Paeonol

CAS# 552-41-0

Paeonol

Catalog No. BCN5738----Order now to get a substantial discount!

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Chemical structure

Paeonol

3D structure

Chemical Properties of Paeonol

Cas No. 552-41-0 SDF Download SDF
PubChem ID 11092 Appearance White-grey powder
Formula C9H10O3 M.Wt 166.2
Type of Compound Phenols Storage Desiccate at -20°C
Synonyms 2'-Hydroxy 4'-methoxyacetophenone; Resacetophenone 4-O-methyl ether
Solubility DMSO : ≥ 38 mg/mL (228.68 mM)
H2O : < 0.1 mg/mL (insoluble)
*"≥" means soluble, but saturation unknown.
Chemical Name 1-(2-hydroxy-4-methoxyphenyl)ethanone
SMILES CC(=O)C1=C(C=C(C=C1)OC)O
Standard InChIKey UILPJVPSNHJFIK-UHFFFAOYSA-N
Standard InChI InChI=1S/C9H10O3/c1-6(10)8-4-3-7(12-2)5-9(8)11/h3-5,11H,1-2H3
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Paeonol

The root of Paeonia moutan Sim.

Biological Activity of Paeonol

DescriptionPaeonol has anticancer, anti-inflammatory, antioxidant and cardiovascular protective activities, it shows a novel inhibitory role on neuroinflammation, and presents a new candidate agent for the development of therapies for inflammation-related neurodegenerative diseases. Paeonol suppresses lipopolysaccharide-induced inflammatory cytokines in macrophage cells and protects mice from lethal endotoxin shock. Paeonol inhibits MAO-A and MAO-B with IC50 of 54.6 μM and 42.5 μM, respectively; it inhibits PGE₂ synthesis and COX-2 expression, and modulates Sirtuin 1, PKCδ and c-Src signaling pathway.
TargetsNO | NOS | AMPK | TNF-α | PKC | PGE | COX | ROS | GSK-3 | p53 | IL Receptor | p38MAPK | JNK | ERK | IkB | Caspase | Bcl-2/Bax | p65 | NF-kB | IKK | MAO-A | MAO-B | Src
In vitro

Paeonol protects against premature senescence in endothelial cells by modulating Sirtuin 1 pathway.[Pubmed: 24768807]

J Ethnopharmacol. 2014 Jun 11;154(2):428-36.

Paeonol is a phenolic compound isolated mainly from Moutan cortex, root bark of Chinese Peony tree. Moutan cortex holds a significant value in traditional Chinese medicine for alleviating various oxidative stress-related diseases mainly atherosclerosis and myocardial infarction. The present study seeks to identify the protective mechanisms of Paeonol in oxidative stress-induced premature senescence in endothelial cells.
METHODS AND RESULTS:
HUVECs were pretreated with Paeonol or DMSO control at different doses for 24h prior to an exposure of 200μM of reactive oxygen species (ROS) inducer, hydrogen peroxide (H2O2). The protective effects of Paeonol against H2O2-induced senescence were evaluated and the activation of Sirtuin 1 pathway by Paeonol pretreatment was investigated in HUVECs. Paeonol attenuated H2O2-induced cell growth arrest at G0/G1 phase, reduced the percentage of SA-β-Gal positive cells and increased BrdU incorporation. In addition, enzymatic Sirt1 activation assay indicated that Paeonol significantly increased lysyl deactylase activity of Sirt1 enzyme with a fold change of 2.4±0.195 (p<0.05). Furthermore, pretreatment with Paeonol significantly decreased the levels of p53, acetyl H3K14 and H4K16 protein expression upregulated by H2O2 stimulation. The changes in the histone protein levels were accompanied with an increase in Sirt1 protein expression level.
CONCLUSIONS:
These findings suggest that Paeonol protects endothelial cells against oxidative stress-induced premature senescence by modulating the expressions of Sirt1 protein and its substrates.

Paeonol suppresses chondrosarcoma metastasis through up-regulation of miR-141 by modulating PKCδ and c-Src signaling pathway.[Pubmed: 24992595]

Int J Mol Sci. 2014 Jul 2;15(7):11760-72.

