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Paeoniflorin

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-P1003

  • Specification : 98%

  • CAS number : 23180-57-6

  • Formula : C23H28O11

  • Molecular Weight : 480.46

  • PUBCHEM ID : 442534

  • Volume : 20mg

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Catalogue Number

BF-P1003

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

480.46

Appearance

White crystal

Botanical Source

Paeonia lactiflora,Paeonia suffruticosa

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

CC12CC3(C4CC1(C4(C(O2)O3)COC(=O)C5=CC=CC=C5)OC6C(C(C(C(O6)CO)O)O)O)O

Synonyms

paeoniflorine/Paeony root/Delmacinone/Paeonia moutan/peoniflorin/Paeonia lactiflora P,E,/Paeoniflorm/PAEONIFLORIN(P)/,Peoniflorin/PACLITAXEL

IUPAC Name

[(1R,2S,3R,5R,6R,8S)-6-hydroxy-8-methyl-3-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-9,10-dioxatetracyclo[4.3.1.02,5.03,8]decan-2-yl]methyl benzoate

Density

1.6±0.1 g/cm3

Solubility

Methanol; Water; Acetontrile; DMSO

Flash Point

238.4±25.0 °C

Boiling Point

690.2±55.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

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#:23180-57-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

28791506

Abstract

Paeoniflorin, a type of bioactive monoterpene glucoside in Paeoniae Radix, possesses anti-oxidative, anti-inflammatory and anti-hyperglycaemic properties. However, the underlying mechanism of paeoniflorin in treating atherosclerosis is unclear. A rat model of high-fat diet-induced atherosclerosis and palmitic acid (PA)-treated vascular smooth muscle cells (VSMCs) were used in this study. The serum concentrations of total cholesterol (TC), triglyceride (TG), low-density lipoprotein-cholesterol (LDL-C) and high-density lipoprotein-cholesterol (HDL-C) were determined, and the results indicated that paeoniflorin remarkably lowered the levels of TC, TG and LDL-C induced by a high-fat diet. Histopathological results showed that paeoniflorin significantly improved the pathological changes in the aorta. In addition, paeoniflorin also maintained a normal weight gain speed. Subsequently, the effects of paeoniflorin on the production of inflammatory cytokines (IL-1β, IL-6 and TNF-α) were detected by qPCR and ELISA. The qPCR and ELISA results showed that paeoniflorin decreased the levels of these inflammatory cytokines. Moreover, the expression of TLR4 and its downstream pathway molecules was measured by Western blot. The results indicated that paeoniflorin significantly reduced the expression of TLR4 and MyD88 as well as the phosphorylation of IκBα and NF-κB p65. Taken together, these results suggested that paeoniflorin could alleviate atherosclerotic inflammation by inhibiting the TLR4/MyD88/NF-κB pathway. Therefore, paeoniflorin may be a potential therapy for atherosclerosis. q

KEYWORDS

NF-κB; atherosclerosis; inflammation; paeoniflorin.

Title

Paeoniflorin Ameliorates Atherosclerosis by Suppressing TLR4-Mediated NF-κB Activation

Author

Huan Li 1 , Yabin Jiao 2 , Mingjun Xie 1

Publish date

2017 Dec

PMID

30149133

Abstract

Systemic lupus erythematosus (SLE) is a chronic and multisystemic autoimmune disease. Interleukin-1 receptor-associated kinase 1 (IRAK1) is associated with the susceptibility of SLE in humans and paeoniflorin has recently been reported to exhibit immunosuppressive properties. The aim of this study was to determine the effect of paeoniflorin on lipopolysaccharide (LPS)-triggered macrophage activation and and its role in LPS-induced IRAK1-nuclear factor κB (NF-κB) signaling pathways. Peritoneal macrophages from lupus-prone MRL/lpr mice and ICR mice were isolated, prepared and cultured. Cells were treated with LPS alone or LPS with paeoniflorin, and macrophage proliferation was analyzed using the CCK8 assay. The expression of IRAK1 in cells was analyzed by immunofluorescence staining. The level of gene expression of IRAK1, NF-κB, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) was measured by RT-PCR, and TNF-α, IL-6 levels in the cell supernatant were determined by ELISA. The protein expression of IRAK1 and downstream molecules tumor necrosis factor receptor-associated factor 6 (TRAF6), inhibitor of nuclear factor kappa-B kinase (IKK), NF-kappa-B inhibitor alpha (IKBα), and NF-κB was detected by Western-blot analysis. Paeoniflorin was found to decrease the phosphorylation of IRAK1 and its downstream proteins induced by LPS and inhibit the expression of TNF-α and IL-6. Taken together, the data obtained indicate that paeoniflorin inhibits LPS-induced cell activation by inhibiting the IRAK1-NF-κB pathway in MRL/lpr mouse macrophages. Therefore, paeoniflorin may be a potential therapy for SLE.

