Selection of Solvent and Positive Control Concentration for Enhanced Ames Test Conditions for N-Nitrosamine Compounds.

The Ames test is a widely used bacterial mutagenicity assay to evaluate the potential of chemical compounds to induce mutations. In recent years, there has been growing concern regarding the presence of N-nitrosamines in pharmaceuticals, food, and other consumer products. N-Nitrosamines are probable mutagens and carcinogens. To address the reduced sensitivity of the standard Ames test for N-nitrosamines, particularly N-nitrosodimethylamine, the European Medicines Agency (EMA) and United States Food and Drug Administration (FDA) have recently published recommendations for enhanced Ames test (EAT) conditions. However, there is a lack of clear guidance on the selection of N-nitrosamine positive control concentrations, particularly for 1-cyclopentyl-4-nitrosopiperazine, and the amount of solvent to be used in the EAT. This study aims to address the current gap in concentration and volume specifications by providing a comprehensive guide to set up enhanced Ames test conditions specifically for N-nitrosamine compounds using appropriate amounts of solvent, new solvents, and strain-specific positive control concentrations.

RNA-Seq analysis of human heart tissue reveals SARS-CoV-2 infection and inappropriate activation of the TNF-NF-κB pathway in cardiomyocytes.

The negative impact of SARS-CoV-2 virus infection on cardiovascular disease (CVD) patients is well established. This research article explores the cellular pathways involved in underlying heart diseases after infection. The systemic inflammatory response to SARS-CoV-2 infection likely exacerbates this increased cardiovascular risk; however, whether the virus directly infects cardiomyocytes remains unknown due to limited multi-omics data. While public transcriptome data exists for COVID-19 infection in different cell types (including cardiomyocytes), infection times vary between studies. We used available RNA-seq data from human heart tissue to delineate SARS-CoV-2 infection and heart failure aetiology specific gene expression signatures. A total of fifty-four samples from four studies were analysed. Our aim was to investigate specific transcriptome changes occurring in cardiac tissue with SARS-CoV-2 infection compared to non-infected controls. Our data establish that SARS-CoV-2 infects cardiomyocytes by the TNF-NF-κB pathway, potentially triggering acute cardiovascular complications and increasing the long-term cardiovascular risk in COVID-19 patients.

Establishment of reference intervals of haematology and biochemistry analytes in ICR mice of different ages.

Outbred stocks of mice are widely used in pre-clinical research as these animals possess a diversified genetic background when compared with inbred strains of mice. It is crucial to assess particular alterations in the physiological and functional profiles of laboratory animals using haematological and biochemical indicators. These values can also differ between laboratories because they are influenced by many different factors. We aimed to provide normal values and reference intervals for selected haematology and biochemistry analytes of 570 ICR mice at three different ages: 6-8 weeks, 10-14 weeks and 6-9 months. Reference values were calculated by non-parametric methods. For comparisons between sexes, the independent-sample t-test and Mann-Whitney test were employed, and analysis of variance was used for age differences. The findings of the study revealed age-related declines in haemoglobin concentration, haematocrit, mean corpuscular volume and mean corpuscular haemoglobin concentrations. Mice aged 6-9 months had statistically higher platelet counts in their blood than mice of other ages. The white blood cell count had a significant age effect and progressively decreased with age. As mice get older, the percentage of neutrophils, monocytes and basophils increases, but the percentage of lymphocytes decreases. For the biochemical values, age-related significant differences in glucose, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and albumin concentrations were found. It was also found that creatinine concentrations were comparable across all age ranges. The values presented in the present work can be used as a reference to interpret clinical pathology data for other studies and to evaluate health status.

Comparative Evaluation of Survival Rate Gingival Health and Patient's Acceptance of Conventional Band and Loop and Prefabricated Band and Loop in Primary Teeth: An In Vivo Study.

