Search Results (7,396)

Brucella infection is associated with an increased risk of adverse obstetric outcomes in humans and animals. Decidualization, a process involving structural and functional changes in endometrial stromal cells, is essential for proper trophoblast implantation and placental development. Trophoblasts’ migration and their ability to invade the decidua and to undergo tubulogenesis, critical for proper implantation and placental development, are normally promoted by decidual cells. We evaluated whether Brucella infection of human endometrial stromal cells (T-HESC cell line) affects their ability to decidualize and to promote trophoblast functions. Infection of T-HESC cells with either B. abortus, B. suis, or B. melitensis resulted in deficient decidualization (as revealed by reduced prolactin levels) and an increased production of proinflammatory chemokines (C-X-C motif chemokine ligand 8 -CXCL8- and C-C motif chemokine ligand 2 -CCL2-) as compared to uninfected cells subjected to decidualization stimuli. In addition, conditioned media (CM) from infected decidualized T-HESC induced an inflammatory response (CXCL8, CCL2 and interleukin-6 -IL-6) in human trophoblasts (Swan-71 cell line) but reduced their ability to produce progesterone. Trophoblasts preincubated with this CM also had reduced migration, invasion, and tubulogenesis capacities, and this impairment was mediated, at least in part, by CXCL8 and CCL2. Moreover, infection of decidual stromal cells impaired the adhesion and spreading of blastocyst-like spheroids formed by Swan-71 cells. Brucella infection also affected the chemotactic capacity of decidual stromal cells for trophoblasts. Overall, these results suggest that Brucella infection of endometrial stromal cells impairs key processes required for successful implantation and placental development. Full article

Excessive alcohol consumption is associated with various health complications, including liver damage and systemic inflammation. Probiotic interventions have emerged as promising strategies to mitigate alcohol-induced harm, yet their mechanisms of action remain incompletely understood. This randomized, double-blind, placebo-controlled clinical trial aimed to evaluate the protective effects of Weizmannia coagulans BC179 in chronic alcohol consumers. Seventy participants with a history of long-term alcohol intake were randomly assigned to receive either BC179 (3 g/day, 1 × 10¹⁰ CFU) or a placebo for a 30-day intervention period. Following alcohol ingestion, dynamic monitoring of blood alcohol concentration (BAC), inflammatory and oxidative stress biomarkers, and serum metabolomic profiles was conducted. BC179 supplementation significantly reduced BAC and enhanced the activities of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), while decreasing levels of alkaline phosphatase (ALP), high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6). Conversely, the anti-inflammatory cytokine interleukin-10 (IL-10), superoxide dismutase (SOD), and glutathione (GSH) were significantly upregulated. Levels of cytochrome P4502E1 (CYP2E1) and malondialdehyde (MDA) were also markedly reduced. Metabolomic analysis revealed significant modulation of taurine and hypotaurine metabolism, as well as downregulation of caffeine-related pathways. Collectively, these findings indicate that W. coagulans BC179 alleviates alcohol-induced discomfort by enhancing alcohol metabolism, attenuating inflammation, reducing oxidative stress, and modulating key metabolic pathways. This probiotic strain may represent a promising adjunctive strategy for managing alcohol-related health issues. Full article