Chondrosarcoma, a primary malignant bone cancer, has potential for local invasion and distant metastasis, especially to the lungs. Patients diagnosed with it show poor prognosis. Paeonol (2'-hydroxy-4'-methoxyacetophenone), the main active compound of traditional Chinese remedy Paeonia lactiflora Pallas, exhibits anti-inflammatory and anti-tumor activity; whether Paeonol regulates metastatic chondrosarcoma is largely unknown.
METHODS AND RESULTS:
Here, we find Paeonol do not increase apoptosis. By contrast, at non-cytotoxic concentrations, Paeonol suppresses migration and invasion of chondrosarcoma cells. We also demonstrate Paeonol enhancing miR-141 expression and miR-141 inhibitor reversing Paeonol-inhibited cell motility; Paeonol also reduces protein kinase C (PKC)d and c-Src kinase activity.
CONCLUSIONS:
Since Paeonol inhibits migration and invasion of human chondrosarcoma via up-regulation of miR-141 via PKCd and c-Src pathways, it thus might be a novel anti-metastasis agent for treatment of metastatic chondrosarcoma.

Paeonol suppresses intercellular adhesion molecule-1 expression in tumor necrosis factor-alpha-stimulated human umbilical vein endothelial cells by blocking p38, ERK and nuclear factor-kappaB signaling pathways.[Pubmed: 17276892 ]

Int Immunopharmacol. 2007 Mar;7(3):343-50.

Paeonol (2'-hydroxy-4'-methoxyacetophenone), the main active compound of the traditionally used Chinese herb Paeonia lactiflora Pallas, has anti-inflammatory, antioxidant and cardiovascular protective activities.
METHODS AND RESULTS:
We studied how the levels of intercellular adhesion molecule-1 (ICAM-1), one of the key molecules in the development of atherosclerosis, might be affected by Paeonol in tumor necrosis factor-alpha (TNF-alpha)-activated human umbilical vein endothelial cells (HUVECs). Paeonol concentration-dependently inhibited the production of ICAM-1; it inhibited nuclear factor-kappaB (NF-kappaB) p65 translocation into the nucleus and the phosphorylation of inhibitory factor kappaBalpha (IkappaBalpha). It also blocked the TNF-alpha-induced phosphorylation of p38 and extracellular signal-regulated kinase (ERK), which are involved in regulating ICAM-1 production by TNF-alpha. Paeonol inhibited U937 monocyte adhesion to HUVECs stimulated by TNF-alpha, suggesting that it may inhibit the binding of monocytes to endothelium by regulating the production of critical adhesion molecules by TNF-alpha. The inhibitory effect of Paeonol on ICAM-1 production might be mediated by inhibiting p38, ERK and NF-kappaB signaling pathways, which are involved in TNF-alpha-induced ICAM-1 production.
CONCLUSIONS:
Thus, Paeonol may be beneficial in the treatment of cardiovascular disorders such as atherosclerosis.

In vivo

Effects of paeonol on anti-neuroinflammatory responses in microglial cells.[Pubmed: 25906473]

Int J Mol Sci. 2015 Apr 21;16(4):8844-60.

Increasing studies suggest that inflammatory processes in the central nervous system mediated by microglial activation plays an important role in numerous neurodegenerative diseases. Development of planning for microglial suppression is considered a key strategy in the search for neuroprotection. Paeonol is a major phenolic component of Moutan Cortex, widely used as a nutrient supplement in Chinese medicine. In this study, we investigated the effects of Paeonol on microglial cells stimulated by inflammagens.
METHODS AND RESULTS:
Paeonol significantly inhibited the release of nitric oxide (NO) and the expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Treatment with Paeonol also reduced reactive oxygen species (ROS) production and inhibited an ATP-induced increased cell migratory activity. Furthermore, the inhibitory effects of neuroinflammation by Paeonol were found to be regulated by phosphorylated adenosine monophosphate-activated protein kinase-α (AMPK-α) and glycogen synthase kinase 3 α/β (GSK 3α/β). Treatment with AMPK or GSK3 inhibitors reverse the inhibitory effect of neuroinflammation by Paeonol in microglial cells. Furthermore, Paeonol treatment also showed significant improvement in the rotarod performance and microglial activation in the mouse model as well.
CONCLUSIONS:
The present study is the first to report a novel inhibitory role of Paeonol on neuroinflammation, and presents a new candidate agent for the development of therapies for inflammation-related neurodegenerative diseases.