Aim: To compare and evaluate the survival rate, gingival health, and patient acceptance of traditional band and loop (B&L) and company-made B&L space maintainers in deciduous teeth-an in vivo study. Materials and methods: A total of 50 patients between 4 and 9 years of age-group, having loss of deciduous first molar in any of the arches, were included in the present study, which was divided into two groups. Group I consisted of the conventional B&L group, and group II consisted of the prefabricated B&L group. Results: The two groups showed no statistical significance in the 1st month, 3rd month, and 6th month in cement loss, failure of soldering, distortion of B&L fracture. The survival rate for the conventional group was 92%, whereas for prefabricated group was 100% at 6 months of follow-up. Company-made B&L showed significantly better gingival health (p = 0.004) at 6 months of follow-up and a better patient's acceptance rate. Conclusion: Prefabricated B&L appliances are newly developed space maintainers that are superior to conventional B&L appliances as they have a higher success rate and are more rational in design. How to cite this article: Dutta S, Gupta S, Tripathi P, et al. Comparative Evaluation of Survival Rate Gingival Health and Patient's Acceptance of Conventional Band and Loop and Prefabricated Band and Loop in Primary Teeth: An In Vivo Study. Int J Clin Pediatr Dent 2024;17(S-1):S73-S77.

Prolyl hydroxylase inhibitor desidustat attenuates autoimmune hemolytic anemia in mice.

Autoimmune hemolytic anemia (AIHA) is a heterogeneous group of diseases mediated by autoantibody directed against RBCs causing hemolysis and anemia. AIHA develops rapidly or over time, depending on the triggering factor. Desidustat is a prolyl hydroxylase inhibitor clinically used for the treatment of chronic kidney disease (CKD)-induced anemia. In this study, we investigated the effect of desidustat in preclinical model of AIHA. We used rat RBC for induction of AIHA in mice. These mice were then treated with desidustat (15 mg/kg, PO, once a day) for eight weeks. Desidustat treatment increased hemoglobin, RBC and hematocrit and decreased WBC and lymphocytes. This treatment suppressed serum LDH, oxidative stress in RBCs, antibody titer and antibody deposition on RBC surface, and increased RBC lifespan. Serum and spleen iron along with spleen mass and oxidative stress were decreased by desidustat. Bone marrow iron was increased and expression of CD71 (cell surface marker for early erythroid progenitor) and TER-119 (cell surface marker for late erythroid progenitor) in bone marrow were found to be elevated by desidustat by treatment. This treatment also suppressed deposition of membrane-bound antibody in late erythroid cells. The treatment showed reduction in total splenic cells, CD71 and TER-119 positive cells in the spleen. Thus, desidustat treatment increased erythropoiesis, early maturation of bone marrow erythroid cells having longer RBC life span due to decrease in the antibody-mediated lysis of RBCs and its progenitors leading to reduced oxidative stress. Thus, desidustat can be a good therapeutic option for treatment of AIHA.

Apigenin-6-C-glucoside ameliorates MASLD in rodent models via selective agonism of adiponectin receptor 2.

Adiponectin plays key roles in energy metabolism and ameliorates inflammation, oxidative stress, and mitochondrial dysfunction via its primary receptors, adiponectin receptors -1 and 2 (AdipoR1 and AdipoR2). Systemic depletion of adiponectin causes various metabolic disorders, including MASLD; however adiponectin supplementation is not yet achievable owing to its large size and oligomerization-associated complexities. Small-molecule AdipoR agonists, thus, may provide viable therapeutic options against metabolic disorders. Using a novel luciferase reporter-based assay here, we have identified Apigenin-6-C-glucoside (ACG), but not apigenin, as a specific agonist for the liver-rich AdipoR isoform, AdipoR2 (EC50: 384 pM) with >10000X preference over AdipoR1. Immunoblot analysis in HEK-293 overexpressing AdipoR2 or HepG2 and PLC/PRF/5 liver cell lines revealed rapid AMPK, p38 activation and induction of typical AdipoR targets PGC-1α and PPARα by ACG at a pharmacologically relevant concentration of 100 nM (reported cMax in mouse; 297 nM). ACG-mediated AdipoR2 activation culminated in a favorable modulation of key metabolic events, including decreased inflammation, oxidative stress, mitochondrial dysfunction, de novo lipogenesis, and increased fatty acid ß-oxidation as determined by immunoblotting, QRT-PCR and extracellular flux analysis. AdipoR2 depletion or AMPK/p38 inhibition dampened these effects. The in vitro results were recapitulated in two different murine models of MASLD, where ACG at 10 mg/kg body weight robustly reduced hepatic steatosis, fibrosis, proinflammatory macrophage numbers, and increased hepatic glycogen content. Together, using in vitro experiments and rodent models, we demonstrate a proof-of-concept for AdipoR2 as a therapeutic target for MASLD and provide novel chemicobiological insights for the generation of translation-worthy pharmacological agents.

State-of-the-Art and New Treatment Approaches for Spinal Cord Tumors.