Inflammatory bowel diseases (IBDs), such as ulcerative colitis, and Crohn’s disease are chronic idiopathic inflammatory diseases of the gastrointestinal system involving interaction between genetic and environmental factors mediating the occurrence of oxidative stress and inflammation. There is no permanent cure for IBD except long-term treatment or surgery (resection of the intestine), and the available agents in the long term appear unsatisfactory and elicit numerous adverse effects. To keep the disease in remission, prevent relapses and minimize adverse effects of currently used medicines, novel dietary compounds of natural origin convincingly appear to be one of the important therapeutic strategies for the pharmacological targeting of oxidative stress and inflammation. Therefore, it is imperative to investigate plant-derived dietary agents to overcome the debilitating conditions of IBD. In the present study, the effect of α-Bisabolol (BSB), a dietary bioactive monoterpene commonly found in many edible plants as well as important components of traditional medicines, was investigated in acetic acid (AA)-induced colitis model in rats. BSB was orally administered to Wistar male rats at a dose of 50 mg/kg/day either for 3 days before or 30 min after induction of IBD for 7 days through intrarectal administration of AA. The changes in body weight, macroscopic and microscopic analysis of the colon and calprotectin levels in the colon of rats from different experimental groups were observed on day 0, 2, 4, and 7. The levels of myeloperoxidase (MPO), a marker of neutrophil activation, reduced glutathione (GSH) and malondialdehyde (MDA), a marker of lipid peroxidation, and the levels of pro-inflammatory cytokines were measured. AA caused a significant reduction in body weight and induced macroscopic and microscopic ulcers, along with a significant decline of endogenous antioxidants (superoxide dismutase (SOD), catalase, and GSH), with a concomitant increase in MDA level and MPO activity. BSB significantly improved the AA-induced reduction in body weight, colonic mucosal histology, inhibited MDA formation, and restored antioxidant levels along with a reduction in MPO activity. AA also induced the release of pro-inflammatory cytokines such as interleukin-1 (IL-1), interleukin-23 (IL-23) and tumor necrosis factor-α (TNF-α). Furthermore, AA also increased levels of calprotectin, a protein released by neutrophils under inflammatory conditions of the gastrointestinal tract. BSB treatment significantly reduced the release of calprotectin and pro-inflammatory cytokines. The findings of the present study demonstrate that BSB has the potential to improve disease activity and rescue colonic tissues from damage by inhibiting oxidative stress, lipid peroxidation and inflammation. The findings are suggestive of the benefits of BSB in IBD treatment and substantiate its usefulness in colitis management, along with its gastroprotective effects in gastric ulcer. Full article

Background and Objectives: Kumazasa extract (KZExt) is a food product obtained by steam extraction of Kumazasa (Sasa senanensis and Sasa kurilensis) leaves under high temperature and pressure. It contains abundant polyphenols, including trans-p-coumaric acid and ferulic acid, as well as xylooligosaccharides. In this study, we investigated the antibacterial, anti-viral, and anti-inflammatory effects of KZExt in vitro and in vivo. Materials and Methods: The anti-oxidant, antibacterial, and anti-viral effects of KZExt were assessed in vitro. Anti-oxidant activity was evaluated based on the scavenging of •OH, •O₂⁻ and ¹O₂. Antibacterial effects were assessed by determining the minimum inhibitory concentration (MIC) using a microdilution method. Anti-influenza activity was measured via plaque formation in MDCK cells. Anti-inflammatory effects were assessed by measuring interleukin (IL)-1β inhibition in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. In vivo, KZExt was administered once (30 min before) in a formalin-induced inflammation model to evaluate pain-related behavior. In the LPS-induced inflammation model, KZExt was administered for five days before LPS injection. Behavioral changes and cytokine levels were assessed 24 h later via the open field test and cytokine quantification. Results: In vitro, KZExt showed antibacterial, anti-influenza, and anti-oxidant effects, and suppressed LPS-induced IL-1β production. In vivo, it significantly reduced the second phase of formalin-induced pain behavior. In the LPS model, although behavioral changes were unaffected, KZExt suppressed IL-6 and interferon-γ production. Conclusions: The antibacterial, anti-viral, and anti-inflammatory effects of KZExt were confirmed in vitro and in vivo. Notably, the anti-inflammatory effect suggests potential immunomodulatory activity. These findings indicate that KZExt may help suppress smoldering inflammation and inflammation associated with various diseases through its combined antibacterial, anti-viral, and immunomodulatory actions. Full article

