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  • Brand : BIOFRON

  • Catalogue Number : BF-V2010

  • Specification : 98%

  • CAS number : 53452-16-7

  • Formula : C32H38O19

  • Molecular Weight : 726.63

  • PUBCHEM ID : 71307582

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Yellow crystalline powder

Botanical Source

Vaccaria hispanica

Structure Type



Standards;Natural Pytochemical;API




(1S)-1,5-Anhydro-2-O-α-L-arabinopyranosyl-1-{2-[4-(β-D-glucopyranosyloxy)phenyl]-5,7-dihydroxy-4-oxo-4H-chromen-6-yl}-D-glucitol/Vaccarin/D-Glucitol, 1,5-anhydro-2-O-α-L-arabinopyranosyl-1-C-[2-[4-(β-D-glucopyranosyloxy)phenyl]-5,7-dihydroxy-4-oxo-4H-1-benzopyran-6-yl]-, (1S)-




1.8±0.1 g/cm3


Methanol; Ethanol; Water; DMSO

Flash Point

345.6±27.8 °C

Boiling Point

1088.1±65.0 °C at 760 mmHg

Melting Point



InChl Key


WGK Germany


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#:53452-16-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Diabetes mellitus is a growing global health issue nearly across the world. Diabetic patients who are prone to develop diabetes-related complications often exhibit progressive neuropathy (painless and sensory loss). It is usual for small wounds to progress to ulceration, which especially worsens with peripheral arterial disease and in the presence of anaerobic bacteria, culminating into gangrene. In our study, vaccarin (VAC), the main active monomer extracted from Chinese herb vaccariae semen, is proven to have a role in promoting diabetic chronic wound healing through a cytoprotective role under high glucose conditions.

We constructed a pressure ulcer on both VAC-treated and control mice based on a type 1 diabetes (T1DM) model. The wound healing index was evaluated by an experimental wound assessment tool (EWAT). We also determined the effect of VAC on the proliferation and cell migration of human microvascular endothelial cells (HMEC-1) by a cell counting kit (CCK-8), a scratch and transwell assay.

The results demonstrated that VAC could promote the proliferation and migration of high glucose-stimulated HMEC-1 cells, which depend on the activation of FOXP2/AGGF1. Activation of the angiogenic factor with G patch and FHA domains 1 (AGGF1) caused enhanced phosphorylation of serine/threonine kinase (Akt) and extracellular regulated protein kinases (Erk1/2). By silencing the expression of forkhead box p2 (FOXP2) protein by siRNA, both mRNA and protein expression of AGGF1 were downregulated, leading to a decreased proliferation and migration of HMEC-1 cells. In addition, a diabetic chronic wound model in vivo unveiled that VAC had a positive effect on chronic wound healing, which involved the activation of the above-mentioned pathways.

In summary, our study found that VAC promoted chronic wound healing in T1DM mice by activating the FOXP2/AGGF1 pathway, indicating that VAC may be a promising candidate for the treatment of the chronic wounds of diabetic patients.


AGGF1; FOXP2; T1DM; diabetic chronic wounds; vaccarin


Vaccarin Regulates Diabetic Chronic Wound Healing through FOXP2/AGGF1 Pathways.


Liu Y1, Sun J1, Ma X1, Li S1, Ai M1, Xu F1, Qiu L1.

Publish date

2020 Mar 13




To explore the potential role and unclear molecular mechanisms of vaccarin in wound healing.

Rats’ skin excision model to study the effects of vaccarin on wound healing in vivo . Hematoxylin and eosin staining was performed to evaluate Histopathologic characteristics. Immunohistochemistry was employed to assess the effects of vaccarin in accelerating angiogenesis. Western blot was used to evaluate relative protein expressed levels.

Vaccarin could significantly promote wound healing and endothelial cells and fibroblasts proliferation in the wound site. Immunohistochemistry and Western blot studies showed that the nodal proteins and receptor (bFGFR) related to angiogenesis signaling pathway were activated, and the microvascular density in the wound site was markedly higher than that in the control group.

The present study was the first to demonstrate that vaccarin is able to induce angiogenesis and accelerate wound healing in vivo by increasing expressions of p-Akt, p-Erk and p-bFGFR. This process is mediated by MAPK/ERK and PI3K/AKT signaling pathways.


Vaccarin hastens wound healing by promoting angiogenesis via activation of MAPK/ERK and PI3K/AKT signaling pathways in vivo.


Hou B1, Cai W2, Chen T3, Zhang Z3, Gong H3, Yang W3, Qiu L4.

Publish date

2020 Feb 7




Oxidized low-density lipoprotein (ox-LDL)-induced endothelial-mesenchymal transition (EndMT), inflammation and apoptosis in endothelial cells play crucial roles in the progression of cardiovascular diseases including atherosclerosis. Vaccarin is a flavonoid glycoside from vaccariae semen associated with powerful cardiovascular protective effects. However, the effects of vaccarin on human umbilical vein endothelial cells (HUVEC) injury in response to ox-LDL remain unknown. Herein, we showed that treatment with vaccarin significantly suppressed ox-LDL-induced HUVEC inflammation, EndMT and apoptosis. Mechanistically, the HUVECs exposed to ox-LDL exhibited enlarged reactive oxygen species (ROS) production and p38 MAPK phosphorylation, which was counteracted by vaccarin. Importantly, ROS activator hydrogen peroxide (H2O2) and p38 MAPK activator anisomycin pretreatment prevent the protective effect of vaccarin on endothelial injury induced by ox-LDL. Our study suggested that vaccarin impeded ox-LDL-triggered HUVEC inflammation, EndMT and apoptosis via inhibition of ROS/p38 MAPK signaling pathway. Vaccarin may have a therapeutic effect on endothelial injury-related disorders.