Spinal cord tumors, though rare, present formidable challenges in clinical management due to their intricate nature. Traditional treatment modalities like surgery, radiation therapy, and chemotherapy have been the mainstay for managing these tumors. However, despite significant advancements, challenges persist, including the limitations of surgical resection and the potential side effects associated with radiation therapy. In response to these limitations, a wave of innovative approaches is reshaping the treatment landscape for spinal cord tumors. Advancements in gene therapy, immunotherapy, and targeted therapy are offering groundbreaking possibilities. Gene therapy holds the potential to modify the genes responsible for tumor growth, while immunotherapy harnesses the body's own immune system to fight cancer cells. Targeted therapy aims to strike a specific vulnerability within the tumor cells, offering a more precise and potentially less toxic approach. Additionally, novel surgical adjuncts are being explored to improve visualization and minimize damage to surrounding healthy tissue during tumor removal. These developments pave the way for a future of personalized medicine for spinal cord tumors. By delving deeper into the molecular makeup of individual tumors, doctors can tailor treatment strategies to target specific mutations and vulnerabilities. This personalized approach offers the potential for more effective interventions with fewer side effects, ultimately leading to improved patient outcomes and a better quality of life. This evolving landscape of spinal cord tumor management signifies the crucial integration of established and innovative strategies to create a brighter future for patients battling this complex condition.

HIF Stabilizer Desidustat Protects against Complement-Mediated Diseases.

Complement cascade is a defence mechanism useful for eliminating pathogenic microorganisms and damaged cells. However, activation of alternative complement system can also cause inflammation and promote kidney and retinal disease progression. Inflammation causes tissue hypoxia, which induces hypoxia-inducible factor (HIF) and HIF helps the body to adapt to inflammation. In this study, we investigated the effect of HIF stabilizer desidustat in complement-mediated diseases. Oral administration of desidustat (15 mg/kg) was effective to reduce the kidney injury in mice that was induced by either lipopolysaccharide (LPS), doxorubicin or bovine serum albumin (BSA)-overload. Complement activation-induced membrane attack complex (MAC) formation and factor B activity were also reduced by desidustat treatment. In addition, desidustat was effective against membranous nephropathy caused by cationic BSA and retinal degeneration induced by sodium iodate in mice. C3-deposition, proteinuria, malondialdehyde, and interleukin-1ß were decreased and superoxide dismutase was increased by desidustat treatment in cBSA-induced membranous nephropathy. Desidustat specifically inhibited alternative complement system, without affecting the lectin-, or classical complement pathway. This effect appears to be mediated by inhibition of factor B. These data demonstrate the potential therapeutic value of HIF stabilization by desidustat in treatment of complement-mediated diseases.

A novel selective NLRP3 inhibitor shows disease-modifying potential in animal models of Parkinson's disease.

Pathological activation of the Nod-like receptor family pyrin domain containing protein 3 (NLRP3) inflammasome signaling underlies many autoimmune and neuroinflammatory conditions. Here we report that, a rationally designed, novel, orally active, selective NLRP3 inflammasome inhibitor, Usnoflast (ZYIL1), showed potent inhibition of ATP, Nigericin and monosodium urate-mediated interleukin (IL)-1ß release in THP-1 cells and human PBMC. In isolated microglia cells, the IC50 of ZYIL1 mediated inhibition of IL-1ß was 43 nM. ZYIL1 displayed good pharmacokinetic profile in mice, rats and primates after oral administration and the concentrations found in the brain and cerebrospinal fluid (CSF) were markedly higher than the IC50 values. In an in vivo model of neuroinflammation, ZYIL1 demonstrated robust suppression of NLRP3 inflammasome activation and IL-1ß upon oral administration. This translated into efficacy in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-Hydroxydopamine (6-OHDA)-induced Parkinson's disease (PD) models in mice. In MPTP and/or 6-OHDA models, treatment with ZYIL1 ameliorated motor deficits, degeneration of nigrostriatal dopaminergic neurons and abnormal accumulation of α-synuclein. There were positive changes in the genes related to walking, locomotor activity, neurogenesis, neuroblast proliferation and neuronal differentiation in the PD brain indicating improvement in neural health which translated into improved mobility. These findings clearly indicate that selective NLRP3 inhibitor ZYIL1, ameliorates neuroinflammation and appears to have the potential for disease modification and progression associated with PD.

Discovery of aminopiperidine based potent & novel topoisomerase inhibitor with broad spectrum anti-bacterial activity.