Lidocaine exhibited anti-inflammatory and immunomodulatory properties. This study aimed to investigate the anti-inflammatory effects of the lidocaine-derived analogs, EI137 and EI341, in a Staphylococcal enterotoxin B (SEB)-induced chronic rhinosinusitis (CRS). A CRS model was established using BALB/c mice via intranasal instillation of SEB. EI137 and EI341 were administered intranasally at 0.5 μg/g and 5 μg/g, respectively. Nasal symptoms and interleukin (IL)-4, IL-10, interferon (IFN)-γ, and tumor necrosis factor (TNF)-α levels in the nasal lavage fluid (NLF) were assessed. The reverse-transcription polymerase chain reaction was used to identify IFN-γ, IL-4, IL-10, and their transcription factors in the sinonasal mucosa. Histological changes were performed to assess inflammatory cell infiltration, epithelial thickness, and mucus-producing cells. SEB induced significant increases in IL-4, IL-10, and TNF-α levels in NLF and sinonasal mucosa, along with marked inflammatory cell infiltration. Intranasal EI137 and EI341 administration significantly reduced Th2 cytokine and its transcription factor, inflammatory cell infiltration, and mucus-producing cell numbers in the sinonasal mucosa. Further, EI137 suppressed Th1 cytokines, whereas EI341 enhanced Th1 responses. Both compounds promoted regulatory T cell responses, as evidenced by increased IL-10 and Foxp3 mRNA expression. EI137 and EI341 demonstrated potent local anti-inflammatory effects in a SEB-induced CRS model by modulating Th2 and Treg responses. EI137 suppressed Th1 inflammation, whereas EI341 enhanced it. These results indicate that EI137 and EI341 are promising topical agents for Th2-dominant inflammatory diseases, with distinct effects on Th1 immune responses. Full article

Lipophenols, combining phenolic and lipid moieties in a single molecule, are valuable candidates for providing enhanced bioactive properties with therapeutic potential, including anti-inflammatory functions associated with immune-mediated diseases such as intestinal bowel disease (IBD). Thus, palmitoyl–epigallocatechin gallate (PEGCG), a lipophilic derivative of epigallocatechin gallate (EGCG), has been highlighted for its enhanced stability in lipid-rich environments and bioavailability due to improved cellular uptake. However, the contribution of lipophilic esterification to PEGCG’s capacity to inhibit inflammation and the development of harmful autoimmune responses remains underexplored. This work uncovered the differential efficiency of EGCG and its palmitoyl derivative in modulating, in vitro, the interleukin profile generated by intestinal epithelium under inflammatory conditions. Therefore, both could attenuate the immune response by lowering macrophage migration and polarisation towards pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes. While the fatty acid moiety gave PEGCG a functional advantage over EGCG in adjusting the interleukin-based response of intestinal epithelium to inflammation—since both of them decreased, to a similar extent, the expression of pro-inflammatory interleukins, namely IL-6, IL-17, IL-18, IL-23, and TNF-α (which lowered by 11.2%, on average)—the former was significantly more efficient in cushioning the increase in IL-1β and IL-12p70 (by 9.2% and 10.4%, respectively). This immune modulation capacity did not significantly impact the migration and expression of costimulatory molecules featuring M1 (CD86⁺) or M2 (CD206⁺) phenotypes by THP-1-derived macrophages, for which both bioactive compounds exhibited equivalent efficiency. Nonetheless, the analysis of the pro- and anti-inflammatory interleukins secreted by differentiated macrophages allowed the identification of an advantage for PEGCG, which decreased the expression of the pro-inflammatory immune mediators IL-1β and IL-12p70, IL-23, and TNF-α more efficiently. These results suggest that lipophilisation of phenolic compounds presents exciting potential for extending their application as functional molecules by combining the effects of their polar head with their ability to interfere with membranes, conveyed by their lipophilic tail. In addition, the enhanced reactivity would confer a higher capacity to interact with cellular signalling molecules and thus inhibit or attenuate the immune response, which is of special interest for preventing the onset and severity of immune-mediated pathologies such as IBD. Full article

