Hesperetin

CAS# 520-33-2

Hesperetin

Catalog No. BCN5657----Order now to get a substantial discount!

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Chemical structure

Hesperetin

3D structure

Chemical Properties of Hesperetin

Cas No. 520-33-2 SDF Download SDF
PubChem ID 72281 Appearance Powder
Formula C16H14O6 M.Wt 302.3
Type of Compound Flavonoids Storage Desiccate at -20°C
Synonyms Eriodictyol 4'-monomethyl ether; Hesperitin; 3',5,7-Trihydroxy 4'-methoxyflavanone
Solubility DMSO : ≥ 33 mg/mL (109.17 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name (2S)-5,7-dihydroxy-2-(3-hydroxy-4-methoxyphenyl)-2,3-dihydrochromen-4-one
SMILES COC1=C(C=C(C=C1)C2CC(=O)C3=C(C=C(C=C3O2)O)O)O
Standard InChIKey AIONOLUJZLIMTK-AWEZNQCLSA-N
Standard InChI InChI=1S/C16H14O6/c1-21-13-3-2-8(4-10(13)18)14-7-12(20)16-11(19)5-9(17)6-15(16)22-14/h2-6,14,17-19H,7H2,1H3/t14-/m0/s1
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 Hesperetin

The peel of Citrus maxima

Biological Activity of Hesperetin

DescriptionHesperetin has antioxidative and anti-inflammatory effects, it inhibits vascular formation by endothelial cells via the inhibition of the PI3K/AKT, ERK and p38 MAPK signaling. Hesperetin-mediated apoptosis of MCF-7 cells involves accumulation of ROS and activation of ASK1/JNK pathway, it induces apoptosis in triple negative breast cancer MDA-MB-231 cells via intrinsic pathway via activation of caspase -9 and -3 and increase in Bax:Bcl-2 ratio.
TargetsCaspase | PARP | Bcl-2/Bax | ROS | JNK | Calcium Channel | ATPase | PI3K | Akt | ERK | p38MAPK | VEGFR | PPAR | TNF-α | p21
In vitro

The pleiotropic effects of fisetin and hesperetin on human acute promyelocytic leukemia cells are mediated through apoptosis, cell cycle arrest, and alterations in signaling networks.[Pubmed: 26081618]

Tumour Biol. 2015 Jun 17.

Fisetin and Hesperetin, flavonoids from various plants, have several pharmaceutical activities including antioxidative, anti-inflammatory, and anticancer effects. However, studies elucidating the role and the mechanism(s) of action of fisetin and Hesperetin in acute promyelocytic leukemia are absent. In this study, we investigated the mechanism of the antiproliferative and apoptotic actions exerted by fisetin and Hesperetin on human HL60 acute promyelocytic leukemia cells.
METHODS AND RESULTS:
The viability of HL60 cells was evaluated using the MTT assay, apoptosis by annexin V/propidium iodide (PI) staining and cell cycle distribution using flow cytometry, and changes in caspase-3 enzyme activity and mitochondrial transmembrane potential. Moreover, we performed whole-genome microarray gene expression analysis to reveal genes affected by fisetin and Hesperetin that can be important for developing of future targeted therapy. Based on data obtained from microarray analysis, we also described biological networks modulated after fisetin and Hesperetin treatment by KEGG and IPA analysis. Fisetin and Hesperetin treatment showed a concentration- and time-dependent inhibition of proliferation and induced G2/M arrest for both agents and G0/G1 arrest for Hesperetin at only the highest concentrations. There was a disruption of mitochondrial membrane potential together with increased caspase-3 activity. Furthermore, fisetin- and Hesperetin-triggered apoptosis was confirmed by annexin V/PI analysis. The microarray gene profiling analysis revealed some important biological pathways including mitogen-activated protein kinases (MAPK) and inhibitor of DNA binding (ID) signaling pathways altered by fisetin and Hesperetin treatment as well as gave a list of genes modulated ≥2-fold involved in cell proliferation, cell division, and apoptosis.
CONCLUSIONS:
Altogether, data suggested that fisetin and Hesperetin have anticancer properties and deserve further investigation.

