Sappanone A inhibits RANKL-induced osteoclastogenesis in BMMs and prevents inflammation-mediated bone loss

Choo, Young-Yeon; Tran, Phuong Thao; Min, Byung‐Sun; Kim, Okwha; Dang, Nguyen Hai; Kwon, Seung‐Hae; Lee, Jeong‐Hyung

doi:10.1016/j.intimp.2017.09.018

Cited by 29 publications

(13 citation statements)

References 31 publications

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“…These results were generally in agreement with Kang et al finding that SA increased the phosphorylation levels of PI3K and Akt in PC-12 cells [8]. However, Choo et al reported the opposite that SA inhibited the activation of the Akt-Gsk-3β signal pathway in receptor activator of nuclear factor-kB ligand (RANKL)-induced osteoclastogenesis in mouse bone marrow macrophages [24]. We speculated that this discrepancy may be ascribed to the difference in cell type and pathophysiological process.…”

Section: Discussionsupporting

confidence: 91%

Sappanone A alleviates hypoxia/reoxygenation-induced cardiomyocytes injury through inhibition of mitochondrial apoptosis and activation of PI3K–Akt–Gsk-3β pathway

Shi¹,

Gao²,

Ji³

et al. 2020

Bioscience Reports

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Myocardial ischemia reperfusion injury (MIRI) is a complex pathophysiological process involved with the activation of oxidative stress, inflammation and apoptosis. Sappanone A (SA), a homoisoflavanone isolated from the heartwood of Caesalpinia sappan L., could exhibit antioxidant, anti-inflammatory and anti-apoptotic activities. Therefore, we assumed that SA has a potential use for preventing against MIRI. The present study aimed to investigate the effect of SA treatment on MIRI and its mechanism. Cardiomyocytes (H9c2 cells) were treated with SA for 1 h, followed by 6 h of hypoxia/3 h of reoxygenation. Cell viability assay was detected by CCK-8 assay. Apoptosis was measured by flow cytometry and Hoechst staining. Mitochondrial permeability transition pore (mPTP) opening and mitochondrial transmembrane potential ( ψm) were measured by spectrophotometry and JC-1 staining. The changes of mitochondrial apoptosis-related proteins and PI3K-Akt-Gsk-3β signaling pathway were evaluated by Western blotting. The results showed that SA pretreatment enhanced the cell viability and decreased the activity of myocardial enzyme in a dose-dependent manner. Moreover, SA pretreatment significantly inhibited apoptosis, blocked mPTP opening, suppressed the release of ψm, prevented the cytochrome c releasing from mitochondria into cytoplasm, and repressed the cleavage of caspase-9 and caspase-3. Furthermore, SA pretreatment increased the phosphorylation levels of Akt and Gsk-3β but not of Stat-3. Meanwhile, the protective effect of SA was abrogated by PI3K inhibitor (LY294002). In conclusion, our results demonstrate that SA could prevent hypoxia/reoxygenation-induced cardiomyocytes injury through inhibition of mitochondrial apoptosis and activation of PI3K-Akt-Gsk-3β pathway. Thus, SA may have a potential use for the prevention of MIRI.

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Section: Discussionsupporting

confidence: 91%

Sappanone A alleviates hypoxia/reoxygenation-induced cardiomyocytes injury through inhibition of mitochondrial apoptosis and activation of PI3K–Akt–Gsk-3β pathway

Shi¹,

Gao²,

Ji³

et al. 2020

Bioscience Reports

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“…The phytochemicals salidroside and sappanone A induced inhibition of inflammation in mice stimulated with LPS (UO) through overexpression of GSK3β and reduction of the relative abundance of phospho-GSK3β-Ser9, respectively ( 100 , 101 ). Isoproterenol inhibition of resistin or its siRNA-gene silencing in PDLC stimulated with nicotine and LPS from P. gingivalis had anti-inflammatory effects associated with activation of GSK3β and inactivation of β-catenin ( 102 ).…”

Section: Strategies To Inhibit the Inflammatory Response By Gsk3β Activationmentioning

confidence: 99%

Glycogen Synthase Kinase 3β Modulates the Inflammatory Response Activated by Bacteria, Viruses, and Parasites

et al. 2021

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Knowledge of glycogen synthase kinase 3β (GSK3β) activity and the molecules identified that regulate its function in infections caused by pathogenic microorganisms is crucial to understanding how the intensity of the inflammatory response can be controlled in the course of infections. In recent years many reports have described small molecular weight synthetic and natural compounds, proteins, and interference RNA with the potential to regulate the GSK3β activity and reduce the deleterious effects of the inflammatory response. Our goal in this review is to summarize the most recent advances on the role of GSK3β in the inflammatory response caused by bacteria, bacterial virulence factors (i.e. LPS and others), viruses, and parasites and how the regulation of its activity, mainly its inhibition by different type of molecules, modulates the inflammation.

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“…This compound induces heme oxygenase (HO)-1 protein and increases nuclear translocation of the nuclear factor-E2-related factor 2 (Nrf2) as well as the expression of Nrf2 target genes, such as NAD(p)H:quinone oxidoreductase 1 (NQO1), in RAW264.7 cells [14]. Additionally, sappanone A has been shown to inhibit RANKL-induced osteoclastogenesis in mouse bone marrow macrophages (BMMs) and suppress inflammation-induced bone loss in a mouse model [15].…”

Section: Introductionmentioning

confidence: 99%

Sappanone A Prevents Left Ventricular Dysfunction in a Rat Myocardial Ischemia Reperfusion Injury Model

Min

Yang

et al. 2020

IJMS

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The incidence of myocardial infarction, among the causes of cardiovascular morbidity and mortality, is increasing globally. In this study, left ventricular (LV) dysfunction, including LV systolic and diastolic function, was investigated in a rat myocardial ischemia/reperfusion injury model with echocardiography. The homoisoflavanone sappanone A is known for its anti-inflammatory effects. Using echocardiography, we found that sappanone A administration significantly improved LV systolic and diastolic function in a rat myocardial ischemia/reperfusion injury model, especially in the early phase development of myocardial infarction. Based on myocardial infarct size, serum cardiac marker assay, and histopathological evaluation, sappanone A showed higher efficacy at the doses used in our experiments than curcumin and was evaluated for its potential to improve LV function.

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Sappanone A inhibits RANKL-induced osteoclastogenesis in BMMs and prevents inflammation-mediated bone loss

Cited by 29 publications

References 31 publications

Sappanone A alleviates hypoxia/reoxygenation-induced cardiomyocytes injury through inhibition of mitochondrial apoptosis and activation of PI3K–Akt–Gsk-3β pathway

Sappanone A alleviates hypoxia/reoxygenation-induced cardiomyocytes injury through inhibition of mitochondrial apoptosis and activation of PI3K–Akt–Gsk-3β pathway

Glycogen Synthase Kinase 3β Modulates the Inflammatory Response Activated by Bacteria, Viruses, and Parasites

Sappanone A Prevents Left Ventricular Dysfunction in a Rat Myocardial Ischemia Reperfusion Injury Model

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