Glaesserella parasuis (GPS) is a Gram-negative, pathogenic bacterium that colonizes the upper respiratory tract of piglets and causes Glässer’s disease with peritonitis under stress conditions. The mechanism underlying GPS-induced peritonitis in piglets remains unclear. Baicalin is one of the main active ingredients of Huangqin (Scutellaria baicalensis), which has a significant anti-inflammatory effect on inflammatory diseases. Therefore, this study aimed to elucidate the molecular mechanism by which baicalin alleviates GPS-induced peritonitis in piglets, specifically focusing on the role of the ADAM17/EGFR signaling axis. We investigated the effects of baicalin in vitro using porcine peritoneal mesothelial cells (PPMCs) and in vivo in GPS-infected piglets. Our results showed that baicalin reduced the expression of the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) in PPMCs and the peritoneum of piglets after GPS infection. Concurrently, baicalin significantly reduced the upregulation of disintegrin and metalloproteinase 17 (ADAM17), phosphorylated epidermal growth factor receptor (p-EGFR)/EGFR, and phosphorylated extracellular signal-regulated kinase (p-ERK)/ERK induced by GPS infection in PPMCs and the peritoneum of piglets. Crucially, in vitro mechanistic investigations revealed that baicalin can significantly reduce the upregulation of ADAM17, p-EGFR/EGFR, p-ERK/ERK, TNF-α, IL-1β, and IL-6 induced by ADAM17 overexpression in PPMCs. Furthermore, ADAM17 small interfering RNA can significantly reduce the upregulation of ADAM17, p-EGFR/EGFR, p-ERK/ERK, TNF-α, IL-1β, and IL-6 induced by GPS infection in PPMCs. These findings demonstrate that baicalin can inhibit the expression of inflammatory factors TNF-α, IL-1β, and IL-6 through the ADAM17/EGFR axis, and then alleviate the peritonitis caused by GPS in piglets. This provides a theoretical basis for developing novel non-antibiotic strategies, including phytochemical therapeutics and feed additives, for preventing and controlling GPS. Full article

Insulin resistance is a key driver of metabolic disorders, including type 2 diabetes and non-alcoholic fatty liver disease (NAFLD), progressing to non-alcoholic steatohepatitis (NASH). This study investigated the effects of geniposide (GP) on insulin sensitivity and hepatic fibrosis in a high-fat diet (HFD)-induced NASH model. C57BL/6 mice were fed an HFD for five weeks and subsequently divided into normal chow (NC), HFD, HFD with GP 50 mg/kg (GP50), and HFD with GP 100 mg/kg (GP100) groups. The treatments were administered orally for 12 weeks. GP treatment significantly reduced body weight as well as epididymal fat and liver weights, while no differences were observed in food intake. Improvements in glucose and lipid metabolism were observed in oral glucose tolerance tests, homeostatic model assessment of insulin resistance (HOMA-IR), and blood lipid profiles. Histological analyses revealed that GP suppressed adipocyte hypertrophy and hepatic lipid accumulation and hepatic fibrosis. To further elucidate molecular mechanisms of GP, quantitative real-time polymerase chain reaction (qRT-PCR) analysis was conducted in the liver tissue. GP downregulated expression of inflammatory markers, including F4/80, tumor necrosis factor (TNF)-α, and interleukin (IL)-6. GP treatment modulated genes involved in insulin signaling including Janus kinase 2 (JAK2), insulin receptor (INSR), insulin receptor substrate 2 (IRS-2), and protein kinase B (AKT1) gene expression levels. This suggests GP suppresses inflammation and mitigates insulin resistance by activating the INSR–IRS2–Akt pathway. Additionally, GP enhanced adenosine monophosphate-activated protein kinase (AMPK) expression, suggesting its potential role in improving glucose and lipid metabolism. In conclusion, GP improves insulin resistance, inflammation, and hepatic fibrosis, highlighting its therapeutic potential for NASH and related metabolic disorders. Full article

Myopia is one of the major public health conditions with significant complications. This study investigates the role of transforming growth factor (TGF)-β2, complement activation, and inflammasome pathways in myopia progression using a Brown Norway rat model. Myopia was induced, and complement regulation was manipulated using gene therapy via adeno-associated virus (AAV) vectors delivering CD55 or CD55 siRNA. Results showed that TGF-β2 exacerbated myopia by upregulating complement components C3 and C5, suppressing CD55, and activating inflammasome pathways through nuclear factor (NF)-κB signaling, leading to axial elongation and increased refractive errors. Overexpression of CD55 via AAV gene therapy effectively counteracted these effects, reducing axial length elongation and inflammation by suppressing inflammasome markers interleukin (IL)-1β and NLR family pyrin domain containing 3 (NLRP3), as confirmed by real-time quantitative PCR and immunofluorescence analyses. Conversely, silencing CD55 intensified TGF-β2-induced effects, further promoting axial elongation and inflammation. These findings highlight the critical role of CD55 in modulating TGF-β2-driven complement and inflammasome activation during myopia progression. The study suggests that gene therapy targeting CD55 could serve as a novel therapeutic strategy to mitigate myopia and related inflammatory processes, offering a promising avenue for managing this significant public health challenge. Full article

