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Nardosinone

$225

  • Brand : BIOFRON

  • Catalogue Number : BF-N4002

  • Specification : 98%(HPLC)

  • CAS number : 23720-80-1

  • Formula : C15H22O3

  • Molecular Weight : 250.33

  • PUBCHEM ID : 168136

  • Volume : 100mg

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Catalogue Number

BF-N4002

Analysis Method

HPLC,NMR,MS

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

250.33

Appearance

Colorless granular crystallization

Botanical Source

Callerya speciosa,Nardostachys jatamansi

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1CCC=C2C1(C3C(CC2=O)OOC3(C)C)C

Synonyms

Nardosinone/5H-Naphtho[2,1-c][1,2]dioxol-5-one, 1,3a,4,7,8,9,9a,9b-octahydro-1,1,9,9a-tetramethyl-, (3aR,9R,9aR,9bS)-/5H-Naphtho[2,1-c][1,2]dioxol-5-one,1,3a,4,7,8,9,9a,9b-octahydro-1,1,9,9a-tetramethyl-, (3aR,9R,9aR,9bS)-/(3aR,9R,9aR,9bS)-1,1,9,9a-Tetramethyl-1,3a,4,7,8,9,9a,9b-octahydro-5H-naphtho[2,1-c][1,2]dioxol-5-one

IUPAC Name

(3aR,9R,9aR,9bS)-1,1,9,9a-tetramethyl-3a,4,7,8,9,9b-hexahydronaphtho[2,1-c]dioxol-5-one

Density

1.1±0.1 g/cm3

Solubility

Ethyl Acetate

Flash Point

142.0±25.2 °C

Boiling Point

330.2±32.0 °C at 760 mmHg

Melting Point

108-110℃

InChl

InChI=1S/C15H22O3/c1-9-6-5-7-10-11(16)8-12-13(15(9,10)4)14(2,3)18-17-12/h7,9,12-13H,5-6,8H2,1-4H3/t9-,12-,13+,15+/m1/s1

InChl Key

KXGHHSIMRWPVQM-JWFUOXDNSA-N

WGK Germany

RID/ADR

HS Code Reference

2938900000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:23720-80-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

28955231

Abstract

Periodontitis is a chronic inflammatory disease that damages the integrity of the tooth-supporting tissues, known as the periodontium, and comprising the gingiva, periodontal ligament and alveolar bone. In this study, the effects of nardosinone (Nd) on bone were tested in a model of lipopolysaccharide (LPS)-induced alveolar bone loss, and the associated mechanisms were elucidated. Nd effectively suppressed LPS-induced alveolar bone loss and reduced osteoclast (OC) numbers in vivo. Nd suppressed receptor activator of nuclear factor-κB ligand (RANKL)-mediated OC differentiation, bone resorption, and F-actin ring formation in a dose-dependent manner. Further investigation revealed that Nd suppressed osteoclastogenesis by suppressing the ERK and JNK signaling pathways, scavenging reactive oxygen species, and suppressing the activation of PLCγ2 that consequently affects the expression and/or activity of the OC-specific transcription factors, c-Fos and nuclear factor of activated T-cells cytoplasmic 1 (NFATc1). In addition, Nd significantly reduced the expression of OC-specific markers in mouse bone marrow-derived pre-OCs, including c-Fos, cathepsin K (Ctsk), VATPase d2, and Nfatc1. Collectively, these findings suggest that Nd has beneficial effects on bone, and the suppression of OC number implies that the effect is exerted directly on osteoclastogenesis.

KEYWORDS

MAPKs; RANKL; alveolar bone resorption; nardosinone; osteoclastogenesis.

Title

Nardosinone Suppresses RANKL-Induced Osteoclastogenesis and Attenuates Lipopolysaccharide-Induced Alveolar Bone Resorption

Author

Chenguang Niu 1 , Fei Xiao 2 , Keyong Yuan 1 , XuChen Hu 1 , Wenzhen Lin 1 , Rui Ma 1 , Xiaoling Zhang 2 , Zhengwei Huang 1

