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Hispidulin

$355

  • Brand : BIOFRON

  • Catalogue Number : BD-P0599

  • Specification : 98.0%(HPLC)

  • CAS number : 1447-88-7

  • Formula : C16H12O6

  • Molecular Weight : 300.3

  • PUBCHEM ID : 5281628

  • Volume : 25mg

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Catalogue Number

BD-P0599

Analysis Method

Specification

98.0%(HPLC)

Storage

-20℃

Molecular Weight

300.3

Appearance

Yellow powder

Botanical Source

This product is isolated and purified from the herbs of Ambrosia artemisiifolia Linn.

Structure Type

Category

SMILES

COC1=C(C2=C(C=C1O)OC(=CC2=O)C3=CC=C(C=C3)O)O

Synonyms

Dinatin/Scutellarein 6-methyl ether/6-O-Methylapigenin/TCMDC-123942/4H-1-Benzopyran-4-one, 5,7-dihydroxy-2-(4-hydroxyphenyl)-6-methoxy-/4',5,7-Trihydroxy-6-methoxyflavone/5,7-dihydroxy-2-(4-hydroxyphenyl)-6-methoxychromen-4-one/Hispidulin/6-O-Methoxyapigenin/5,7,4'-trihydroxy-6-methoxyflavone/5,7-Dihydroxy-2-(4-hydroxyphenyl)-6-methoxy-4H-chromen-4-one/Flavone, 4',5,7-trihydroxy-6-methoxy-

IUPAC Name

Applications

J Ethnopharmacol. 2015 May 26;166:18-22. Hispidulin, a constituent of Clerodendrum inerme that remitted motor tics, alleviated methamphetamine-induced hyperlocomotion without motor impairment in mice.[Pubmed: 25764963]Previously, we found a patient with an intractable motor tic disorder that could be ameliorated by the ground leaf juice of Clerodendrum inerme (CI). Furthermore, the ethanol extract of CI leaves effectively ameliorated methamphetamine-induced hyperlocomotion (MIH) in mice, an animal model mimicking the hyper-dopaminergic status of tic disorders/Tourette syndrome, schizophrenia, or obsessive-compulsive disorder. Here, we for the first time identified a constituent able to reduce MIH from the CI ethanol extract that might represent a novel lead for the treatment of such disorders. METHODS AND RESULTS:The ethanol extract of CI was sub-divided into n-hexane, dichloromethane, n-butanol and water fractions. Using MIH alleviation as a bioassay, active compounds were identified in these fractions using silica gel chromatography, recrystallization and proton NMR spectroscopy. The dichloromethane and n-hexane fractions were active in the bioassay. Further subfractionation and re-crystallization resulted in an active compound that was identified to be Hispidulin by proton NMR spectroscopy. Hispidulin significantly alleviated MIH in mice at doses that did not affect their spontaneous locomotor activity or performance in the rotarod test, a measure for motor coordination. CONCLUSIONS: Hispidulin is a flavonoid that has been isolated from several plants and reported to have anti-oxidative, anti-inflammatory and anti-cancer activities. Here, we for the very first time found that Hispidulin can also alleviate MIH at doses that did not impair motor activity, suggesting a therapeutic potential of Hispidulin in hyper-dopaminergic disorders.

Density

1.5±0.1 g/cm3

Solubility

Methanol; DMF

Flash Point

230.1±25.0 °C

Boiling Point

601.5±55.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

IHFBPDAQLQOCBX-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:1447-88-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

29656183

Abstract

Hispidulin, a phenolic flavonoid, exerts potent cytotoxicity towards a variety of human cancers. However, the effects of hispidulin on hepatocellular carcinoma (HCC) and underlying molecular mechanisms of its action remain elusive. The present study investigated the effect of hispidulin on HCC in experimental models, including tumor cell lines and mouse tumor xenograft. Results demonstrated that hispidulin was cytotoxic and anti-proliferative to HCC cell lines (SMMC7721 and Bel7402). Hispidulin activated caspase-3 and triggered apoptosis in HCC cells. Moreover, hispidulin inhibited cell migration and invasion by inhibiting the expression of matrix metalloproteinases (MMP-2, MMP-9) and by inducing tissue inhibitor of metalloproteinase-3 (TIMP-3) expression. Hispidulin activated peroxisome proliferator-activated receptor γ (PPARγ) signaling which mainly contributed to its cytotoxicity in HCC cells. Remarkably, GW9662 (a PPARγ inhibitor) or PPARγ targeting siRNA significantly abrogated the anti-proliferative, pro-apoptotic, and anti-metastatic effects of hispidulin in HCC cells. Furthermore, hispidulin induced activation of PPARγ which was associated with increased phosphorylation of AMPK, ERK, JNK in HCC cells. Compound C (an AMPK inhibitor) or PD98059 (a MEK inhibitor) partly reversed the effects of hispidulin on PPARγ signaling in HCC cells. In contrast, no significant changes in PPARγ signaling were observed in HCC cells pretreated with SP600125 (a JNK inhibitor), while SP6000125 significantly inhibited the anti-cancer effects of hispidulin in HCC cells. Hispidulin administration effectively suppressed Bel7402 xenograft tumor growth and lung metastasis in vivo. Our findings indicate that PPARγ activation by hispidulin effectively suppressed HCC cell growth and metastasis both in vitro and in vivo.

