 500mg/kg BW as evidenced by their ability to reduce paw edema, percentage inhibition and prolonged latency time and proinflammatory cytokines, such as interleukin-6 (IL-6), tumor necrosis factor (TNF-α), and C-reactive protein (CRP). The EAF also normalized the oxidative stress levels of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GPX), reduced glutathione (GSH) and catalase (CAT) when compared to the standard drug indomethacin. The present study concluded that ethyl acetate fraction (EAF) of combined ZMZS extract has remarkable antioxidant as well as anti-inflammatory and analgesic potentials possibly due to interactions of total phenolic and total flavonoid contents.

The Impact of Microplastics in Food and Drugs on Human Health: A Review of the MENA Region

Microplastics (MPs), defined as plastic particles smaller than 5 mm, have emerged as a global environmental and public health crisis, infiltrating air, water, soil, and food systems worldwide. MPs originate from the breakdown of larger plastic debris, single-use plastics, and industrial processes, entering food. Emerging evidence underscores the ability of MPs to cross biological barriers, including the blood–brain barrier, triggering neuroinflammatory responses and contributing to neurodegenerative diseases such as Alzheimer’s and Parkinson’s. Polystyrene (PS), a common type of MP, activates microglial cells, releasing pro-inflammatory cytokines like tumor necrosis factor (TNF-α) and interleukins, which increase neuronal damage. MPs have also been linked to cardiovascular diseases, with studies detecting polyethylene (PE) and polyvinyl chloride (PVC) in carotid artery plaques, increasing the risk of myocardial infarction and stroke. Furthermore, MPs disrupt endocrine function, alter lipid metabolism, and induce gut microbiome imbalances, posing multifaceted health risks. In the MENA region, MP pollution is particularly severe, with the Mediterranean Sea receiving an estimated 570,000 tons of plastic annually, equivalent to 33,800 plastic bottles per minute. Studies in Egypt, Lebanon, and Tunisia document high MP concentrations in marine ecosystems, with herbivorous fish like Siganus rivulatus containing over 1000 MPs per individual due to the ingestion of contaminated seaweed. Despite these findings, public awareness and regulatory frameworks remain inadequate, with only 24% of Egyptians demonstrating sufficient knowledge of safe plastic use. This review emphasizes the urgent need for region-specific research, policy interventions, and public awareness campaigns to address MP pollution. Recommendations include sustainable waste management practices, the promotion of biodegradable alternatives, and enhanced monitoring systems to mitigate the health and environmental impacts of MPs in the MENA region.

Deciphering the Pharmacological Mechanism of Compound Purpura Decoction in Treating Henoch-Schonlein Purpura by Network Pharmacology, Molecular Docking, and Experimental Validation.

Henoch-Schonlein purpura (HSP) is an immunoglobulin A(IgA)-mediated systemic vasculitis that frequently developsin children. Compound purpura decoction (CPD), a classical herbal combination, exerts favourable effectson the clinical symptoms and prognosis of HSP;however, theunderlying molecular mechanism remains unclear. Firstly, HPLCanalysis identified fivebioactive components in CPD, including protocatechuic acid, chlorogenic acid, mangiferin, baicalin,and buddleoside, with concentrations of 0.011±0.02 mg/g, 0.577±0.33 mg/g, 0.150±0.05 mg/g, 1.132±0.23 mg/g, and 0.369±0.23 mg/g, respectively.Additionally,we established an animal model of allergic purpura to evaluatethe therapeutic effects of CPD on HSP. CPD effectively alleviated renal and cutaneous vasculitis and reducedIgA deposition. CPD could regulatethe Treg/Th17 cell balance, decrease the levels of the proinflammatory factors IL-6 and TNF-α,and suppress the expression ofC3 and C5 (p<0.05).Network pharmacology analysissuggested that the mechanism of CPD in HSP treatment mainly involved EGFR-related targets and pathways, followed by molecular docking confirming strong binding affinity between EGFR and the bioactive components(binding energy <-4.25 kcal/mol). Real-time quantitative PCR (RT-qPCR) and western blot showed that CPD suppressed the activation of the EGFR/ERK signaling pathway(p<0.05), which could be associated with the inhibition of complement system activation.

Effects of WN1703 on Cardiovascular Function in Chronic Hyperuricemia Rats and Myocardial Injury Mechanism Exploration in H9C2 Cells.

