Animal Model for Glucocorticoid Induced Osteoporosis: A Systematic Review from 2011 to 2021

Xavier, Andy; Toumi, Hechmi; Lespessailles, Éric

doi:10.3390/ijms23010377

Cited by 17 publications

(9 citation statements)

References 103 publications

(89 reference statements)

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“…To detect whether QCT has effects on anti-osteoporosis, dexamethasone (DEX), a kind of glucocorticoid, was used to construct a zebrafish model [ 32 ]. We used alizarin red staining to investigate the effects of bone formation ( Figure 7 A).…”

Section: Resultsmentioning

confidence: 99%

Exploring Quercetin Anti-Osteoporosis Pharmacological Mechanisms with In Silico and In Vivo Models

Yuan

Cai

et al. 2022

Life

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Since osteoporosis critically influences the lives of patients with a high incidence, effective therapeutic treatments are important. Quercetin has been well recognized as a bone-sparing agent and thus the underlying mechanisms warrant further investigation. In the current study, the network pharmacology strategy and zebrafish model were utilized to explain the potential pharmacological effects of quercetin on osteoporosis. The potential targets and related signaling pathways were explored through overlapping target prediction, protein–protein interaction network construction, and functional enrichment analysis. Furthermore, we performed docking studies to verify the specific interactions between quercetin and crucial targets. Consequently, 55 targets were related to osteoporosis disease among the 159 targets of quercetin obtained by three database sources. Thirty hub targets were filtered through the cytoNCA plugin. Additionally, the Gene Ontology functions in the top 10 respective biological processes, molecular functions, and cell components as well as the top 20 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were depicted. The most significance difference in the KEGG pathways was the TNF signaling pathway, consisting of the Nuclear Factor Kappa B Subunit (NF-κB), Extracellular Regulated Protein Kinases (ERK) 1/2, Activator Protein 1 (AP-1), Interleukin 6 (IL6), Transcription factor AP-1 (Jun), and Phosphatidylinositol 3 Kinase (PI3K), which were probably involved in the pharmacological effects. Moreover, molecular docking studies revealed that the top three entries were Interleukin 1 Beta (IL1B), the Nuclear Factor NF-Kappa-B p65 Subunit (RelA), and the Nuclear Factor Kappa B Subunit 1 (NFKB1), respectively. Finally, these results were verified by alizarin red-stained mineralized bone in zebrafish and related qPCR experiments. The findings probably facilitate the mechanism elucidation related to quercetin anti-osteoporosis action.

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Section: Resultsmentioning

confidence: 99%

Exploring Quercetin Anti-Osteoporosis Pharmacological Mechanisms with In Silico and In Vivo Models

Yuan

Cai

et al. 2022

Life

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“…(2,3) GIO is the leading cause of secondary osteoporosis (a condition caused by another disease or treatment of another disease) and has been well documented in both the basic science and clinical literature. (4)(5)(6) GIO significantly increases the risk of osteoporosis-related fractures in chronic GC users and leads to increased morbidity and mortality. (7)(8)(9) Current therapeutic options to treat GIO include bisphosphonates, denosumab, and intermittent parathyroid hormone (iPTH), among others.…”

Section: Introductionmentioning

confidence: 99%

Lactobacillus Reuteri 6475 Prevents Bone Loss in a Clinically Relevant Oral Model of Glucocorticoid‐Induced Osteoporosis in Male CD‐1 Mice

