Chrysin CAS NO.480-40-0

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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.

Chemical Properties of Chrysin

Cas No.	480-40-0	SDF
PubChem ID	5281607	Appearance	Yellow powder
Formula	C15H10O4	M.Wt	254.2
Type of Compound	Flavonoids	Storage	Desiccate at -20°C
Synonyms	5,7-Dihydroxyflavone
Solubility	DMSO : ≥ 100 mg/mL (393.33 mM) *"≥" means soluble, but saturation unknown.
Chemical Name	5,7-dihydroxy-2-phenylchromen-4-one
SMILES	C1=CC=C(C=C1)C2=CC(=O)C3=C(C=C(C=C3O2)O)O
Standard InChIKey	RTIXKCRFFJGDFG-UHFFFAOYSA-N
Standard InChI	InChI=1S/C15H10O4/c16-10-6-11(17)15-12(18)8-13(19-14(15)7-10)9-4-2-1-3-5-9/h1-8,16-17H
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 Chrysin

The bark of Oroxylum indicum

Biological Activity of Chrysin

Description	Chrysin, a naturally-occurring ligand for benzodiazepine receptors, with anticonvulsant , anti-inflammation, anti-cancer, hepatoprotective, and anti-oxidation properties. Chrysin induced apoptosis is mediated through caspase activation and Akt inactivation in U937 leukemia cells; it prevented the development of DN in HFD/STZ-induced type 2 diabetic rats through anti-inflammatory effects in the kidney by specifically targeting the TNF-α pathway.
Targets	NOS | COX | TNF-α | PGE | IL Receptor | PI3K | Akt | Caspase | NF-kB | TGF-β/Smad
In vivo	Chrysin suppresses renal carcinogenesis via amelioration of hyperproliferation, oxidative stress and inflammation: plausible role of NF-κB.[Pubmed: 23194824] Toxicol Lett. 2013 Feb 4;216(2-3):146-58. Flavonoid family is a rich source of polyphenolic compounds and hence possess strong antioxidant and anti inflammatory properties. The aim of this study was to determine the efficacy of Chrysin; a bio-active flavonoid as an anticancer agent. METHODS AND RESULTS: Renal cancer was initiated by single intraperitoneal (i.p.) injection of N-nitrosodiethylamine (DEN 200 mg/kg BW body weight) and promoted by twice weekly administration of ferric nitrilotriacetate (Fe-NTA) 9 mg Fe/kg BW for 16 wk. In the present study, we report the chemopreventive effects of Chrysin against (Fe-NTA) induced renal oxidative stress, inflammation, hyperproliferative response, and two-stage renal carcinogenesis. To ascertain the molecular mechanism implicated in the antitumor promoting activity of Chrysin, its effect was investigated on markers of tumor promotion and inflammation: ornithine decarboxylase (ODC) activity, proliferating cell nuclear antigen (PCNA), inducible nitric oxide synthase (iNOS) and cyclo-oxygenase-2 (COX-2) expression, and on levels of proinflammatory cytokines interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and prostaglandin E(2) (PGE(2)). Pretreatment of animals with Chrysin at both doses (20 and 40 mg/kg body weight) markedly inhibited all. Further, Fe-NTA enhances renal lipid peroxidation, with concomitant reduction in reduced glutathione content (GSH), antioxidant enzymes, and phase II metabolizing enzymes. It induces serum toxicity markers, viz., blood urea nitrogen (BUN), creatinine and lactate dehydrogenase (LDH). Prophylactic treatment of animals with Chrysin before the administration of Fe-NTA was effective in modulating oxidative and renal injury markers and resulted in the diminution of Fe-NTA mediated injury. CONCLUSIONS: These results suggest Chrysin as an effective chemopreventive agent having the capability to obstruct DEN initiated and Fe-NTA promoted renal cancer in the rat model. Chrysin inhibits cell invasion by inhibition of Recepteur d'origine Nantais via suppressing early growth response-1 and NF-κB transcription factor activities in gastric cancer cells.[Pubmed: 25625479] Int J Oncol. 2015 Apr;46(4):1835-43. Cell invasion is one of crucial reasons for cancer metastasis and malignancy. Recepteur d'origine Nantais (RON) has been reported to play an important role in the cancer cell invasion process. High accumulation and activation of RON has been implicated in gastric adenocarcinoma AGS cells. Chrysin is a naturally occurring phytochemical, a type of flavonoid, which has been reported to suppress tumor metastasis. However, the effects of Chrysin on RON expression in gastric cancer are not well studied. METHODS AND RESULTS: In the present study, we examined whether Chrysin affects RON expression in gastric cancer, and if so, its underlying mechanism. We examined the effect of Chrysin on RON expression and activity, via RT-PCR, promoter study, and western blotting in human gastric cancer AGS cells. Chrysin significantly inhibited endogenous and inducible RON expression in a dose-dependent manner. After demonstrating that Egr-1 and NF-κB are the critically required transcription factors for RON expression, we discovered that Chrysin suppressed Egr-1 and NF-κB transcription factor activities. Additionally, the phorbol-12-myristate-13-acetate- (PMA) induced cell invasion was partially abrogated by Chrysin and an RON antibody. CONCLUSIONS: Our results suggest that Chrysin has anticancer effects at least by suppressing RON expression through blocking Egr-1 and NF-κB in gastric cancer AGS cells. Possible anxiolytic effects of chrysin, a central benzodiazepine receptor ligand isolated from Passiflora coerulea.[Pubmed: 7906886] Pharmacol Biochem Behav. 1994 Jan;47(1):1-4. The pharmacological effects of 5,7-dihydroxyflavone (Chrysin), a naturally occurring monoflavonoid that displaces [3H]flunitrazepam binding to the central benzodiazepine (BDZ) receptors, were examined in mice. METHODS AND RESULTS: In the elevated plus-maze test of anxiety, diazepam (DZ, 0.3-0.6 mg/kg) or Chrysin (1 mg/kg) induced increases in the number of entries into the open arms and in the time spent on the open arms, consistent with an anxiolytic action of both compounds. The effects of Chrysin on the elevated plus-maze was abolished by pretreatment with the specific BDZ receptor antagonist Ro 15-1788 (3 mg/kg). In the holeboard, diazepam (1 mg/kg) and Chrysin (3 mg/kg) increased the time spent head-dipping. In contrast, high doses of DZ (6 mg/kg) but not of Chrysin produced a decrease in the number of head dips and in the time spent head-dipping. In the horizontal wire test, diazepam (6 mg/kg) had a myorelaxant action. In contrast, Chrysin (0.6-30 mg/kg) produced no effects in this test. CONCLUSIONS: These data suggest that Chrysin possesses anxiolytic actions without inducing sedation and muscle relaxation. We postulate that this natural monoflavonoid is a partial agonist of the central BDZ receptors.