Hyperuricemia, a prevalent condition, is typically preceded by disturbances in purine metabolism and is frequently associated with hyperlipidemia and other dysfunctions of metabolism. WN1703 demonstrated an inhibitory activity against xanthine oxidoreductase (XOR) that was comparable to febuxostat in our prior investigation. In this study, we assessed the cardiovascular safety of WN1703 in a chronic hyperuricemia rat model induced by potassium oxonate in combination with hypoxanthine. We investigated the changes in cardiovascular biomarkers in chronic hyperuricemia rats treated with febuxostat and WN1703, including creatine kinase (CK), CK-MB, B type natriuretic peptide (BNP), Corin protein (CRN), Neprilysin (NEP), myeloperoxidase (MPO), 8-hydroxy-2-deoxyguanosine (8-OHdG), tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), and interleukin-8 (IL-8). Additionally, we validated the potential mechanism of cardiac injury induced by WN1703 in H9C2 cells, guided by cardiotoxicity predictions from the cardioToxCSM database and network pharmacology. We observed that excessively rapid urate-lowering, oxidative stress, and inflammation could disrupt myocardial functional homeostasis and increase the risk of cardiovascular injury in hyperuricemia rats, and WN1703 treatment effectively reduced the levels oxidative stress marker 8-OHdG and inflammatory factor TNF-α. Despite the absence of organic damage to the heart with prolonged treatment of febuxostat and WN1703, potential hazard of cardiovascular injury could be associated with the modulation of the TGFβ and RHO/ROCK signaling pathways by febuxostat and WN1703. This could offer new insights into the mechanisms underlying the adverse effects caused by XOR inhibitors.

Apoptosis, MAPK signaling pathway affected in tilapia liver following nano-microplastics and sulfamethoxazole acute co-exposure

Apoptosis, MAPK signaling pathway affected in tilapia liver following nano-microplastics and sulfamethoxazole acute co-exposure

Network pharmacology and molecular docking technology-based predictive study and potential targets analysis of icariin for the treatment of diabetic nephropathy.

Network pharmacology and molecular docking technology-based predictive study and potential targets analysis of icariin for the treatment of diabetic nephropathy.

Preparation and anti-inflammation activity of λ-carrageenan oligosaccharides degraded by a novel λ-carrageenase Car3193.

Preparation and anti-inflammation activity of λ-carrageenan oligosaccharides degraded by a novel λ-carrageenase Car3193.

The Exosomes Derived From Bone Marrow Mesenchymal Stem Cells Alleviate Inflammatory Injury in Heart Failure Disease by Enhancing the Expression of KLF4.

The aim of this study is to investigate the impact and mechanism of action of exosomes derived from bone marrow mesenchymal stem cells (BMSCs) in the treatment of heart failure (HF). The analysis of gene sequencing data set was employed to identify potential therapeutic target proteins for HF. Subsequently, H9C2 cells and Sprague-Dawley (SD) rats were utilized as experimental models to simulate doxorubicin hydrochloride (Doxorubicin, Dox)-induced myocardial injury. This approach was employed to investigate the expression changes of inflammatory factors, including TNF-α, IL-6, IL-1β, sST2, and Gal-3, as well as the alterations in their expression following exosome treatment. Meanwhile, the mechanism of exosomes in relieving HF and inhibiting inflammation were investigated using constructed KLF 4 knockout cell lines and SD rats. BMSC-derived exosomes were capable of enhancing the expression level of KLF4 in cardiomyocytes, decreasing the expression levels of myocardial damage markers BNP and hs-TnI, as well as inflammatory factors TNF-α, IL-6, IL-1β, sST2, and Gal-3, thereby alleviating HF injury. In vitro and in vivo experiments have shown that exosomal treatment decreases the expression of BNP and hs-TnI, which are indicators of myocardial injury, along with the release of inflammatory cytokines in cardiomyocytes. Concurrently, the expression of KLF4 was downregulated, leading to a significant reduction in this physiological modulation. BMSC-derived exosomes exhibit superior therapeutic potential for HF by enhancing the expression of KLF4 and mitigating inflammation in myocardial tissue.

Arsenic exposure induces neural cells senescence and abnormal lipid droplet accumulation leading to social memory impairment in mice.

Arsenic exposure induces neural cells senescence and abnormal lipid droplet accumulation leading to social memory impairment in mice.

Rational design, synthesis and anti-inflammatory activity of 6-substituted dihydrobenzophenanthridine derivatives.

Rational design, synthesis and anti-inflammatory activity of 6-substituted dihydrobenzophenanthridine derivatives.

Laminarin Alleviates Acute Lung Injury Induced by LPS Through Inhibition of M1 Macrophage Polarisation.