Bacterial DNA gyrase and topoisomerase IV inhibition has emerged as a promising strategy for the cure of infections caused by antibiotic-resistant bacteria. The Novel Bacterial Topoisomerase Inhibitors (NBTIs) bind to a different site from that of the quinolones with novel mechanism of action. This evades the existing target-mediated bacterial resistance associated with quinolones. This article presents our efforts to identify in vitro potent and broad-spectrum antibacterial agent 4l.

Correction: Jain et al. Proteomic Approach for Comparative Analysis of the Spike Protein of SARS-CoV-2 Omicron (B.1.1.529) Variant and Other Pango Lineages. Proteomes 2022, 10, 34.

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Safety Assessment of a Novel Intravenous Diclofenac Sodium Formulation Following 28-Day Repeated Administration in Wistar Rats.

These toxicity studies aimed to assess the safety and tolerability of a novel intravenous diclofenac sodium (37.5 mg/mL) formulation containing povidone K12 (80 mg/mL) as the key excipient in Wistar rats. This formulation was tested at doses of 3, 7, and 15 mg/kg/day and was administered daily for 28 days by intravenous route. Toxicokinetic estimation revealed a dose-proportional increase in plasma exposure to diclofenac. The formulation was well tolerated in males; however, mortality was observed in females (2/15) at the highest dose (15 mg/kg/day). Adverse gastrointestinal events related to NSAIDS and a few other treatment-related effects on clinical and anatomic pathology were noted at the 15 mg/kg/day dose, which normalized at the end of the 2-week recovery period. In addition, the excipient povidone K12 was present in a higher amount than the approved Inactive Ingredient Database (IID) limit in the proposed novel formulation. It was qualified through a separate 28-day repeated dose toxicity study by intravenous route in Wistar rats. Povidone K12 was found to be well tolerated and safe up to a dose of 165 mg/kg/day. No treatment-related adverse effects were observed in this study. In conclusion, repeated administration of a novel intravenous formulation containing diclofenac sodium was found to be safe up to the dose of 7 mg/kg/day in female rats and 15 mg/kg/day in male rats.

Comparative evaluation of clinical success of Stainless Steel and Bioflx crowns in primary molar - A 12 month split mouth prospective randomized clinical trial.

PURPOSE: The purpose of this clinical trial was to assess and compare the clinical outcomes of Bioflx crowns (BFCs) with stainless steel crowns (SSCs) in primary molars (PMs). MATERIALS AND METHODS: This prospective split-mouth randomized controlled clinical trial was conducted between March 2022 and June 2023. Thirty-eight patients (17 females and 21 males) with a mean age of 5.21 years participated in this study. Each child (n = 38) received both SSC and BFC. Clinical and radiographic follow-up was performed at baseline, 3, 6, and 12 months using the modified United States Public Health System scoring criteria to evaluate various parameters. RESULTS: At the 3 and 6 months' follow-up, no significant difference was observed between the two groups. However, at 1-year follow-up, a statistically significant difference (P < 0.05) was evident in the frequency between the two groups for the criteria of crown retention after cementation and anatomic form of the crown, indicating a preference for SSC over prototype 1 BFC. CONCLUSION: The 12-month results indicate that BFC performed similarly to the established SSC for the restoration of PMs providing better esthetics.

Unveiling stress markers: A systematic review investigating psychological stress biomarkers.

Psychological stress is a ubiquitous facet of modern life, impacting individuals across diverse contexts and demographics. Understanding its physiological manifestations through biomarkers has gained substantial attention within the scientific community. A comprehensive search was conducted across multiple databases for peer-reviewed articles published within the past decade. Preliminary findings reveal many biomarkers associated with psychological stress across different biological systems, including the hypothalamic-pituitary-adrenal axis, immune system, cardiovascular system, and central nervous system. This systematic review explores psychological, physiological, and biochemical biomarkers associated with stress. Analyzing recent literature, it synthesizes findings across these three categories, elucidating their respective roles in stress response mechanisms. Psychological markers involve subjective assessments like self-reported stress levels, perceived stress scales, or psychometric evaluations measuring anxiety, depression, or coping mechanisms. Physiological markers include heart rate variability, blood pressure, and immune system responses such as cytokine levels or inflammatory markers. Biochemical markers involve hormones or chemicals linked to stress. It includes cortisol, catecholamines, copeptin, salivary amylase, IL-6, and C-reactive protein.

Network pharmacology-based approach to elucidate the pharmacologic mechanisms of natural compounds from Dictyostelium discoideum for Alzheimer's disease treatment.