Hesperetin Induces Apoptosis in Breast Carcinoma by Triggering Accumulation of ROS and Activation of ASK1/JNK Pathway.[Pubmed: 25204891]

J Cell Physiol. 2015 Aug;230(8):1729-39.

Hesperetin, a flavanone glycoside predominantly found in citrus fruits, exhibits a wide array of biological properties. In the present study Hesperetin exhibited a significant cytotoxic effect in human breast carcinoma MCF-7 cells in a concentration- and time-dependent manner without affecting normal (HMEC) as well as immortalized normal mammary epithelial cells (MCF-10A).
METHODS AND RESULTS:
The cytotoxic effect of Hesperetin was due to the induction of apoptosis as evident from the phosphatidyl-serine externalization, DNA fragmentation, caspase-7 activation, and PARP cleavage. Apoptosis was associated with caspase-9 activation, mitochondrial membrane potential loss, release of cytochrome c, and increase in Bax:Bcl-2 ratio. Pre-treatment with caspase-9 specific inhibitor (Z-LEHD-fmk) markedly attenuated apoptosis suggesting an involvement of intrinsic mitochondrial apoptotic cascade. Further, DCFDA flow-cytometric analysis revealed triggering of ROS in a time-dependent manner. Pre-treatment with ROS scavenger N-acetylcysteine (NAC) and glutathione markedly abrogated Hesperetin-mediated apoptosis whereas carbonyl cyanide m-chlorophenylhydrazone (CCCP) pretreatment along with DHR123-based flow-cytometry indicated the generation of cytosolic ROS. Profiling of MAPKs revealed activation of JNK upon Hesperetin treatment which was abrogated upon NAC pre-treatment. Additionally, inhibition of JNK by SP600125 significantly reversed Hesperetin-mediated apoptosis. The activation of JNK was associated with the activation of ASK1.
CONCLUSIONS:
Silencing of ASK1 resulted in significant attenuation of JNK activation as well as reversed the Hesperetin-mediated apoptosis suggesting that Hesperetin-mediated apoptosis of MCF-7 cells involves accumulation of ROS and activation of ASK1/JNK pathway. In addition, Hesperetin also induced apoptosis in triple negative breast cancer MDA-MB-231 cells via intrinsic pathway via activation of caspase -9 and -3 and increase in Bax:Bcl-2 ratio.

Hesperetin inhibit adipocyte differentiation and enhance Bax- and p21-mediated adipolysis in human mesenchymal stem cell adipogenesis.[Pubmed: 25345581]

J Biochem Mol Toxicol. 2015 Mar;29(3):99-108.

We aimed to explore the antiadipogenic and adipolysis effect of Hesperetin in human mesenchymal stem cells (hMSCs)-induced adipogenesis.
METHODS AND RESULTS:
IC50 value of Hesperetin was higher for hMSCs such as 149.2 ± 13.2 μmol for 24 h and 89.4 ± 11.4 μmol in 48 h, whereas in preadipocytes was 87.6 ± 9.5 μmol and 72.4 ± 5.6 μmol in 24 h and 48 h, respectively. Hesperetin treatment (5, 10, and 20 μmol) to adipogenesis-induced hMSCs (Group 1) and preadipocytes (Group 2) resulted in a significantly (p < 0.05) increased lipolysis. The treatment with Hesperetin decreased the expression of resistin, adiponectin, aP2, LPL, PPAR-γ, and TNF-α in Groups 1 and 2, whereas a significant increase was observed in Bcl, Bax, and p21 expression in Group 2 compared to untreated preadipocytes. hMSCs cultured in adipogenic medium along with Hesperetin significantly inhibited adipocyte differentiation and increased the proapoptotic gene expression levels in preadipocyte.
CONCLUSIONS:
Our result indicates the antiadipogenic and adipolysis effects of Hesperetin.

Protocol of Hesperetin

Cell Research

Hesperetin Inhibits Vascular Formation by Suppressing of the PI3K/AKT, ERK, and p38 MAPK Signaling Pathways.[Pubmed: 25580394]

Hesperetin induces the apoptosis of hepatocellular carcinoma cells via mitochondrial pathway mediated by the increased intracellular reactive oxygen species, ATP and calcium.[Pubmed: 25737432]

Med Oncol. 2015 Apr;32(4):101.