Protocol of Paeonol

Cell Research

Paeonol exerts an anticancer effect on human colorectal cancer cells through inhibition of PGE₂ synthesis and COX-2 expression.[Pubmed: 25322760]

Oncol Rep. 2014 Dec;32(6):2845-53.

Cyclooxygenase-2 (COX-2) and its metabolite prostaglandin E2 (PGE2) can potentially affect most of the events in cancer development, including promotion of proliferation, resistance to apoptosis, angiogenesis, immune suppression and invasion. However, worldwide attention has predominantly centered on the cardiovascular toxicity of selective COX-2 inhibitors. Paeonol is a major active extract from the root bark of Paeonia suffruticosa Andrews with anti‑inflammatory, anti-oxidant, anti-allergic, anti-oxidation and antitumor effects. In the present study, we investigated the underlying mechanisms of Paeonol in inducing apoptosis and aimed to ascertain whether its antitumor effect is associated with a reduction in COX-2 expression and a decrease in the levels of PGE2 in colorectal cancer cells.
METHODS AND RESULTS:
We observed that Paeonol inhibited cell proliferation and induced apoptosis in a dose- and time-dependent manner in colorectal cancer cells, which was associated with a reduction in COX-2 expression and PGE2 synthesis. Treatment with the selective COX-2 inhibitor, celecoxib, or transient transfection of colorectal cancer cells with COX-2 siRNA, also inhibited cell proliferation and induced apoptosis. Western blot analysis showed that Paeonol inhibited the activation of NF-κB, an upstream regulator of COX-2, and its translocation to the nucleus. Treatment with increasing doses of Paeonol led to increased expression of pro-apoptotic factor Bax and decreased expression of anti-apoptotic factor Bcl-2. Caspase-3 and caspase-9 were activated, and Paeonol induced loss of mitochondrial membrane potential, suggesting that the apoptosis induced by Paeonol was mediated by mitochondrial pathways. In addition, Paeonol significantly suppressed tumor growth in a xenograft tumor mouse model in a dose-dependent manner.
CONCLUSIONS:
Our findings indicate that Paeonol exerts an antitumor effect on human colorectal cancer cells by inhibiting PGE2 production and COX-2 expression. We expect that Paeonol may replace selective COX-2 inhibitors due to their toxic effects, and may offer a new strategy for the therapy of colorectal cancer.

Animal Research

Paeonol suppresses lipopolysaccharide-induced inflammatory cytokines in macrophage cells and protects mice from lethal endotoxin shock.[Pubmed: 23413967]

Fundam Clin Pharmacol. 2014 Jun;28(3):268-76.

Paeonol (2'-hydroxy-4'-methoxyacetophenone) is the main phenolic compound of the radix of Paeonia suffruticosa which has been used as traditional Chinese medicine. In this study, we primarily investigated the anti-inflammatory effects and the underlying mechanisms of Paeonol in RAW macrophage cells; and based on these effects, we assessed the protective effects of Paeonol on lipopolysaccharide-induced endotoxemia in mice.
METHODS AND RESULTS:
The in vitro study showed that Paeonol regulated the production of TNF-α, IL-1β, IL-6, and IL-10 via inactivation of IκBα, ERK1/2, JNK, and p38 MAPK. In mouse model of lipopolysaccharide-induced endotoxemia, pro- and anti-inflammatory cytokines are significantly regulated, and thus the survival rates of lipolysaccharide-challenged mice are improved by Paeonol (150, 200, or 250 mg/kg).
CONCLUSIONS:
Therefore, Paeonol has a beneficial activity against lipopolysaccharide-induced inflammation in RAW 264.7 cell and mouse models.