Alzheimer's disease (AD) is increasingly becoming a major public health concern in our society. While many studies have explored the use of natural polyketides, alkaloids, and other chemical components in AD treatment, there is an urgent need to clarify the concept of multi-target treatment for AD. This study focuses on using network pharmacology approach to elucidate how secondary metabolites from Dictyostelium discoideum affect AD through multi-target or indirect mechanisms. The secondary metabolites produced by D. discoideum during their development were obtained from literature sources and PubChem. Disease targets were selected using GeneCards, DisGeNET, and CTD databases, while compound-based targets were identified through Swiss target prediction and Venn diagrams were used to find intersections between these targets. A network depicting the interplay among disease, drugs, active ingredients, and key target proteins (PPI network) was formed utilizing the STRING (Protein-Protein Interaction Networks Functional Enrichment Analysis) database. To anticipate the function and mechanism of the screened compounds, GO and KEGG enrichment analyses were conducted and visually presented using graphs and bubble charts. After the screening phase, the top interacting targets in the PPI network and the compound with the most active target were chosen for subsequent molecular docking and molecular dynamic simulation studies. This study identified nearly 50 potential targeting genes for each of the screened compounds and revealed multiple signaling pathways. Among these pathways, the inflammatory pathway stood out. COX-2, a receptor associated with neuroinflammation, showed differential expression in various stages of AD, particularly in pyramidal neurons during the early stages of the disease. This increase in COX-2 expression is likely induce by higher levels of IL-1, which is associated with neuritic plaques and microglial cells in AD. Molecular docking investigations demonstrated a strong binding interaction between the terpene compound PQA-11 and the neuroinflammatory receptor COX2, with a substantial binding affinity of -8.4 kcal/mol. Subsequently, a thorough analysis of the docked complex (COX2-PQA11) through Molecular Dynamics Simulation showed lower RMSD, minimal RMSF fluctuations, and a reduced total energy of -291.35 kJ/mol compared to the standard drug. These findings suggest that the therapeutic effect of PQA-11 operates through the inflammatory pathway, laying the groundwork for further in-depth research into the role of secondary metabolites in AD treatment.

Immunization of laboratory animal workers: occupational health and safety aspects.

Occupational immunization is an integral part of institutional occupational safety and health (OSH) programs. Laboratory animal workers (LAWs) are personnel working with various small and large vertebrate animals. LAWs are at the risk of contracting a myriad of zoonotic infections as they are occupationally exposed to animals and their biological products. Immunizing employees against such zoonotic pathogens is the best way to prevent disease transmission. This review provides information on various zoonotic diseases, vaccines available to protect against such infections, and vaccination schedules. Certain sections of institutional occupational immunization programs such as risk evaluation, immunizing special categories of personnel and exemption from immunization among others are also described. Additionally, the authors have discussed various probable modes of impact through which occupational immunization of laboratory animal workers fulfills different United Nations Sustainable Development Goals.

Age-related changes in hematological and biochemical profiles of Wistar rats.

BACKGROUND: Wistar rats are extensively used as the model for assessing toxicity and efficacy in preclinical research. Hematological and biochemical laboratory data are essential for evaluating specific variations in the physiological and functional profile of a laboratory animal. Establishing hematological and biochemical reference values for Wistar (han) rats at various age intervals was the goal of this work. Male and female Wistar rats (n = 660) of ages 6-8 weeks, 10-14 weeks and > 6 months were used in the experiment. Blood and serum were collected from these rats under fasting conditions. RESULTS: We observed that the majority of hematological and biochemical parameters were significantly influenced by sex and age. Hematological changes were significantly correlated to aging were increased red blood cells, hemoglobin, hematocrit, neutrophils, monocytes and eosinophils in both sexes, as well as decreased platelet, mean corpuscular volume, mean corpuscular hemoglobin and lymphocytes in both sexes. White blood cells of male rats were considerably higher than those of female rats in all age ranges. For biochemistry, increase in glucose, total protein and creatinine were seen in both sexes, along with increases in urea in females and alanine aminotransferase in males. Age was significantly associated with decreased alkaline phosphatase in both sexes. CONCLUSIONS: When using Wistar rats as a model, these reference values may be useful in evaluating the results.

The Perspective of Using Flow Cytometry for Unpuzzling Hypoxia-Inducible Factors Signalling.