Hesperetin, a flavonoid from citrus fruits, has been proved to possess biological activity on various types of human cancers. However, few related studies on hepatocellular carcinoma are available. In this study, we aimed to investigate the effect of Hesperetin on hepatocellular carcinoma cells in vitro and in vivo and clarify its potentially specific mechanism.
METHODS AND RESULTS:
Compared with the control group, the proliferations of hepatocellular carcinoma cells in Hesperetin groups were significantly inhibited (P < 0.05), and a dose- and time-dependent inhibition of cell viability was observed. When pretreated with H2O2 (1 mM) or N-acetyl-L-cysteine (5 mM), the inhibition of cell viability by Hesperetin was enhanced or reduced, respectively (P < 0.05). Similarly, the levels of intracellular ROS, ATP and Ca(2+) changed in different groups (P < 0.05). The results of Hoechst 33258 staining showed that the percentages of apoptotic cells in Hesperetin groups are remarkably higher than that in control group (P < 0.05). And the results of Western blot showed that Hesperetin caused an increase in the levels of cytosolic AIF, cytosolic Apaf-1, cytosolic Cyt C, caspase-3, caspase-9 and Bax and a decrease in that of Bcl-2, mitochondrial AIF, mitochondrial Apaf-1 and mitochondrial Cyt C (P < 0.05). Meanwhile, Hesperetin significantly inhibited the growth of xenograft tumors.
CONCLUSIONS:
Our study suggests that Hesperetin could inhibit the proliferation and induce the apoptosis of hepatocellular carcinoma via triggering the activation of the mitochondrial pathway by increasing the levels of intracellular ROS, ATP and Ca(2+).

Prev Nutr Food Sci. 2014 Dec;19(4):299-306.

Hesperetin has been shown to possess a potential anti-angiogenic effect, including vascular formation by endothelial cells. However, the mechanisms underlying the potential anti-angiogenic activity of Hesperetin are not fully understood. In the present study, we evaluated whether Hesperetin has anti-angiogenic effects in human umbilical vascular endothelial cells (HUVECs).
METHODS AND RESULTS:
HUVECs were treated with 50 ng/mL vascular endothelial growth factor (VEGF) to induce proliferation as well as vascular formation, followed by treatment with several doses of Hesperetin (25, 50, and 100 μM) for 24 h. Cell proliferation and vascular formation were analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and tube formation assay, respectively. In addition, cell signaling related to cell proliferation and vascular formation was analyzed by western blot. Furthermore, a mouse aorta ring assay was performed to confirm the effect of Hesperetin on vascular formation. Hesperetin treatment did not cause differences in HUVECs proliferation. However, Hesperetin significantly inhibited VEGF-induced cell migration and tube formation of HUVECs (P<0.05). Moreover, Hesperetin suppressed the expression of ERK, p38 MAPK, and PI3K/AKT in the VEGF-induced HUVECs. In an ex vivo model, Hesperetin also suppressed microvessel sprouting of mouse aortic rings.
CONCLUSIONS:
Taken together, the findings suggest that Hesperetin inhibited vascular formation by endothelial cells via the inhibition of the PI3K/AKT, ERK and p38 MAPK signaling.

Hesperetin Dilution Calculator

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Preparing Stock Solutions of Hesperetin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.308 mL 16.5399 mL 33.0797 mL 66.1594 mL 82.6993 mL
5 mM 0.6616 mL 3.308 mL 6.6159 mL 13.2319 mL 16.5399 mL
10 mM 0.3308 mL 1.654 mL 3.308 mL 6.6159 mL 8.2699 mL
50 mM 0.0662 mL 0.3308 mL 0.6616 mL 1.3232 mL 1.654 mL
100 mM 0.0331 mL 0.1654 mL 0.3308 mL 0.6616 mL 0.827 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 Hesperetin

Hesperetin is a natural flavanone, and acts as a potent and broad-spectrum inhibitor against human UGT activity.