Paeonol Dilution Calculator

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Preparing Stock Solutions of Paeonol

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 6.0168 mL 30.0842 mL 60.1685 mL 120.3369 mL 150.4212 mL
5 mM 1.2034 mL 6.0168 mL 12.0337 mL 24.0674 mL 30.0842 mL
10 mM 0.6017 mL 3.0084 mL 6.0168 mL 12.0337 mL 15.0421 mL
50 mM 0.1203 mL 0.6017 mL 1.2034 mL 2.4067 mL 3.0084 mL
100 mM 0.0602 mL 0.3008 mL 0.6017 mL 1.2034 mL 1.5042 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Paeonol

Paeonol is an active extraction from the root of Paeonia suffruticosa, Paeonol inhibits MAO-A and MAO-B with IC50 of 54.6 μM and 42.5 μM, respectively.

In Vitro:Paeonol is found to be inhibitory against MAO A in a dose-dependent manner with IC50 value of 54.6 μM. Paeonol is shown to inhibit MAO-B in a dose-dependent manner with the IC50 of 42.5 μM. For Paeonol, the Ki is estimated to be 51.1 μM. The inhibition of Paeonol on MAO B is of competitive type with Ki value of 38.2 μM[1].

In Vivo:The 200 mg/kg Paeonol+I/R group [AN/V (%): 7.6±2.2, p<0.01] and 100 mg/kg Paeonol+I/R group [AN/V (%): 9.4±2.8, p<0.05] both show lesser extents of no-reflow area in the ventricles compared with the I/R group [AN/V (%): 18.2±2.9]. In particular, the 200 mg/kg Paeonol + I/R group experienced markedly alleviated no-reflow in the whole heart [AN/WH (%): 4.6±1, p<0.05] compared with the I/R group [AN/WH (%): 10.0±1.9][2].

References:
[1]. Kong LD, et al. Inhibition of MAO A and B by some plant-derived alkaloids, phenols and anthraquinones. J Ethnopharmacol. 2004 Apr;91(2-3):351-5. [2]. Ma L, et al. Paeonol Protects Rat Heart by Improving Regional Blood Perfusion during No-Reflow. Front Physiol. 2016 Jul 21;7:298.

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References on Paeonol

Effects of paeonol on anti-neuroinflammatory responses in microglial cells.[Pubmed:25906473]

Int J Mol Sci. 2015 Apr 21;16(4):8844-60.

Increasing studies suggest that inflammatory processes in the central nervous system mediated by microglial activation plays an important role in numerous neurodegenerative diseases. Development of planning for microglial suppression is considered a key strategy in the search for neuroprotection. Paeonol is a major phenolic component of Moutan Cortex, widely used as a nutrient supplement in Chinese medicine. In this study, we investigated the effects of Paeonol on microglial cells stimulated by inflammagens. Paeonol significantly inhibited the release of nitric oxide (NO) and the expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Treatment with Paeonol also reduced reactive oxygen species (ROS) production and inhibited an ATP-induced increased cell migratory activity. Furthermore, the inhibitory effects of neuroinflammation by Paeonol were found to be regulated by phosphorylated adenosine monophosphate-activated protein kinase-alpha (AMPK-alpha) and glycogen synthase kinase 3 alpha/beta (GSK 3alpha/beta). Treatment with AMPK or GSK3 inhibitors reverse the inhibitory effect of neuroinflammation by Paeonol in microglial cells. Furthermore, Paeonol treatment also showed significant improvement in the rotarod performance and microglial activation in the mouse model as well. The present study is the first to report a novel inhibitory role of Paeonol on neuroinflammation, and presents a new candidate agent for the development of therapies for inflammation-related neurodegenerative diseases.

Paeonol suppresses lipopolysaccharide-induced inflammatory cytokines in macrophage cells and protects mice from lethal endotoxin shock.[Pubmed:23413967]

Fundam Clin Pharmacol. 2014 Jun;28(3):268-76.