KEYWORDS

NF-κB; atherosclerosis; inflammation; paeoniflorin.

Title

Paeoniflorin Inhibits Activation of the IRAK1-NF-κB Signaling Pathway in Peritoneal Macrophages From Lupus-Prone MRL/lpr Mice

Author

Lina Ji 1 , Xiaoli Hou 2 , Wenhong Liu 1 , Xian Deng 1 , Ziyan Jiang 1 , Kaichen Huang 1 , Rongqun Li 3

Publish date

2018 Nov

PMID

28899493

Abstract

Background: Paeoniflorin, a monoterpene glycoside, exerts protective vascular effects, showing good antioxidant properties. However, whether Paeoniflorin has protective effect against the oxidative damage induced by advanced oxidation protein products (AOPPs) in Human umbilical vein endothelial cells (HUVECs) is unknown, as is the underlying mechanism.
Purpose: The present study was designed to investigate the effect of Paeoniflorin on oxidative damage of HUVECs and elucidate its underlying molecular mechanisms.
Methods: The fluorescence intensity of 2′, 7′-dichlorofluorescein-diacetate (DCFH-DA) staining was detected for intracellular reactive oxygen species (ROS) production. The increases mitochondrial membrane potential (MMP) was measured via flow cytometry and confocal microscopy using MitoTracker® Deep Red/ MitoTracker® Green staining. The intracellular adenosine triphosphate (ATP) was measured by ATP Determination Kit according to the manufacturer’s protocol. Nox2, Nox4, hypoxia inducible factor-1α (HIF-1α), vascular endothelial growth factor (VEGF) and nuclear factor-κB (NF-κB) p65 expressions were detected by western blot.
Results: Our results showed that Paeoniflorin increases MMP and ATP levels of HUVECs induced by AOPPs, and attenuates NF-κB p65 expression on HUVECs might mainly result from its antioxidant capability by suppressing ROS production. Moreover, we also found that Paeoniflorin can suppress HIF-1α and VEGF protein expression through a decrease of ROS production via down-regulation of Nox2/Nox4 expression in HUVECs. AOPP-induced RAGE mRNA up-regulation was blocked by Paeoniflorin treatment in HUVECs.
Conclusion: Our results provided the first experimental that Paeoniflorin protects against AOPP-induced oxidative damage in HUVECs, mainly through a mechanism involving a decrease in ROS production by the inhibition of Nox2/Nox4 and RAGE expression; restored ATP depletion and mitochondria dysfunction via ROS suppression; and down-regulated HIF-1α/VEGF, possibly via the ROS-NF-κB axis.

KEYWORDS

AOPPs; HIF-1α; Paeoniflorin; Reactive oxygen species; VEGF.

Title

Protective Effects of Paeoniflorin Against AOPP-induced Oxidative Injury in HUVECs by Blocking the ROS-HIF-1α/VEGF Pathway

Author

Shaolian Song 1 , Xiaoyan Xiao 2 , Dan Guo 2 , Liqian Mo 2 , Can Bu 2 , Wenbin Ye 3 , Quanwen Den 2 , Shiting Liu 2 , Xixiao Yang 4

Publish date

2017 Oct 15


Description :

Paeoniflorin is a herbal constituent extracted from the root of Paeonia albiflora Pall.Target: OthersPaeoniflorin (PF) is the principal bioactive component of Radix Paeo- niae alba, which is widely used in Traditional Chinese Medicine for the treatment of neurodegenerative disorders such as Parkinson's disease(PD) [1]. Paeoniflorin, a compound found in white peony that inhibited the production of testosterone and promoted the activity of aromatase, which converts testosterone into estrogen [2]. Treatment of cells with paeoniflorin but not glycyrrhizin resulted in enhanced phosphorylation and acquisition of the deoxyribonucleic acid-binding ability of heat shock transcription factor 1 (HSF1), as well as the formation of characteristic HSF1 granules in the nucleus, suggesting that the induction of HSPs by paeoniflorin is mediated by the activation of HSF1. Also, thermotolerance was induced by treatment with paeoniflorin but not glycyrrhizin. Paeoniflorin had no toxic effect at concentrations as high as 80 microg/ mL (166.4 microM). To our knowledge, this is the first report on the induction of HSPs by herbal medicines [3].