In Vitro:Hesperetin has the retention of antioxidant potential in self nano-emulsifying drug delivery system[1]. Hesperetin and NGR display broad-spectrum inhibition against human UGTs. Besides, Hesperetin exhibits strong inhibitory effects on UGT1A1, 1A3 and 1A9 (both IC50 and Ki values lower than 10 µM) and moderately inhibits UGT1A4, UGT1A7, UGT1A8 (IC50 values 29.68-63.87 µM)[2]. Hesperetin interacts with different types of proteins involving hydrogen bonds, pi-pi effects, pi-cation bonding and pi-sigma interactions with varying binding energies. Hesperetin exhibits drug-like properties which projects its potential as a therapeutic option for CHIKV infection[3]. Hesperetin dose-dependently reduces GCDCA-induced caspase-3 activity in cultured primary rat hepatocytes. Hesperetin also dose-dependently reduces CM-induced Nos2 (iNOS) expression in hepatocytes. Interestingly, hesperetin-induced expression of the antioxidant gene haem oxygenase 1 (HO-1) about fourfold compared with cytokine mixture alone[5].

In Vivo:Preadministration of Hesperetin (40 mg/kg b.w., oral) significantly attenuates the Cd-induced oxidative stress and mitochondrial dysfunction, restores the antioxidant and membrane-bound enzyme activities and decreases apoptosis in the brain of rats[4]. Hesperetin (200 mg/kg) attenuates Con A-induced hepatocyte apoptosis and hepatic Nos2 (iNOS) expression in mice. Hesperetin co-treatment also decreases the occurrence of apoptotic bodies, hydropic degeneration, nuclear fragments, autolysis and haemorrhage. The number of leukocytes infiltrated in liver tissue of mice with D-GalN/LPS-induced fulminant hepatitis are significantly decreased by hesperetin in a murine model[5].

References:
[1]. Arya A, et al. Bioflavonoid hesperetin overcome bicalutamide induced toxicity by co-delivery in novel SNEDDS formulations: Optimization, in vivo evaluation and uptake mechanism. Mater Sci Eng C Mater Biol Appl. 2017 Feb 1;71:954-964. [2]. Liu D, et al. Inhibitory Effect of Hesperetin and Naringenin on Human UDP-Glucuronosyltransferase Enzymes: Implications for Herb-Drug Interactions. Biol Pharm Bull. 2016;39(12):2052-2059. [3]. Oo A, et al. In silico study on anti-Chikungunya virus activity of hesperetin. PeerJ. 2016 Oct 26;4:e2602. eCollection 2016. [4]. Shagirtha K, et al. Neuroprotective efficacy of hesperetin against cadmium induced oxidative stress in the brain of rats. Toxicol Ind Health. 2016 Nov 1. pii: 0748233716665301. [5]. Bai X, et al. The protective effect of the natural compound hesperetin against fulminant hepatitis in vivo and in vitro. Br J Pharmacol. 2017 Jan;174(1):41-56.

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References on Hesperetin

Hesperetin Induces Apoptosis in Breast Carcinoma by Triggering Accumulation of ROS and Activation of ASK1/JNK Pathway.[Pubmed:25204891]

J Cell Physiol. 2015 Aug;230(8):1729-39.

Hesperetin, a flavanone glycoside predominantly found in citrus fruits, exhibits a wide array of biological properties. In the present study Hesperetin exhibited a significant cytotoxic effect in human breast carcinoma MCF-7 cells in a concentration- and time-dependent manner without affecting normal (HMEC) as well as immortalized normal mammary epithelial cells (MCF-10A). The cytotoxic effect of Hesperetin was due to the induction of apoptosis as evident from the phosphatidyl-serine externalization, DNA fragmentation, caspase-7 activation, and PARP cleavage. Apoptosis was associated with caspase-9 activation, mitochondrial membrane potential loss, release of cytochrome c, and increase in Bax:Bcl-2 ratio. Pre-treatment with caspase-9 specific inhibitor (Z-LEHD-fmk) markedly attenuated apoptosis suggesting an involvement of intrinsic mitochondrial apoptotic cascade. Further, DCFDA flow-cytometric analysis revealed triggering of ROS in a time-dependent manner. Pre-treatment with ROS scavenger N-acetylcysteine (NAC) and glutathione markedly abrogated Hesperetin-mediated apoptosis whereas carbonyl cyanide m-chlorophenylhydrazone (CCCP) pretreatment along with DHR123-based flow-cytometry indicated the generation of cytosolic ROS. Profiling of MAPKs revealed activation of JNK upon Hesperetin treatment which was abrogated upon NAC pre-treatment. Additionally, inhibition of JNK by SP600125 significantly reversed Hesperetin-mediated apoptosis. The activation of JNK was associated with the activation of ASK1. Silencing of ASK1 resulted in significant attenuation of JNK activation as well as reversed the Hesperetin-mediated apoptosis suggesting that Hesperetin-mediated apoptosis of MCF-7 cells involves accumulation of ROS and activation of ASK1/JNK pathway. In addition, Hesperetin also induced apoptosis in triple negative breast cancer MDA-MB-231 cells via intrinsic pathway via activation of caspase -9 and -3 and increase in Bax:Bcl-2 ratio.