Hypoxia-inducible factors (HIFs) are transcription factors that are responsible for adapting to the changes in oxygen levels in the cellular environment. HIF activity determines the expression of cellular proteins that control the development and physiology of the cells and pathophysiology of a disease. Understanding the role of specific HIF (HIF-1-3) in cellular function is essential for development of the HIF-targeted therapies. In this review, we have discussed the use of flow cytometry in analysing HIF function in cells. Proper understanding of HIF-signalling will help to design pharmacological interventions HIF-mediated therapy. We have discussed the role of HIF-signalling in various diseases such as cancer, renal and liver diseases, ulcerative colitis, arthritis, diabetes and diabetic complications, psoriasis, and wound healing. We have also discussed protocols that help to decipher the role of HIFs in these diseases that would eventually help to design promising therapies.

14-3-3 proteins-a moonlight protein complex with therapeutic potential in neurological disorder: in-depth review with Alzheimer's disease.

Alzheimer's disease (AD) affects millions of people worldwide and is a gradually worsening neurodegenerative condition. The accumulation of abnormal proteins, such as tau and beta-amyloid, in the brain is a hallmark of AD pathology. 14-3-3 proteins have been implicated in AD pathology in several ways. One proposed mechanism is that 14-3-3 proteins interact with tau protein and modulate its phosphorylation, aggregation, and toxicity. Tau is a protein associated with microtubules, playing a role in maintaining the structural integrity of neuronal cytoskeleton. However, in the context of Alzheimer's disease (AD), an abnormal increase in its phosphorylation occurs. This leads to the aggregation of tau into neurofibrillary tangles, which is a distinctive feature of this condition. Studies have shown that 14-3-3 proteins can bind to phosphorylated tau and regulate its function and stability. In addition, 14-3-3 proteins have been shown to interact with beta-amyloid (Aß), the primary component of amyloid plaques in AD. 14-3-3 proteins can regulate the clearance of Aß through the lysosomal degradation pathway by interacting with the lysosomal membrane protein LAMP2A. Dysfunction of lysosomal degradation pathway is thought to contribute to the accumulation of Aß in the brain and the progression of AD. Furthermore, 14-3-3 proteins have been found to be downregulated in the brains of AD patients, suggesting that their dysregulation may contribute to AD pathology. For example, decreased levels of 14-3-3 proteins in cerebrospinal fluid have been suggested as a biomarker for AD. Overall, these findings suggest that 14-3-3 proteins may play an important role in AD pathology and may represent a potential therapeutic target for the disease. However, further research is needed to fully understand the mechanisms underlying the involvement of 14-3-3 proteins in AD and to explore their potential as a therapeutic target.

HIF-PHD inhibitor desidustat ameliorates iron deficiency anemia.

Iron deficiency anemia is caused by many pathological conditions like chronic kidney disease (CKD), inflammation, malnutrition and gastrointestinal abnormality. Current treatments that are erythropoiesis stimulating agents (ESAs) and iron supplementation are inadequate and often lead to tolerance and/or toxicity. Desidustat, a prolyl hydroxylase (PHD) inhibitor, is clinically used for the treatment of anemia with CKD. In this study, we investigated the effect of desidustat on iron deficiency anemia (IDA). IDA was induced in C57BL6/J mice by iron deficient diet feeding. These mice were then treated with desidustat (15 mg/kg, PO) and FeSO4 (20 mg/kg) for five weeks and effect of the treatment on hematology, iron homeostasis, and bone marrow histology was observed. Effect of desidustat on iron metabolism in inflammation (LPS)-induced iron deficiency was also assessed. Both, Desidustat and FeSO4, increased MCV (mean corpuscular volume), MCH (mean corpuscular hemoglobin), hemoglobin, and HCT (hematocrit) in blood and increased iron in serum, liver, and spleen. Desidustat increased MCHC (mean corpuscular hemoglobin concentration) while FeSO4 treatment did not alter it. FeSO4 treatment significantly increased iron deposition in liver, and spleen, while desidustat increased iron in circulation and demonstrated efficient iron utilization. Desidustat increased iron absorption, serum iron and decreased hepcidin without altering tissue iron, while FeSO4 increased serum and tissue iron by increasing hepcidin in LPS-induced iron deficiency. Desidustat increased erythroid population, especially iron-dependent polychromatic normoblasts and orthochromatic normoblasts, while FeSO4 did not improve cell architecture. PHD inhibition by desidustat improved iron utilization in iron deficiency anemia, by efficient erythropoiesis.