We Offer Worldwide Shipping
Login Wishlist

Protocatechualdehyde

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-P3020

  • Specification : 98%

  • CAS number : 139-85-5

  • Formula : C7H6O3

  • Molecular Weight : 138.12

  • PUBCHEM ID : 8768

  • Volume : 50mg

In stock

Quantity
Checkout Bulk Order?

Catalogue Number

BF-P3020

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

138.12

Appearance

White crystalline powder

Botanical Source

Salvia miltiorrhiza

Structure Type

Phenolics

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC(=C(C=C1C=O)O)O

Synonyms

Benzaldehyde, 3,4-dihydroxy-/1,2-dihydroxy-4-formylbenzene/3,4-Dihydroxy benzaldehyde/4-formyl-1,2-benzenediol/3,4-Dihydroxybenzyl aldehyde/RANCINAMYCIN IV/4-formyl-1,2-dihydroxybenzene/3,4-Dihydroxybenzaldehyde/Protocatechuic aldehyde/Protocatechualdehyde

IUPAC Name

3,4-dihydroxybenzaldehyde

Density

1.4±0.1 g/cm3

Solubility

Methanol; Water

Flash Point

146.7±18.3 °C

Boiling Point

295.4±20.0 °C at 760 mmHg

Melting Point

150-157 °C(lit.)

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2912490000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:139-85-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

26780453

Abstract

Oxidative stress is closely related to the pathogenesis of ischemic stroke. Protocatechualdehyde (PCA) is a phenolic acid compound that has the putative antioxidant activities. The present study was aimed to investigate the molecular mechanisms involved in the antioxidative effect of PCA against cerebral ischemia/reperfusion (I/R) injury. The experiment stroke model was produced in Sprague-Dawley rats via middle cerebral artery occlusion (MCAO). To model ischemia-like conditions in vitro, differentiated SH-SY5Y cells were exposed to transient oxygen and glucose deprivation (OGD). Treatment with PCA significantly improved neurologic score, reduced infarct volume and necrotic neurons, and also decreased reactive oxygen species (ROS) production, 4-hydroxynonenal (4-HNE), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) contents at 24 h after reperfusion. Meanwhile, PCA significantly increased the transcription nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expressions in the ischemic cerebral cortex as shown by immunofluorescence staining and Western blot analysis. In vitro experiment showed that PCA protected differentiated SH-SY5Y cells against OGD-induced injury. Likewise, PCA also increased markedly the Nrf2 and HO-1 expressions in a dose-dependent manner. The neuroprotection effect of PCA was abolished by knockdown of Nrf2 and HO-1. Moreover, knockdown of protein kinase Cε (PKCε) also blocked PCA-induced Nfr2 nuclear translocation, HO-1 expression, and neuroprotection. Taken together, these results provide evidences that PCA can protect against cerebral ischemia-reperfusion-induced oxidative injury, and the neuroprotective effect involves the PKCε/Nrf2/HO-1 pathway.

KEYWORDS

HO-1; Ischemic stroke; Nrf2; Oxidative stress; PKCε.

Title

Protocatechualdehyde Protects Against Cerebral Ischemia-Reperfusion-Induced Oxidative Injury Via Protein Kinase Cε/Nrf2/HO-1 Pathway

Author

Chao Guo 1 , Shiquan Wang 2 , Jialin Duan 1 , Na Jia 1 , Yanrong Zhu 1 , Yi Ding 1 , Yue Guan 1 , Guo Wei 1 , Ying Yin 1 , Miaomaio Xi 3 , Aidong Wen 4 `

Publish date

2017 Mar

PMID

31082368

Abstract

Myocardial fibrosis is associated with cardiovascular remodeling, which is characterized by abnormal collagen architecture. However, there are not yet effective strategies targeting this abnormal pathological process. The purpose of our study is to investigate the effect of protocatechualdehyde (PCA) on myocardial fibrosis for exploring the underlying target protein and molecular mechanism. We found PCA significantly suppressed isoprenaline (ISO)-induced fibrosis and collagen deposition in myocardial tissue. Then, the direct pharmacological target of PCA was identified as collagen I using cellular thermal shift assay (CETSA) coupled with stable isotope labeling with amino acids in cell culture (SILAC) technology. Surface plasmon resonance (SPR) analysis further confirmed the specific binding of PCA with collagen I. Moreover, collagen self-assembly assay and atomic force microscope analysis confirmed that PCA directly modulated collagen conformational dynamics. LC-MS/MS analysis was applied to determine lysine residues as the binding sites of PCA on collagen I by covalently cross-linking reaction. Collectively, our study suggests that PCA controls cardiovascular remodeling by mediating diffuse interstitial myocardial fibrosis. Moreover, directly targeting collagen may be a promising strategy for the treatment of heart failure and resultant myocardial fibrosis.

KEYWORDS

Collagen; Conformational dynamics; Myocardial fibrosis; Protocatechualdehyde; Target identification.

Title

Protocatechualdehyde Reduces Myocardial Fibrosis by Directly Targeting Conformational Dynamics of Collagen

Author

Yan-Jun Wan 1 , Qiang Guo 1 , Dan Liu 2 , Yong Jiang 1 , Ke-Wu Zeng 3 , Peng-Fei Tu 4

Publish date

2019 Jul 15

PMID

27447597

Abstract

Protocatechualdehyde (PCA) extracted from Phellinus gilvus exhibits anti-cancer activity in human colorectal carcinoma cells (HT-29). However, the underlying mechanisms remain poorly understood. We performed an in vitro study involving MTT, flow cytometry, RT-PCR, and western blot analyses to investigate the effects of PCA treatment on cell proliferation, cell cycle distribution, apoptosis, and expression of several cell cycle-related genes in HT-29 cells. The treatment enhanced S-phase cell cycle and apoptosis in HT-29 cells in a dose-dependent manner. Western blot results showed that PCA treatment decreased the expression levels of cyclin A, cyclin D1, and p27(KIP1) but increased those of cyclin-dependent kinase 2 (CDK2) in HT-29 cells. Furthermore, the expression levels of B-cell lymphoma/leukemia-2 (Bcl-2) and B-cell lymphoma/leukemia-xL (Bcl-xL) were down-regulated, whereas the levels of BH3-interacting domain death agonist (Bid), Bcl-2 homologous antagonist/killer (Bak), and cytosolic cytochrome c were significantly upregulated. Thus, the enzymes caspases-9, -3, -8, and -6 were found to be activated in HT-29 cells with PCA treatment. These results indicate that PCA-induced S-phase cell cycle arrest and apoptosis involve p27(KIP1)-mediated activation of the cyclin-A/D1-Cdk2 signaling pathway and the mitochondrial apoptotic pathway.

KEYWORDS

HT-29 cells; Phellinus gilvus; S-phase arrest; apoptosis; protocatechualdehyde.

Title

Protocatechualdehyde Induces S-Phase Arrest and Apoptosis by Stimulating the p27(KIP1)-Cyclin A/D1-CDK2 and Mitochondrial Apoptotic Pathways in HT-29 Cells

Author

Shi Zhong 1 , You-Gui Li 2 , Dong-Feng Ji 3 , Tian-Bao Lin 4 , Zhi-Qiang Lv 5

Publish date

2016 Jul 19


Description :

Protocatechualdehyde (Catechaldehyde), a natural polyphenol compound isolated from the roots of radix Salviae Miltiorrhizae, is associated with a wide variety of biological activities and has been widely used in medicine as an antioxidant, anti-aging, an antibacterial and anti-inflammatory agent[1].