Hesperetin Inhibits Vascular Formation by Suppressing of the PI3K/AKT, ERK, and p38 MAPK Signaling Pathways.[Pubmed:25580394]

Prev Nutr Food Sci. 2014 Dec;19(4):299-306.

Hesperetin has been shown to possess a potential anti-angiogenic effect, including vascular formation by endothelial cells. However, the mechanisms underlying the potential anti-angiogenic activity of Hesperetin are not fully understood. In the present study, we evaluated whether Hesperetin has anti-angiogenic effects in human umbilical vascular endothelial cells (HUVECs). HUVECs were treated with 50 ng/mL vascular endothelial growth factor (VEGF) to induce proliferation as well as vascular formation, followed by treatment with several doses of Hesperetin (25, 50, and 100 muM) for 24 h. Cell proliferation and vascular formation were analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and tube formation assay, respectively. In addition, cell signaling related to cell proliferation and vascular formation was analyzed by western blot. Furthermore, a mouse aorta ring assay was performed to confirm the effect of Hesperetin on vascular formation. Hesperetin treatment did not cause differences in HUVECs proliferation. However, Hesperetin significantly inhibited VEGF-induced cell migration and tube formation of HUVECs (P<0.05). Moreover, Hesperetin suppressed the expression of ERK, p38 MAPK, and PI3K/AKT in the VEGF-induced HUVECs. In an ex vivo model, Hesperetin also suppressed microvessel sprouting of mouse aortic rings. Taken together, the findings suggest that Hesperetin inhibited vascular formation by endothelial cells via the inhibition of the PI3K/AKT, ERK and p38 MAPK signaling.

Hesperetin inhibit adipocyte differentiation and enhance Bax- and p21-mediated adipolysis in human mesenchymal stem cell adipogenesis.[Pubmed:25345581]

J Biochem Mol Toxicol. 2015 Mar;29(3):99-108.

We aimed to explore the antiadipogenic and adipolysis effect of Hesperetin in human mesenchymal stem cells (hMSCs)-induced adipogenesis. IC50 value of Hesperetin was higher for hMSCs such as 149.2 +/- 13.2 mumol for 24 h and 89.4 +/- 11.4 mumol in 48 h, whereas in preadipocytes was 87.6 +/- 9.5 mumol and 72.4 +/- 5.6 mumol in 24 h and 48 h, respectively. Hesperetin treatment (5, 10, and 20 mumol) to adipogenesis-induced hMSCs (Group 1) and preadipocytes (Group 2) resulted in a significantly (p < 0.05) increased lipolysis. The treatment with Hesperetin decreased the expression of resistin, adiponectin, aP2, LPL, PPAR-gamma, and TNF-alpha in Groups 1 and 2, whereas a significant increase was observed in Bcl, Bax, and p21 expression in Group 2 compared to untreated preadipocytes. hMSCs cultured in adipogenic medium along with Hesperetin significantly inhibited adipocyte differentiation and increased the proapoptotic gene expression levels in preadipocyte. Our result indicates the antiadipogenic and adipolysis effects of Hesperetin.

The pleiotropic effects of fisetin and hesperetin on human acute promyelocytic leukemia cells are mediated through apoptosis, cell cycle arrest, and alterations in signaling networks.[Pubmed:26081618]

Tumour Biol. 2015 Nov;36(11):8973-84.