Inflammatory bowel disease (IBD) and primary sclerosing cholangitis (PSC) are chronic immune-mediated inflammatory diseases (IMIDs) that affect the gastrointestinal and hepatobiliary systems. They are characterized by persistent inflammation, potentially progressive fibrosis, and an elevated risk of developing cholangiocarcinoma and colorectal cancer. IBD and PSC share phenotypical, genetic, and immunological features, largely due to the central role of immune cell dysregulation. Despite their increasing global prevalence, the underlying drivers remain poorly understood, and effective treatment options are still lacking. Efforts towards an improved comprehension of their pathogenic mechanisms are therefore pivotal. Emerging evidence highlights the role of canonical ASC-dependent inflammasomes—multiprotein bioactive Interleukin (IL)-1-producing complexes of the innate immune system—and serum amyloid A (SAA) as key structures of gastrointestinal and hepatobiliary inflammation, tissue remodeling, stromal crosstalk, and fibrosis. In this review, we explore immunological connections and analogies between IBD and PSC, highlighting the converging roles of canonical ASC-dependent inflammasomes, the IL-1 superfamily, SAA, and sustained gut microbiota-driven chronic inflammation in disease pathology and their surging potential as therapeutic targets across the gut–liver axis. Full article

Spinal health depends on the dynamic interplay between mechanical forces, biochemical signaling, and cellular behavior. This review explores how key molecular pathways, including integrin, yeas-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), Piezo, and Wingless/Integrated (Wnt) with β-catenin, actively shape the structural and functional integrity of spinal tissues. These signaling mechanisms respond to physical cues and interact with inflammatory mediators such as interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α), driving changes that lead to disc degeneration, vertebral fractures, spinal cord injury, and ligament failure. New research is emerging that shows scaffold designs that can directly harness these pathways. Further, new stem cell-based therapies have been shown to promote disc regeneration through targeted differentiation and paracrine signaling. Interestingly, many novel bone and ligament scaffolds are modulating anti-inflammatory signals to enhance tissue repair and integration, as well as prevent scaffold degradation. Neural scaffolds are also arising. These mimic spinal biomechanics and activate Piezo signaling to guide axonal growth and restore motor function. Scientists have begun combining these biological platforms with brain–computer interface technology to restore movement and sensory feedback in patients with severe spinal damage. Although this technology is not fully clinically ready, this field is advancing rapidly. As implantable technology can now mimic physiological processes, molecular signaling, biomechanical design, and neurotechnology opens new possibilities for restoring spinal function and improving the quality of life for individuals with spinal disorders. Full article

Mistletoe (Viscum album L.) has been used in complementary cancer therapy for decades, but its mechanisms remained poorly understood until recently. This review synthesizes transformative advances in mistletoe cancer research from 2020 to 2025, focusing on newly discovered molecular mechanisms, immunomodulatory properties, and clinical applications. We conducted a comprehensive analysis of controlled studies, mechanistic investigations, and real-world evidence published between 2020 and 2025. The discovery of mistletoe-induced immunogenic cell death (ICD) represents a paradigm shift in understanding its anticancer effects. Mistletoe extracts trigger endoplasmic reticulum stress, leading to calreticulin exposure in 18–51% of cancer cells and a 7-fold increase in adenosine triphosphate (ATP) release. Three-dimensional culture models revealed enhanced macrophage reprogramming effects, with a 15.8% increase in pro-inflammatory interleukin (IL)-6 and a 26.4% reduction in immunosuppressive IL-10. Real-world evidence from over 400 non-small-cell lung cancer patients shows that combining mistletoe with programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) inhibitors doubles median overall survival (6.8 to 13.8 months), with biomarker-selected populations experiencing up to a 91.2% reduction in death risk. The Johns Hopkins Phase I trial established intravenous administration safety at 600 mg three times weekly. Advanced analytical approaches including metabolomics, chronobiology, and machine learning are enabling precision medicine applications. These findings position mistletoe as a scientifically validated component of integrative oncology, bridging traditional medicine with evidence-based cancer care. Future research should focus on ferroptosis mechanisms, single-cell immune profiling, and standardized clinical protocols. Full article