Protocol of Chrysin

Cell Research

Chrysin-induced apoptosis is mediated through caspase activation and Akt inactivation in U937 leukemia cells.[Pubmed: 15555556 ] Biochem Biophys Res Commun. 2004 Dec 24;325(4):1215-22. Chrysin is a natural, biologically active compound extracted from many plants, honey, and propolis. It possesses potent anti-inflammation, anti-cancer, and anti-oxidation properties. The mechanism by Chrysin is a natural, biologically active compound extracted from many plants, honey, and propolis. It possesses potent anti-inflammation, anti-cancer, and anti-oxidation properties. The mechanism by which Chrysin initiates apoptosis remains poorly understood. METHODS AND RESULTS: In the present report, we investigated the effect of Chrysin on the apoptotic pathway in U937 human promonocytic cells. We show that Chrysin induces apoptosis in association with the activation of caspase 3 and that Akt signal pathway plays a crucial role in Chrysin-induced apoptosis in U937 cells. Furthermore, we have shown that inhibition of Akt phosphorylation in U937 cells by the specific PI3K inhibitor, LY294002 significantly, enhanced apoptosis. Overexpression of a constitutively active Akt (myr-Akt) in U937 cells inhibited the induction of apoptosis, activation of caspase 3, and PLC-gamma1 cleavage by Chrysin. CONCLUSIONS: Together, these findings suggest that the Akt pathway plays a major role in regulating the apoptotic response of human leukemia cells to Chrysin and raise the possibility that combined interruption of Chrysin and PI3K/Akt-related pathways may represent a novel therapeutic strategy in hematological malignancies.