Fisetin and Hesperetin, flavonoids from various plants, have several pharmaceutical activities including antioxidative, anti-inflammatory, and anticancer effects. However, studies elucidating the role and the mechanism(s) of action of fisetin and Hesperetin in acute promyelocytic leukemia are absent. In this study, we investigated the mechanism of the antiproliferative and apoptotic actions exerted by fisetin and Hesperetin on human HL60 acute promyelocytic leukemia cells. The viability of HL60 cells was evaluated using the MTT assay, apoptosis by annexin V/propidium iodide (PI) staining and cell cycle distribution using flow cytometry, and changes in caspase-3 enzyme activity and mitochondrial transmembrane potential. Moreover, we performed whole-genome microarray gene expression analysis to reveal genes affected by fisetin and Hesperetin that can be important for developing of future targeted therapy. Based on data obtained from microarray analysis, we also described biological networks modulated after fisetin and Hesperetin treatment by KEGG and IPA analysis. Fisetin and Hesperetin treatment showed a concentration- and time-dependent inhibition of proliferation and induced G2/M arrest for both agents and G0/G1 arrest for Hesperetin at only the highest concentrations. There was a disruption of mitochondrial membrane potential together with increased caspase-3 activity. Furthermore, fisetin- and Hesperetin-triggered apoptosis was confirmed by annexin V/PI analysis. The microarray gene profiling analysis revealed some important biological pathways including mitogen-activated protein kinases (MAPK) and inhibitor of DNA binding (ID) signaling pathways altered by fisetin and Hesperetin treatment as well as gave a list of genes modulated >/=2-fold involved in cell proliferation, cell division, and apoptosis. Altogether, data suggested that fisetin and Hesperetin have anticancer properties and deserve further investigation.

Hesperetin induces the apoptosis of hepatocellular carcinoma cells via mitochondrial pathway mediated by the increased intracellular reactive oxygen species, ATP and calcium.[Pubmed:25737432]

Med Oncol. 2015 Apr;32(4):101.

Hesperetin, a flavonoid from citrus fruits, has been proved to possess biological activity on various types of human cancers. However, few related studies on hepatocellular carcinoma are available. In this study, we aimed to investigate the effect of Hesperetin on hepatocellular carcinoma cells in vitro and in vivo and clarify its potentially specific mechanism. Compared with the control group, the proliferations of hepatocellular carcinoma cells in Hesperetin groups were significantly inhibited (P < 0.05), and a dose- and time-dependent inhibition of cell viability was observed. When pretreated with H2O2 (1 mM) or N-acetyl-L-cysteine (5 mM), the inhibition of cell viability by Hesperetin was enhanced or reduced, respectively (P < 0.05). Similarly, the levels of intracellular ROS, ATP and Ca(2+) changed in different groups (P < 0.05). The results of Hoechst 33258 staining showed that the percentages of apoptotic cells in Hesperetin groups are remarkably higher than that in control group (P < 0.05). And the results of Western blot showed that Hesperetin caused an increase in the levels of cytosolic AIF, cytosolic Apaf-1, cytosolic Cyt C, caspase-3, caspase-9 and Bax and a decrease in that of Bcl-2, mitochondrial AIF, mitochondrial Apaf-1 and mitochondrial Cyt C (P < 0.05). Meanwhile, Hesperetin significantly inhibited the growth of xenograft tumors. Our study suggests that Hesperetin could inhibit the proliferation and induce the apoptosis of hepatocellular carcinoma via triggering the activation of the mitochondrial pathway by increasing the levels of intracellular ROS, ATP and Ca(2+).

Description

Hesperetin is a natural flavanone, and acts as a potent and broad-spectrum inhibitor against human UGT activity. Hesperetin induces apoptosis via p38 MAPK activation.

Keywords:

Hesperetin,520-33-2,Eriodictyol 4'-monomethyl ether; Hesperitin; 3',5,7-Trihydroxy 4'-methoxyflavanone,Natural Products, buy Hesperetin , Hesperetin supplier , purchase Hesperetin , Hesperetin cost , Hesperetin manufacturer , order Hesperetin , high purity Hesperetin

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