EndMT; HUVECs; apoptosis; inflammation; ox-LDL; vaccarin


Vaccarin prevents ox-LDL-induced HUVEC EndMT, inflammation and apoptosis by suppressing ROS/p38 MAPK signaling.


Gong L1, Lei Y1, Liu Y1, Tan F1, Li S1, Wang X1, Xu M1, Cai W1, Du B1, Xu F1, Zhou Y1, Han H2, Sun H3, Qiu L1.

Publish date

2019 Apr 15

Description :

Vaccarin promotes endothelial cell proliferation in association with neovascularization in vitro and in vivo. PUMID/DOI:25815517 Mol Med Rep. 2015 Jul;12(1):1131-6. Angiogenesis is a major pathological component of several diseases, including traumatic vascular disease and coronary heart disease. The purpose of the present study was to determine the effects of vaccarin on endothelial cell migration and neovascularization, which are important and necessary components of wound healing. The present study investigated and confirmed neovascularization induced by vaccarin in vitro and in vivo. In vitro, the effects of vaccarin (1.08 and 2.15 μM) on proliferation, migration and tube formation of human microvascular endothelial cells (HMEC)-1 were evaluated via sulforhodamine B assay and migration and tube formation assay, respectively. Furthermore, a mouse Matrigel plus model was used to detect capillary-like tube structures in vivo. Immunohistochemistry was used to detect the protein expression of cluster of differentiation 31 (CD31), p-AKT and p-extracellular-signal-regulated kinases (Erk). Vaccarin significantly promoted HMEC-1 proliferation and migration and tube formation of HMEC-1 at a dose of 2.15 μM. In vivo, vaccarin delivered by daily oral administration significantly improved epidermal growth factor-induced angiogenesis in an intradermal inoculation mouse model. The mouse Matrigel model study also revealed that vaccarin significantly promoted neovascularization via detection of CD31 levels and enhanced protein expression of p-Akt and p?Erk. In addition, vaccarin also promoted expression of CD31. Vaccarin attenuates the human EA.hy926 endothelial cell oxidative stress injury through inhibition of Notch signaling PUMID/DOI:25352009 Int J Mol Med. 2015 Jan;35(1):135-42. Endothelial cell injury is an essential component of atherosclerosis and hypertension. Atherosclerosis and other macrovascular diseases are the most common complications of diabetes. Vaccarin is a major flavonoid glycoside in Vaccariae semen, and is expected to be useful in the treatment of vascular diseases. The aim of the present study was to evaluate the possible effects of Vaccarin in human umbilical vein endothelial cells (EA.hy926) induced by hydrogen peroxide (H2O2) and its underlying mechanism in the prevention and treatment of H2O2 injury. In this study, the EA.hy926 cells were exposed to 250, 500 and 1000 µM H2O2 for 2 and 4 h in the absence or presence of Vaccarin, and the cell injury induced by H2O2 was examined via SRB. Cell migratory ability, lactate dehydrogenase (LDH) leakage, malondialdehyde (MDA) levels and decreasing superoxide dismutase (SOD) activity were evaluated by the wound healing assay and corresponding assay kits. Cell apoptosis was detected by flow cytometry with Annexin V-fluorescein isothiocyanate/propidium iodide Apoptosis Detection kit and Hoechst staining. Furthermore, western blot detected the protein expressions of Notch1, Hes1 and caspase-3. Following treatment with H2O2, it was found that H2O2 stimulated cell injury in a dose-dependent manner, including reducing cell viability and cell migratory ability, increasing LDH leakage and MDA levels, and decreasing SOD activity. H2O2 further accelerated cell apoptosis via activation of Notch1 and the downstream molecule Hes1. Preincubation with Vaccarin was found to protect EA.hy926 cells from H2O2-induced cell oxidative stress injury, which promoted cell viability and cell migratory ability, inhibited the level of LDH and MDA, but enhanced the activity of SOD. In particular, in addition to downregulation Notch signaling, Vaccarin treatments also downregulated caspase-3, a cell apoptotic pathway-related protein. These findings indicated that Vaccarin may be able to selectively protect vascular endothelium from dysfunction induced by H2O2. Microwave-assisted extraction and antioxidant activity of vaccarin from the seeds of Vaccaria segetalis PUMID/DOI:无 Sep. Purif. Technol. 2014, 133(36):91-8. Microwave-assisted extraction (MAE) of Vaccarin from the seeds of Vaccaria segetalis was optimized in this study. Compared with the conventional extraction methods, maceration extraction (ME), ultrasonic-assisted extraction (UAE) and heat reflux extraction (HRE), MAE possessed higher efficiency for the extraction of Vaccarin. The MAE conditions including methanol concentration, temperature, liquid/solid ratio, and microwave power were studied and optimized. The maximum extraction rate of Vaccarin reached 0.52%, under the optimal conditions: methanol concentration 57%, temperature 65 °C, liquid/solid ratio 50 mL/g, and microwave power 400 W. At these optimal extraction parameters, the maximum extraction rate of Vaccarin obtained experimentally was found to be very close to its predicted value. Furthermore, MAE extract of Vaccarin exhibited substantial free radical-scavenging activity with an IC50 value of 0.48 mg/mL, which indicated crude extracts possess good potential in food and pharmaceutical industry.