Publish date

2017 Sep 12

PMID

24337842

Abstract

Pathological cardiac hypertrophy induced by angiotensin II (AngII) can subsequently give rise to heart failure, a leading cause of mortality. Nardosinone is a pharmacologically active compound extracted from the roots of Nardostachys chinensis, a well-known traditional Chinese medicine. In order to investigate the effects of nardosinone on AngII-induced cardiac cell hypertrophy and the related mechanisms, the myoblast cell line H9c2, derived from embryonic rat heart, was treated with nardosinone (25, 50, 100, and 200 μmol/L) or AngII (1 μmol/L). Then cell surface area and mRNA expression of classical markers of hypertrophy were detected. The related protein levels in PI3K/Akt/mTOR and MEK/ERK signaling pathways were examined by Western blotting. It was found that pretreatment with nardosinone could significantly inhibit the enlargement of cell surface area induced by AngII. The mRNA expression of ANP, BNP and β-MHC was obviously elevated in AngII-treated H9c2 cells, which could be effectively blocked by nardosinone at the concentration of 100 μmol/L. Further study revealed that the protective effects of nardosinone might be mediated by repressing the phosphorylation of related proteins in PI3K/Akt and MEK/ERK signaling pathways. It was suggested that the inhibitory effect of nardosinone on Ang II-induced hypertrophy in H9c2 cells might be mediated by targeting PI3K/Akt and MEK/ERK signaling pathways.

KEYWORDS

MAPKs; RANKL; alveolar bone resorption; nardosinone; osteoclastogenesis.

Title

Nardosinone Protects H9c2 Cardiac Cells From Angiotensin II-induced Hypertrophy

Author

Meng Du 1 2 , Kun Huang 1 2 , Lu Gao 2 , Liu Yang 2 , Wen-Shuo Wang 3 , Bo Wang 3 , Kai Huang 4 5 , Dan Huang 6 7

Publish date

2013 Dec

PMID

24614893

Abstract

In this study, we investigated the impact of Nardosinone, a bioactive component in Nardostachys root, on the proliferation and differentiation of neural stem cells. The neural stem cells were isolated from cerebrums of embryonic day 14 CD1 mice. The proliferation of cells was monitored using the cell counting kit-8 assay, bromodeoxyuridine incorporation and cell cycle analysis. Cell migration and differentiation were investigated with the neurosphere assay and cell specific markers, respectively. The results showed that Nardosinone promotes cells proliferation and increases cells migration distance in a dose-dependent manner. Nardosinone also induces the selective differentiation of neural stem cells to neurons and oligodendrocytes, as indicated by the expression of microtubule-associated protein-2 and myelin basic protein, respectively. Nardosinone also increases the expression of phospho-extracellular signal-regulated kinase and phospho-cAMP response element binding protein during proliferation and differentiation. In conclusion, this study reveals the regulatory effects of Nardosinone on neural stem cells, which may have significant implications for the treatment of brain injury and neurodegenerative diseases.

Title

Nardosinone Improves the Proliferation, Migration and Selective Differentiation of Mouse Embryonic Neural Stem Cells

Author

Ze-Hui Li 1 , Wei Li 2 , Jin-Li Shi 2 , Min-Ke Tang 2

Publish date

2014 Mar 10


Description :

