Hawthorn Extract

Name: Hawthorn Extract
Brand: MedChemExpress
SKU: HY-N13250

Cat. No.: HY-N13250: Data Sheet
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Hawthorn Extract is an orally active hawthorn extract. Hawthorn Extract decreases Bax expression and increases Bcl-2 expression in the aorta. Hawthorn Extract regulates the AMPK signaling pathway, induces apoptosis, enhances the hepatic antioxidant system, and ameliorates symptoms of liver injury, inflammation and cancer. Hawthorn Extract reduces plasma levels of pro-inflammatory factors, increases plasma levels of anti-inflammatory adiponectin, and alleviates atherosclerotic plaque lesions in the aorta. Hawthorn Extract improves symptoms associated with chronic heart failure. Hawthorn Extract inhibits FMLP-induced superoxide anion production, Elastase release, ILB₄ generation and calcium signaling in neutrophils, and also reduces LPS-induced cytokine production in neutrophils. Hawthorn Extract induces autophagy and inhibits the proliferation of intestinal stem cells. Hawthorn Extract can be used in research related to atherosclerosis, hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease, hepatocellular carcinoma, chronic heart failure and hypotension.

For research use only. We do not sell to patients.

Hawthorn Extract Chemical Structure

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5 mg	In-stock	Estimated Time of Arrival: December 31
10 mg	In-stock	Estimated Time of Arrival: December 31
25 mg	In-stock	Estimated Time of Arrival: December 31
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NUAK1 NUAK2 AMPK AMPK α1β1γ1 AMPK α2β1γ1 AMPK α1β2γ1 AMPK α2β2γ1 BRSK1 BRSK2 HUNK AMPKα

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Bcl-2 Bcl-xL Bcl-W Mcl-1 Bfl-1 Bcl-B Bax Bak Bim BNIP3 Bad

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IL-1 IL-2 IL-3 IL-4 IL-5 IL-6 IL-8 IL-10 IL-12 IL-13 IL-15 IL-17 IL-23 IL-7 IL-33 IL-22 IL-18

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Caspase 1 Caspase 2 Caspase 3 Caspase 4 Caspase 5 Caspase 6 Caspase 7 Caspase 8 Caspase 9 Caspase 10 Caspase 12 Caspase Caspase 11 Caspase-13

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PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

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Akt Akt1 Akt2 Akt3

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Description

Hawthorn Extract is an orally active hawthorn extract. Hawthorn Extract decreases Bax expression and increases Bcl-2 expression in the aorta. Hawthorn Extract regulates the AMPK signaling pathway, induces apoptosis, enhances the hepatic antioxidant system, and ameliorates symptoms of liver injury, inflammation and cancer. Hawthorn Extract reduces plasma levels of pro-inflammatory factors, increases plasma levels of anti-inflammatory adiponectin, and alleviates atherosclerotic plaque lesions in the aorta. Hawthorn Extract improves symptoms associated with chronic heart failure^[3]. Hawthorn Extract inhibits FMLP-induced superoxide anion production, Elastase release, ILB₄ generation and calcium signaling in neutrophils, and also reduces LPS-induced cytokine production in neutrophils. Hawthorn Extract induces autophagy and inhibits the proliferation of intestinal stem cells. Hawthorn Extract can be used in research related to atherosclerosis, hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease, hepatocellular carcinoma, chronic heart failure and hypotension^[1]^[2]^[3]^[4]^[5]^[6].

In Vitro

Hawthorn extract (0.4-1%) protects human hepatocellular carcinoma HepG2 cells against alcohol-induced injury^[2].
Hawthorn extract (0.5-8.66 μg/mL) reduces the viability of human hepatocellular carcinoma HepG2 cells; among them, the ethanol extract of C. pinnatifida fruit (0.8 mg/mL) induces cell apoptosis by altering the mRNA/protein levels of caspase-3, Bax and Bcl-2, the IC₅₀ of the 80% acetone extract of C. pinnatifida fruit is 11.58 μg/mL, and the IC₅₀ of the 80% ethanol extract of stems, flowers and fruits of C. armena is 8.66 μg/mL^[2].
Hawthorn extract blocks repolarizing potassium currents in isolated guinea pig ventricular myocytes, mimicking the activity of class III antiarrhythmic drugs^[3].
Hawthorn extract (0.75-250 μg/mL; 5 min preincubation, 60 min incubation with FMLP) potently inhibits FMLP-induced superoxide anion production in human peripheral blood neutrophils, with an IC₅₀ of 43.6 μg/mL^[5].
Hawthorn extract (0.75-250 μg/mL; 5 min preincubation, followed by incubation with FMLP) potently inhibits FMLP (HY-P0224)-induced elastase release from human peripheral blood neutrophils, with an IC₅₀ of 21.9 μg/mL, and exerts no direct inhibitory effect on elastase activity^[5].
Hawthorn extract (0.75-250 μg/mL; 30 min preincubation) potently inhibits FMLP-induced chemotactic migration of human peripheral blood neutrophils, with an IC₅₀ of 31.6 μg/mL^[5].
Hawthorn extract (125 μg/mL; 60 min preincubation, 5 min cytochalasin B treatment, 5 min FMLP incubation) significantly inhibits FMLP-induced production of LTB₄ in human peripheral blood neutrophils, without affecting basal LTB₄ release^[5].
Hawthorn extract (125 μg/mL; 1 h preincubation, 8 h incubation with LPS) significantly inhibits LPS (HY-D1056)-induced production of TNF-α and IL-8 in human peripheral blood neutrophils, without affecting the baseline levels of cytokines^[5].
Hawthorn extract (0.75-125 μg/mL; 10 min preincubation, FMLP stimulation) potently inhibits FMLP-induced elevation of [Ca²⁺]_i in human peripheral blood neutrophils, with an IC₅₀ of 17.4 μg/mL; at concentrations of 20 μg/mL and 125 μg/mL, it also blocks extracellular calcium influx, intracellular calcium release, and capacitative calcium influx^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Migration Assay ^[5]