Paeonol (2'-hydroxy-4'-methoxyacetophenone) is the main phenolic compound of the radix of Paeonia suffruticosa which has been used as traditional Chinese medicine. In this study, we primarily investigated the anti-inflammatory effects and the underlying mechanisms of Paeonol in RAW macrophage cells; and based on these effects, we assessed the protective effects of Paeonol on lipopolysaccharide-induced endotoxemia in mice. The in vitro study showed that Paeonol regulated the production of TNF-alpha, IL-1beta, IL-6, and IL-10 via inactivation of IkappaBalpha, ERK1/2, JNK, and p38 MAPK. In mouse model of lipopolysaccharide-induced endotoxemia, pro- and anti-inflammatory cytokines are significantly regulated, and thus the survival rates of lipolysaccharide-challenged mice are improved by Paeonol (150, 200, or 250 mg/kg). Therefore, Paeonol has a beneficial activity against lipopolysaccharide-induced inflammation in RAW 264.7 cell and mouse models.

Paeonol suppresses intercellular adhesion molecule-1 expression in tumor necrosis factor-alpha-stimulated human umbilical vein endothelial cells by blocking p38, ERK and nuclear factor-kappaB signaling pathways.[Pubmed:17276892]

Int Immunopharmacol. 2007 Mar;7(3):343-50.

Paeonol (2'-hydroxy-4'-methoxyacetophenone), the main active compound of the traditionally used Chinese herb Paeonia lactiflora Pallas, has anti-inflammatory, antioxidant and cardiovascular protective activities. We studied how the levels of intercellular adhesion molecule-1 (ICAM-1), one of the key molecules in the development of atherosclerosis, might be affected by Paeonol in tumor necrosis factor-alpha (TNF-alpha)-activated human umbilical vein endothelial cells (HUVECs). Paeonol concentration-dependently inhibited the production of ICAM-1; it inhibited nuclear factor-kappaB (NF-kappaB) p65 translocation into the nucleus and the phosphorylation of inhibitory factor kappaBalpha (IkappaBalpha). It also blocked the TNF-alpha-induced phosphorylation of p38 and extracellular signal-regulated kinase (ERK), which are involved in regulating ICAM-1 production by TNF-alpha. Paeonol inhibited U937 monocyte adhesion to HUVECs stimulated by TNF-alpha, suggesting that it may inhibit the binding of monocytes to endothelium by regulating the production of critical adhesion molecules by TNF-alpha. The inhibitory effect of Paeonol on ICAM-1 production might be mediated by inhibiting p38, ERK and NF-kappaB signaling pathways, which are involved in TNF-alpha-induced ICAM-1 production. Thus, Paeonol may be beneficial in the treatment of cardiovascular disorders such as atherosclerosis.

Paeonol protects against premature senescence in endothelial cells by modulating Sirtuin 1 pathway.[Pubmed:24768807]

J Ethnopharmacol. 2014 Jun 11;154(2):428-36.

ETHNOPHARMACOLOGICAL RELEVANCE: Paeonol is a phenolic compound isolated mainly from Moutan cortex, root bark of Chinese Peony tree. Moutan cortex holds a significant value in traditional Chinese medicine for alleviating various oxidative stress-related diseases mainly atherosclerosis and myocardial infarction. The present study seeks to identify the protective mechanisms of Paeonol in oxidative stress-induced premature senescence in endothelial cells. MATERIALS AND METHODS: HUVECs were pretreated with Paeonol or DMSO control at different doses for 24h prior to an exposure of 200muM of reactive oxygen species (ROS) inducer, hydrogen peroxide (H2O2). The protective effects of Paeonol against H2O2-induced senescence were evaluated and the activation of Sirtuin 1 pathway by Paeonol pretreatment was investigated in HUVECs. RESULTS: Paeonol attenuated H2O2-induced cell growth arrest at G0/G1 phase, reduced the percentage of SA-beta-Gal positive cells and increased BrdU incorporation. In addition, enzymatic Sirt1 activation assay indicated that Paeonol significantly increased lysyl deactylase activity of Sirt1 enzyme with a fold change of 2.4+/-0.195 (p<0.05). Furthermore, pretreatment with Paeonol significantly decreased the levels of p53, acetyl H3K14 and H4K16 protein expression upregulated by H2O2 stimulation. The changes in the histone protein levels were accompanied with an increase in Sirt1 protein expression level. CONCLUSION: These findings suggest that Paeonol protects endothelial cells against oxidative stress-induced premature senescence by modulating the expressions of Sirt1 protein and its substrates.