The lipopolysaccharide-induced acute lung injury (ALI) mouse model is used to simulate human acute respiratory distress syndrome (ARDS), which has a high mortality rate. An imbalance between M1 and M2 macrophages, characterised by an increase in M1 macrophages, was observed in sepsis-induced ALI. We report that laminarin, an active ingredient found in algae, exhibits exceptional performance in a mouse model of sepsis-induced ALI. It ameliorates lung edema, enhances the survival rate of mice and reduces the levels of the inflammatory factors TNF-α and IL-6. Furthermore, laminarin reduced the expression of CD86, which are markers associated with M1 macrophages. Laminarin treatment reduces the secretion of TNF-α and IL-6 in LPS-stimulated macrophages. Laminarin treatment also decreases glucose uptake in LPS-stimulated macrophages. Transcriptome sequencing reveals that genes downregulated in LPS-stimulated macrophages following laminarin treatment are predominantly enriched in the HIF-1α signalling pathway. Experimental validation confirms that laminarin treatment of LPS-stimulated macrophages reduces the expression of HIF-1α and significantly decreases the expression of related indicators ROS and NLRP3. After using siRNA to knock down HIF-1α in RAW264.7 cells, the inhibitory effect of laminarin on LPS-induced M1 polarisation of macrophages is abolished. This suggests that laminarin may potentially inhibit macrophage polarisation towards the M1 phenotype by downregulating the HIF-1α signal. In conclusion, the data presented in our study demonstrate that laminarin can effectively reduce M1 macrophage polarisation by downregulating HIF-1α signalling. This makes it a novel candidate drug for the treatment of LPS-induced ALI.

Long term effects of gamma radiation on inflammatory and apoptotic biomarkers in nuclear medicine staff.

Long term effects of gamma radiation on inflammatory and apoptotic biomarkers in nuclear medicine staff.

The Effect and Significance of Mild Hypothermia Adjuvant Therapy on Serum IL-6 and TNF-α in Neonatal Hypoxic-Ischemic Encephalopathy

Objective: To investigate the effect of systemic mild hypothermia therapy on peripheral blood interleukin-6 (IL-6) and tumor necrosis factor (TNF-α) in neonates with hypoxic-ischemic encephalopathy (HIE) within 6 hours after birth. Methods: Forty neonates with HIE within 6 hours after birth, who were admitted to the neonatal intensive care unit of Shangqiu First People's Hospital in Henan Province from October 2021 to October 2023, were selected as the research objects. They were divided into the mild hypothermia group and the conventional treatment group according to the treatment method. The children in the conventional treatment group received conventional supportive treatment, while those in the mild hypothermia group were given head mild hypothermia treatment and conventional supportive treatment. Peripheral blood IL-6 and TNF-α were measured in all children at admission and 72 hours after treatment. Neonatal Behavioral Neurological Assessment (NBNA) scale scores were performed at 14 and 28 days after birth. Results: There was no significant difference in the levels of blood IL-6 and TNF-α in HIE children of the conventional treatment group 72 hours after treatment compared with those at admission (P &gt; 0.05). 2. The levels of blood IL-6 and TNF-α in HIE children of the mild hypothermia group 72 hours after treatment were significantly lower than those at admission (P &lt; 0.05). 3. 72 hours after treatment, the levels of blood IL-6 and TNF-α in moderate HIE children of the mild hypothermia group were significantly lower than those in moderate HIE children of the conventional treatment group (P &lt; 0.05). 4. 72 hours after treatment, the levels of blood IL-6 and TNF-α in severe HIE children of the mild hypothermia group were significantly lower than those in severe HIE children of the conventional treatment group (P &lt; 0.05). 5. At 14 and 28 days after birth, the NBNA scores of HIE children in the mild hypothermia group were significantly higher than those in the conventional treatment group (P &lt; 0.05). Conclusion Head mild hypothermia treatment for HIE children within 6 hours after birth has an obvious effect. Head mild hypothermia treatment can reduce the levels of serum IL-6 and TNF-α in HIE children, inhibit the indirect neurotoxic effect caused by the increase of IL-6 and TNF-α levels, play a role in brain protection, improve the NBNA score, and obtain a better prognosis.

The effect of melatonin administration on motor recovery after spinal cord injury in animal models: a systematic review and meta-analysis.