KEYWORDS

AMPK; ERK; Hepatocellular carcinoma (HCC); Hispidulin; PPARγ.

Title

Hispidulin Inhibits Hepatocellular Carcinoma Growth and Metastasis Through AMPK and ERK Signaling Mediated Activation of PPARγ

Author

Mei Han 1 , Hui Gao 2 , Ping Ju 3 , Ming-Quan Gao 1 , Yin-Ping Yuan 4 , Xue-Hong Chen 5 , Kai-Li Liu 1 , Yan-Tao Han 5 , Zhi-Wu Han 6

Publish date

2018 Jul

PMID

30055130

Abstract

Hispidulin, a natural flavone, has been reported to have diverse pharmacological effects, including antifungal, antioxidant, and antithrombotic properties. However, an anti-adipogenic effect has not yet been reported, which is the focus of the current study. Hispidulin suppressed the differentiation of adipocytes and cellular lipid accumulation without cytotoxicity. Treatment with hispidulin at concentrations of 10, 20, and 40 μM reduced intracellular lipids by 88.1%, 81.9%, and 75.8%, respectively. In addition, hispidulin reduced mRNA and protein expression of peroxisome proliferator-activated receptor gamma (PPARγ) and adiponectin. To our knowledge, these results are the first evidence of the anti-adipogenic effects of hispidulin in 3T3-L1 adipocytes, indicating that hispidulin has potential as a novel anti-obesity therapeutic.

KEYWORDS

3T3-L1 adipocytes; Anti-adipogenic; Hispidulin; PPARγ; Sage.

Title

Hispidulin Inhibits Adipogenesis in 3T3-L1 Adipocytes Through PPARγ Pathway

Author

Seul Gi Lee 1 , Jin Soo Kim 1 , Kyoungjin Min 2 , Taeg Kyu Kwon 2 , Ju-Ock Nam 3

Publish date

2018 Sep 25

PMID

29091891

Abstract

Aim: As a widely used general anesthetic, sevoflurane has been found to induce cognitive and memory defectsin the elderly. This may increase the risk of Alzheimer’s disease. This study explores the neuroprotective effect of hispidulin, a natural flavone compound, against sevoflurane-induced memory dysfunction.
Methods: The effect of sevoflurane exposure on memory function was evaluated by novel object recognition and Y-maze testing using an aged rat model. The apoptotic cell death in the hippocampus of rats was assessed using a TUNEL assay. The levels of protein markers for cell apoptosis in the hippocampus were examined by western blot. The effect of sevoflurane and hispidulin on the accumulation of Aβ was also examined. In addition, the attenuating effect of hispidulin on sevoflurane-induced neuroinflammation was assessed by measuring the expression of pro-inflammatory cytokines and the translocation of NF-κB p65 from cytosol to nucleus. The activation of Nrf2 in the hippocampus was also detected. Moreover, the effect of hispidulin on sevoflurane-induced apoptosis, Aβ accumulation, and neuroinflammation was also examined in human neuroglioma H4 cells, which served as an in vitro model.To further examine the role of Nrf2 in the neuroprotective activity of hispidulin against sevoflurane-neurotoxicity, H4 cells were transfected with Nrf2 targeting siRNA, which led to a significant reduction in Nrf2 expression.
Results: Both novel object recognition and Y-maze testing showed that sevoflurane significantly impaired the memory of aged rats, which was significantly reversed by pretreatment with hispidulin. Mechanistically, our findings revealed that hispidulin significantly attenuated sevoflurane-induced apoptotic cell death, Aβ accumulation, and neuroinflammation. In agreement with in vivo studies, hispidulin was also able to attenuate sevoflurane-induced apoptosis, increases of Aβ levels, and neuroinflammation in H4 cells. Moreover, our results showed that Nrf2 activation mediated the neuroprotective effect of hispidulin against sevoflurane-induced neurotoxicity by demonstrating that knockdown of Nrf2 in H4 cells significantly compromised its protective effects.
Conclusion: As our study provides in vitro and in vivo evidence that hispidulin can offer protection against sevoflurane-induced neurological dysfunction, hispidulin has the potential to be a neuroprotective agent that can improve the cognitive and memory function of elderly patients undergoing anesthesia.

KEYWORDS

Hispidulin; Memory dysfunction; Nrf2; Sevoflurane.

Title

Hispidulin Prevents Sevoflurane- Induced Memory Dysfunction in Aged Rats

Author

Lubin Huang 1 , Kejing Huang 2 , Hong Ning 3

Publish date

2018 Jan