Chargo,

Schepper,

Rios‐Arce

et al. 2023

JBMR Plus

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Glucocorticoids (GCs) are commonly used anti‐inflammatory medications with significant side effects, including glucocorticoid‐induced osteoporosis (GIO). We have previously demonstrated that chronic subcutaneous GC treatment in mice leads to gut barrier dysfunction and trabecular bone loss. We further showed that treating with probiotics or barrier enhancers improves gut barrier function and prevents GIO. The overall goal of this study was to test if probiotics could prevent GC‐induced gut barrier dysfunction and bone loss in a clinically relevant oral‐GC model of GIO. Eight‐week‐old male CD‐1 mice were treated with vehicle or corticosterone in the drinking water for 4 weeks and administered probiotics Lactobacillus reuteri ATCC 6475 (LR 6475) or VSL#3 thrice weekly via oral gavage. As expected, GC treatment led to significant gut barrier dysfunction (assessed by measuring serum endotoxin levels) and bone loss after 4 weeks. Serum endotoxin levels significantly and negatively correlated with bone volume. Importantly, LR 6475 treatment effectively prevented both GC‐induced increase in serum endotoxin and trabecular bone loss. VSL#3 had intermediate results, not differing from either control or GC‐treated animals. GC‐induced reductions in femur length, cortical thickness, and cortical area were not affected by probiotic treatment. Taken together, these results are the first to demonstrate that LR 6475 effectively prevents the detrimental effects of GC treatment on gut barrier, which correlates with enhanced trabecular bone health in an oral mouse model of GIO. © 2023 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.

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“…Through a preliminary search of eight databases, 445 studies were identified. In addition, seven articles from our records met the requirements for this meta-analysis but did not appear in the search results, and we included those ( Xavier et al, 2021 ). After removing duplicate studies, 285 articles remained, and we performed title and abstract readings to exclude 265 articles, including 238 irrelevant studies, 16 studies whose interventions did not meet inclusion requirements, five literature reviews, three conference abstracts, and three articles for which the full text was not available.…”

Section: Resultsmentioning

confidence: 99%

Effectiveness and mechanism of metformin in animal models of pulmonary fibrosis: A preclinical systematic review and meta-analysis

Xiao

Chen

et al. 2022

Front. Pharmacol.

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Background: Pulmonary fibrosis (PF) is a lung disease with no curative drug, characterized by a progressive decrease in lung function. Metformin (MET) is a hypoglycemic agent with the advantages of high safety and low cost and has been used in several in vivo trials to treat fibrotic diseases.Objective: This study aimed to explore the efficacy and safety of MET in treating PF and elaborate on its mechanism.Methods: Eight databases were searched for in vivo animal trials of MET for PF from the time of database creation until 1 March 2022. The risk of bias quality assessment of the included studies was conducted using SYRCLE’s risk of bias assessment. Pulmonary inflammation and fibrosis scores were the primary outcomes of this study. Hydroxyproline (HYP), type I collagen (collagen I), α-smooth muscle actin (α-SMA), transforming growth factor-β (TGF-β), Smad, AMP-activated protein kinase (AMPK), and extracellular signal–regulated kinase (ERK) protein expression in lung tissues and animal mortality were secondary outcomes. Effect magnitudes were combined and calculated using Revman 5.3 and Stata 16.0 to assess the efficacy and safety of MET in animal models of PF. Inter-study heterogeneity was examined using the I2 or Q test, and publication bias was assessed using funnel plots and Egger’s test.Results: A total of 19 studies involving 368 animals were included, with a mean risk of bias of 5.9. The meta-analysis showed that MET significantly suppressed the level of inflammation and degree of PF in the lung tissue of the PF animal model. MET also reduced the content of HYP, collagen I, α-SMA, and TGF-β and phosphorylation levels of Smad2, Smad3, p-smad2/3/smad2/3, ERK1/2, and p-ERK1/2/ERK1/2 in lung tissues. MET also elevated AMPK/p-AMPK levels in lung tissues and significantly reduced animal mortality.Conclusion: The results of this study suggest that MET has a protective effect on lung tissues in PF animal models and may be a potential therapeutic candidate for PF treatment.Systematic Review Registration:https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=327285, identifier CRD42022327285.

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Animal Model for Glucocorticoid Induced Osteoporosis: A Systematic Review from 2011 to 2021

Cited by 17 publications

References 103 publications

Exploring Quercetin Anti-Osteoporosis Pharmacological Mechanisms with In Silico and In Vivo Models

Exploring Quercetin Anti-Osteoporosis Pharmacological Mechanisms with In Silico and In Vivo Models

Lactobacillus Reuteri 6475 Prevents Bone Loss in a Clinically Relevant Oral Model of Glucocorticoid‐Induced Osteoporosis in Male CD‐1 Mice

Effectiveness and mechanism of metformin in animal models of pulmonary fibrosis: A preclinical systematic review and meta-analysis

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