Paeonol suppresses chondrosarcoma metastasis through up-regulation of miR-141 by modulating PKCdelta and c-Src signaling pathway.[Pubmed:24992595]

Int J Mol Sci. 2014 Jul 2;15(7):11760-72.

Chondrosarcoma, a primary malignant bone cancer, has potential for local invasion and distant metastasis, especially to the lungs. Patients diagnosed with it show poor prognosis. Paeonol (2'-hydroxy-4'-methoxyacetophenone), the main active compound of traditional Chinese remedy Paeonia lactiflora Pallas, exhibits anti-inflammatory and anti-tumor activity; whether Paeonol regulates metastatic chondrosarcoma is largely unknown. Here, we find Paeonol do not increase apoptosis. By contrast, at non-cytotoxic concentrations, Paeonol suppresses migration and invasion of chondrosarcoma cells. We also demonstrate Paeonol enhancing miR-141 expression and miR-141 inhibitor reversing Paeonol-inhibited cell motility; Paeonol also reduces protein kinase C (PKC)d and c-Src kinase activity. Since Paeonol inhibits migration and invasion of human chondrosarcoma via up-regulation of miR-141 via PKCd and c-Src pathways, it thus might be a novel anti-metastasis agent for treatment of metastatic chondrosarcoma.

Paeonol exerts an anticancer effect on human colorectal cancer cells through inhibition of PGE(2) synthesis and COX-2 expression.[Pubmed:25322760]

Oncol Rep. 2014 Dec;32(6):2845-53.

Cyclooxygenase-2 (COX-2) and its metabolite prostaglandin E2 (PGE2) can potentially affect most of the events in cancer development, including promotion of proliferation, resistance to apoptosis, angiogenesis, immune suppression and invasion. However, worldwide attention has predominantly centered on the cardiovascular toxicity of selective COX-2 inhibitors. Paeonol is a major active extract from the root bark of Paeonia suffruticosa Andrews with antiinflammatory, anti-oxidant, anti-allergic, anti-oxidation and antitumor effects. In the present study, we investigated the underlying mechanisms of Paeonol in inducing apoptosis and aimed to ascertain whether its antitumor effect is associated with a reduction in COX-2 expression and a decrease in the levels of PGE2 in colorectal cancer cells. We observed that Paeonol inhibited cell proliferation and induced apoptosis in a dose- and time-dependent manner in colorectal cancer cells, which was associated with a reduction in COX-2 expression and PGE2 synthesis. Treatment with the selective COX-2 inhibitor, celecoxib, or transient transfection of colorectal cancer cells with COX-2 siRNA, also inhibited cell proliferation and induced apoptosis. Western blot analysis showed that Paeonol inhibited the activation of NF-kappaB, an upstream regulator of COX-2, and its translocation to the nucleus. Treatment with increasing doses of Paeonol led to increased expression of pro-apoptotic factor Bax and decreased expression of anti-apoptotic factor Bcl-2. Caspase-3 and caspase-9 were activated, and Paeonol induced loss of mitochondrial membrane potential, suggesting that the apoptosis induced by Paeonol was mediated by mitochondrial pathways. In addition, Paeonol significantly suppressed tumor growth in a xenograft tumor mouse model in a dose-dependent manner. Our findings indicate that Paeonol exerts an antitumor effect on human colorectal cancer cells by inhibiting PGE2 production and COX-2 expression. We expect that Paeonol may replace selective COX-2 inhibitors due to their toxic effects, and may offer a new strategy for the therapy of colorectal cancer.

Description

Paeonol is an active extraction from the root of Paeonia suffruticosa, Paeonol inhibits MAO-A and MAO-B with IC50 of 54.6 μM and 42.5 μM, respectively.

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