Toxoplasma gondii is a globally distributed protozoan parasite and a major cause of congenital infections, particularly in South America. Current therapies for congenital toxoplasmosis are limited by toxicity, long treatment regimens, and suboptimal efficacy, highlighting the urgent need for safer and more effective alternatives. In this study, we evaluated the antiparasitic effects of crude ethanolic extract of Brazilian Red Propolis (BRP) and its isolated compounds, focusing on 7-O-methylvestitol, in human trophoblast (BeWo) cells and third-trimester placental explants. Both BRP and 7-O-methylvestitol significantly reduced T. gondii adhesion, invasion, and intracellular replication, without compromising host cell viability. Ultrastructural analyses revealed irreversible parasite damage, and cytokine profiling demonstrated immunomodulatory effects, with enhanced production of interleukin (IL)-6, IL-8, and macrophage migration inhibitory factor (MIF) in BeWo cells and downregulation of IL-6, MIF, and tumor Necrosis Factor (TNF) in infected placental villi. Notably, 7-O-methylvestitol reproduced and, in some assays, surpassed the antiparasitic activity of BRP, suggesting it as a key bioactive constituent responsible for the therapeutic potential of the extract. These findings support the identification of 7-O-methylvestitol as a promising lead compound for structure-based drug design and repositioning strategies, advancing the development of novel, safe, and targeted therapies against congenital toxoplasmosis. Full article

Inflammatory bowel disease (IBD) is a relapsing–remitting condition resulting in chronic inflammation of the gastrointestinal tract. Present methods are either inadequate or not viable for continuous tracking of disease progression in individuals. In this study, we present the development towards an implantable biosensor for detecting interleukin-6 (IL-6), an important cytokine implicated in IBD. The optimised sensor design includes a gold surface functionalised with a known IL-6-specific aptamer, integrating a recognition sequence and an electrochemical redox probe. The IL-6 aptasensor demonstrated a sensitivity of up to 40% and selectivity up to 10% to the IL-6 target in vitro. Sensors were found to degrade over 7 days when exposed to recombinant IL-6, with the degradation rate rapidly increasing when exposed to intestinal mucosa. A feasibility in vivo experiment with a newly designed implantable gut sensor array confirmed rapid degradation over a 5-h implantation period. We achieved up to a 93% reduction in sensor degradation rates, with a polyvinyl alcohol–methyl acrylate hydrogel coating that aimed to reduce nonspecific interactions in complex analytes compared to uncoated sensors. Degradation was linked to desorption of the monolayer leading to breakage of gold thiol bonds. While there are key challenges to be resolved before a stable implantable IBD sensor is realised, this work highlights the potential of aptamer-based biosensors as effective tools for long-term diagnostic monitoring in IBD. Full article

Artemin is a neurotrophic factor that belongs to the four-member family of Glial-derived growth factors. This study aims to investigate changes in artemin correlated with anxiety and depression-like behaviors in a neuroinflammation rodent model. In adult male Wistar rats, neuroinflammation was established through administration of 2 mg/kg LPS. Anxiety-like behaviors and locomotor activity were evaluated by the open field test. The sucrose preference test and the splash test analyzed depression-like behaviors. Tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and artemin levels were measured in the prefrontal cortex, striatum, and serum. In the neuroinflammation group, rearing, total distance traveled, time spent in the central region, and sucrose solution consumption decreased in the open-field test (p < 0.0001). Grooming time and frequency were shortened, and grooming latency was prolonged in the neuroinflammation group (p < 0.0001). TNF-α was significantly increased in the prefrontal cortex (p < 0.05) and striatum (p < 0.01). lL-1β did not change between groups (p > 0.05). Artemin levels decreased in the prefrontal cortex and striatum (p < 0.05). No difference was observed in serum artemin levels; however, artemin levels of brain regions were higher than those in the serum. An increase in anxiety–depression-like behaviors has accompanied decreased levels of artemin in the brain. Artemin may be a target molecule in psychiatric disorders. Further studies are needed to examine the role of artemin in neuropsychiatric disorders. Full article