Nardosinone protects H9c2 cardiac cells from angiotensin II-induced hypertrophy. PUMID/DOI:24337842 J Huazhong Univ Sci Technolog Med Sci. 2013 Dec;33(6):822-6 Pathological cardiac hypertrophy induced by angiotensin II (AngII) can subsequently give rise to heart failure, a leading cause of mortality. Nardosinone is a pharmacologically active compound extracted from the roots of Nardostachys chinensis, a well-known traditional Chinese medicine. In order to investigate the effects of Nardosinone on AngII-induced cardiac cell hypertrophy and the related mechanisms, the myoblast cell line H9c2, derived from embryonic rat heart, was treated with Nardosinone (25, 50, 100, and 200 μmol/L) or AngII (1 μmol/L). Then cell surface area and mRNA expression of classical markers of hypertrophy were detected. The related protein levels in PI3K/Akt/mTOR and MEK/ERK signaling pathways were examined by Western blotting. It was found that pretreatment with Nardosinone could significantly inhibit the enlargement of cell surface area induced by AngII. The mRNA expression of ANP, BNP and β-MHC was obviously elevated in AngII-treated H9c2 cells, which could be effectively blocked by Nardosinone at the concentration of 100 μmol/L. Further study revealed that the protective effects of Nardosinone might be mediated by repressing the phosphorylation of related proteins in PI3K/Akt and MEK/ERK signaling pathways. It was suggested that the inhibitory effect of Nardosinone on Ang II-induced hypertrophy in H9c2 cells might be mediated by targeting PI3K/Akt and MEK/ERK signaling pathways. Nardosinone improves the proliferation, migration and selective differentiation of mouse embryonic neural stem cells. PUMID/DOI:24614893 PLoS One. 2014 Mar 10;9(3):e91260. In this study, we investigated the impact of Nardosinone, a bioactive component in Nardostachys root, on the proliferation and differentiation of neural stem cells. The neural stem cells were isolated from cerebrums of embryonic day 14 CD1 mice. The proliferation of cells was monitored using the cell counting kit-8 assay, bromodeoxyuridine incorporation and cell cycle analysis. Cell migration and differentiation were investigated with the neurosphere assay and cell specific markers, respectively. The results showed that Nardosinone promotes cells proliferation and increases cells migration distance in a dose-dependent manner. Nardosinone also induces the selective differentiation of neural stem cells to neurons and oligodendrocytes, as indicated by the expression of microtubule-associated protein-2 and myelin basic protein, respectively. Nardosinone also increases the expression of phospho-extracellular signal-regulated kinase and phospho-cAMP response element binding protein during proliferation and differentiation. In conclusion, this study reveals the regulatory effects of Nardosinone on neural stem cells, which may have significant implications for the treatment of brain injury and neurodegenerative diseases. Nardosinone reduces neuronal injury induced by oxygen-glucose deprivation in primary cortical cultures PUMID/DOI:24358776 Yao Xue Xue Bao. 2013 Sep;48(9):1422-9. The aim of the study is to investigate the effect of Nardosinone (Nar) on neuronal injury induced by oxygen-glucose deprivation (OGD) in primary cortical cultures isolated from embryos at gestational day 14. MTT method was used to determine the dosage regimen of Nar in primary neuronal cultures and observe the influence of Nardosinone on the neurons suffering OGD; Western blotting analysis was used to detect expressions of protein kinase A (PKA), Ras related protein 1 (Rap1), mitogen-activated protein kinase kinase 1 (MEK1) and phospho-extracellular signal-regulated kinase 1/2 (p-ERK1/2) of OGD-injured or uninjured primary cultured neurons after Nardosinone treatment. Results showed that Nar (50 and 100 micromol x L(-1)) improved the cell viability during OGD damage (P < 0.01) and increased the expression of PKA, Rap1, MEK1 and p-ERK1/2 in injured neurons. Additionally, elevations of PKA, Rapl, MEK1 and p-ERK1/2 in uninjured neurons were caused by Nardosinone (50, 100 and 200 micromol x L(-1)) with a dose-dependent tenclency as well (P < 0.01). In conclusion, Nardosinone could protect against the neuronal injury exposed to OGD, which may be relevant to the promotion of PKA and ERK signaling pathway. Nardosinone, the first enhancer of neurite outgrowth-promoting activity of staurosporine and dibutyryl cyclic AMP in PC12D cells. PUMID/DOI:14604758 Brain Res Dev Brain Res. 2003 Nov 12;145(2):177-83. Nardosinone was isolated as an enhancer of nerve growth factor (NGF) from Nardostachys chinensis [Neurosci. Lett. 273 (1999) 53]. Nardosinone (0.1-100 microM) enhanced dibutyryl cyclic AMP (dbcAMP, 0.3 mM)- and staurosporine (10 nM)-induced neurite outgrowth from PC12D cells in a concentration-dependent manner. PD98059 (20 microM), a potent mitogen-activated protein (MAP) kinase kinase inhibitor, partially blocked enhancements of dbcAMP (0.3 mM)- or staurosporine (10 nM)-induced neurite outgrowth by Nardosinone. Nardosinone alone had no effect on the phosphorylation of MAP kinase. The dbcAMP-induced increase in phosphorylation of MAP kinase was not affected by Nardosinone. Staurosporine almost unaffected the phosphorylation of MAP kinase, and Nardosinone potentiated the staurosporine-induced neurite outgrowth without stimulation of the phosphorylation of MAP kinase. Since it is known that MAP kinase signaling is required for neurite outgrowth in PC12D cells, these results suggest that Nardosinone enhances staurosporine- or dbcAMP-induced neurite outgrowth from PC12D cells, probably by amplifying both the MAP kinase-dependent and -independent signaling pathways of dbcAMP and staurosporine. It is also suggested that Nardosinone enhances a downstream step of MAP kinase in the MAP kinase-dependent signaling pathway. Nardosinone is the first enhancer of the neuritogenic action of dbcAMP and staurosporine and may become a useful pharmacological tool for studying the mechanism of action of not only NGF but also both the neuritogenic substances