In this study, the effects of the antioxidant melatonin on motor function after spinal cord injury were investigated in preclinical studies. IRAN METHODS: The search strategy was designed based on keywords related to melatonin and spinal cord injury. The primary screening was based on title and abstract, and the secondary screening was based on the full text of the articles. After extracting data from the articles, statistical analysis was performed using STATA software. Standardized mean differences were used to analyze the results of the included studies. Subgroup analysis and quality control of articles were also performed. Based on the results of 29 separate experiments, melatonin showed a significant strong effect compared to the untreated group. The results showed that IP injection and multiple administrations days had the strong effect in the first three days as well as after 3-4 weeks. But more studies are needed to draw conclusions about its longer term effects. The analysis of MDA, SOD and GSH redox factors showed that the amount of MDA decreased and the amount of GSH increased in the treated animals. Also, the inflammatory factors IL-1Β and TNF-α as well as apoptosis and the rate of neuronal cell death, were reduced in animals that received melatonin, while the number of viable neurons was increased in melatonin treated animals. Melatonin is an antioxidant supplement, which can be considered for clinical trials in human SCI patients. IRAN University of medical sciences.

Evaluating the Efficacy of Gelatin-Chitosan-Tetraethyl Orthosilicate Calcium Hydroxide Composite as a Dental Pulp Medicament on COX-2, PGP 9.5, TNF-α Expression and Neutrophil number

Introduction Calcium hydroxide (Ca(OH)2) is the material of choice for pulp therapy. However, Ca(OH)2 has drawbacks such as toxicity, poor sealing, and tunnel defect formation. Alternative materials have been developed to provide more biocompatible materials with better dentin formation ability. The objective of this study was to evaluate the effect of composites containing gelatin (G), chitosan (CH), tetraethyl orthosilicate (TEOS), and Ca(OH)2, namely G-CH-TEOS-Ca (OH)2 (Extended data) on inflammation of the dental pulp (expression of COX-2, PGP 9.5, TNF-α, and neutrophil number). Materials and methods A total of 16 Wistar rat models of acute pulp injury were prepared and divided into two groups, treatment and control, 8 with each. In the treatment group, we applied a pulp-capping material using G-CH-TEOS-Ca (OH)2 and Ca(OH)2. On the 1st and 3rd days, rats were sacrificed. Tissue samples from 4 rats in each group were processed for histological preparation. COX-2, PGP 9.5, and TNF-α were observed using immunohistochemical (IHC) staining, and neutrophil numbers were observed using hematoxylin-eosin staining. Image analysis of COX-2, PGP 9.5, and TNF-α expression was performed using ImageJ software. Results The results showed a decrease significantly in COX-2 expression while PGP 9.5 and TNF-α expression were significantly higher than those in the control group. Neutrophil numbers were lower in the treatment group than in the control group, but the difference was not statistically significant. Conclusion The G-CH-TEOS-Ca (OH)2 composite material may have potential as an exposed pulp medicament by reducing mediator of inflammation (COX-2 expression) and increasing the regeneration factor (TNF-α expression) and nerve (PGP 9.5 expression).

The potential role of GLP-1 receptor agonists in osteoarthritis.

Osteoarthritis (OA) is the most common form of arthritis, affecting over 500 million people globally. Current treatments are primarily symptom-focused, with no approved therapies to halt disease progression. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), widely used in type 2 diabetes (T2D) and obesity, demonstrate significant weight loss and glucose-lowering effects and have been shown to possess anti-inflammatory properties. Given the central role of inflammation and metabolic dysfunction in OA, this review examines the potential utility of GLP-1 RAs in OA management, focusing on both indirect effects, such as weight reduction, and possible direct effects on inflammatory pathways and cartilage preservation. Clinical studies suggest that GLP-1 RAs may benefit people with OA by reducing weight, improving glycemic control, and modulating inflammatory markers relevant to OA progression. Notable findings include significant weight loss and pain reduction in people with knee OA (KOA) treated with semaglutide in the STEP-9 trial. In other studies, GLP-1 RAs have shown potential to lower oxidative stress and pro-inflammatory cytokines, such as tumor necrosis factor (TNF-α) and interleukin (IL)-6, with reductions in OA-related pain and functional impairment observed in some cohorts. However, results vary, with some studies showing limited effects, potentially linked to the degree of weight loss achieved. Although some studies report variability in pain relief, likely influenced by the degree of weight loss achieved, GLP-1 RAs have shown overall promise in reducing both OA symptoms and markers associated with disease progression. This emerging evidence supports the utility of GLP-1 RAs as a potential disease-modifying option for OA, offering a dual benefit in metabolic and joint health. Future research should focus on establishing the long-term efficacy and safety and elucidating the mechanism by which GLP-1 RAs influence OA pathology.