Cell Line:	FMLP-induced human peripheral blood neutrophils
Concentration:	0.75-250 μg/mL
Incubation Time:	30 min
Result:	Inhibited FMLP-induced chemotactic migration.

In Vivo

Hawthorn extract (50 mg/kg; p.o.; daily; 16 weeks) exhibits anti-atherosclerotic efficacy in ApoE^-/- mice, reduces aortic plaque area to 20.3%, and regulates lipid profiles, inflammatory factors, and apoptosis-related markers by inhibiting inflammatory and apoptotic signaling pathways^[1].
Hawthorn extract (1-3 mg/mL; oral administration; continuous dietary supplementation) extends the lifespan of *Drosophila melanogaster* by up to 13.7% (average lifespan of male flies in the 3 mg/mL group), while improving their stress tolerance, enhancing antioxidant activity, maintaining intestinal homeostasis, inhibiting PI3K-Akt pathway activity, and activating autophagy^[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	ApoE-/- (8-week-old male, 19-21 g, fed high-fat diet for 16 weeks)^[1]
Dosage:	50 mg/kg
Administration:	p.o.; daily; 16 weeks
Result:	Significantly decreased plasma levels of total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C), and increased plasma high-density lipoprotein cholesterol (HDL-C). Reduced the percentage of aortic plaque area from 61.2% to 20.3%. Decreased plasma levels of monocyte chemoattractant protein-1 (MCP-1), interleukin-1β (IL-1β), and hypersensitive C-reactive protein (hs-CRP), and increased plasma adiponectin (APN) level. Reduced aortic protein and mRNA expression of Bax, and increased aortic protein and mRNA expression of Bcl-2.

Animal Model:	w¹¹¹⁸ strain; Esg-Gal4 USA-GFP transgenic strain (male and female, 2 days old at study start)^[6]
Dosage:	1 mg/mL; 3 mg/mL
Administration:	p.o.; continuous dietary supplementation
Result:	Extended both the mean and maximum lifespan of fruit flies. Reduced the reproductive capacity of fruit flies. Enhanced the climbing ability of fruit flies. Extended the mean survival time of fruit flies under conditions of paraquat exposure, H₂O₂-induced oxidative stress, heat shock, and starvation stress. Reduced the recovery time of fruit flies following cold shock. Increased the activity levels of SOD1, SOD2, and CAT within fruit flies, while simultaneously reducing MDA content. Reduced the proportion of "Smurf" fruit flies (those exhibiting intestinal barrier dysfunction). Reduced the colony-forming unit (CFU) counts of LMRS, ACE, and NR bacterial colonies within the fruit fly gut. Reduced the proliferation rate of intestinal stem cells (ISCs) in fruit flies. Increased the level of lysosomal staining in fruit flies. Increased the mRNA expression levels of Atg1, Atg5, Atg8a, and Atg8b within fruit flies. Increased the mRNA expression levels of SOD1, SOD2, and CAT within fruit flies; decreased the mRNA expression levels of PI3K and Akt-1; and increased the mRNA expression level of FOXO.

Appearance

Solid

Color

Yellow to brown

SMILES

[Hawthorn Extract]

Initial Source

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Store at room temperature, keep dry and cool

In solvent	-80°C	1 year
	-20°C	6 months

Purity & Documentation

Select Batch:

Data Sheet (276 KB) SDS (251 KB)

COA (241 KB)

Handling Instructions (2659 KB)

References

[1]. Wang SZ, et al. Hawthorn Extract Alleviates Atherosclerosis through Regulating Inflammation and Apoptosis Related Factors: An Experimental Study. Chin J Integr Med. 2019;25(2):108-115.

[2]. Kim E, et al. Potential Roles and Key Mechanisms of Hawthorn Extract against Various Liver Diseases. Nutrients. 2022;14(4):867. Published 2022 Feb 18.

[3]. Pittler MH, et al. Hawthorn extract for treating chronic heart failure. Cochrane Database Syst Rev. 2008 Jan 23;2008(1):CD005312.

[4]. Csupor D, et al. The combination of hawthorn extract and camphor significantly increases blood pressure: A meta-analysis and systematic review. Phytomedicine. 2019;63:152984.

[5]. Dalli E, et al. Hawthorn extract inhibits human isolated neutrophil functions. Pharmacol Res. 2008;57(6):445-450.

[6]. Wang Y, et al. Hawthorn extract inhibited the PI3k/Akt pathway to prolong the lifespan of Drosophila melanogaster. J Food Biochem. 2022;46(8):e14169.