Animal Research

Chrysin (5,7-di-OH-flavone), a naturally-occurring ligand for benzodiazepine receptors, with anticonvulsant properties.[Pubmed: 2173925] Chrysin, an anti-inflammatory molecule, abrogates renal dysfunction in type 2 diabetic rats.[Pubmed: 24848621] Effect of chrysin on hepatoprotective and antioxidant status in D-galactosamine-induced hepatitis in rats.[Pubmed: 20056116 ] Eur J Pharmacol. 2010 Apr 10;631(1-3):36-41. Chrysin is a natural, biologically active compound present in many plants and possesses potent anti-inflammatory, anticancer and antioxidation properties. This work was designed to investigate the effect of Chrysin, on the hepatoprotective efficacy in d-galactosamine-intoxication rats. METHODS AND RESULTS: D-galactosamine-induced toxicity was manifested by the elevation of serum hepatic marker enzyme activities (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma-glutamyl transpeptidase) and the lipid peroxidation process and by decreasing the antioxidant capacity of the plasma, erythrocyte and tissues. Treatment with Chrysin (25, 50 and 100mg/kg body weight) decreased hepatic marker enzyme activities and lipid peroxidation products such as thiobarbituric acid reactive substances, lipid hydroperoxides and conjugated dienes, increased the activities of free-radical scavenging enzymes superoxide dismutase, catalase and glutathione peroxidase and the levels of non-enzymatic antioxidants reduced glutathione, vitamin C and vitamin E. CONCLUSIONS: These findings demonstrate that Chrysin acts as a hepatoprotective and antioxidant agent against d-galactosamine-induced hepatotoxicity. Toxicol Appl Pharmacol. 2014 Aug 15;279(1):1-7. Diabetic nepropathy (DN) is considered as the leading cause of end-stage renal disease (ESRD) worldwide, but the current available treatments are limited. Recent experimental evidences support the role of chronic microinflammation in the development of DN. Therefore, the tumor necrosis factor-alpha (TNF-α) pathway has emerged as a new therapeutic target for the treatment of DN. METHODS AND RESULTS: We investigated the nephroprotective effects of Chrysin (5, 7-dihydroxyflavone) in a high fat diet/streptozotocin (HFD/STZ)-induced type 2 diabetic Wistar albino rat model. Chrysin is a potent anti-inflammatory compound that is abundantly found in plant extracts, honey and bee propolis. The treatment with Chrysin for 16weeks post induction of diabetes significantly abrogated renal dysfunction and oxidative stress. Chrysin treatment considerably reduced renal TNF-α expression and inhibited the nuclear transcription factor-kappa B (NF-кB) activation. Furthermore, Chrysin treatment improved renal pathology and suppressed transforming growth factor-beta (TGF-β), fibronectin and collagen-IV protein expressions in renal tissues. Chrysin also significantly reduced the serum levels of pro-inflammatory cytokines, interleukin-1beta (IL-1β) and IL-6. Moreover, there were no appreciable differences in fasting blood glucose and serum insulin levels between the Chrysin treated groups compared to the HFD/STZ-treated group. CONCLUSIONS: Hence, our results suggest that Chrysin prevents the development of DN in HFD/STZ-induced type 2 diabetic rats through anti-inflammatory effects in the kidney by specifically targeting the TNF-α pathway. Biochem Pharmacol. 1990 Nov 15;40(10):2227-31. Chrysin (5,7-di-OH-flavone) was identified in Passiflora coerulea L., a plant used as a sedative in folkloric medicine. METHODS AND RESULTS: Chrysin was found to be a ligand for the benzodiazepine receptors, both central (Ki = 3 microM, competitive mechanism) and peripheral (Ki = 13 microM, mixed-type mechanism). Administered to mice by the intracerebroventricular route, Chrysin was able to prevent the expression of tonic-clonic seizures induced by pentylenetertrazol. Ro 15-1788, a central benzodiazepine receptor antagonist, abolished this effect. CONCLUSIONS: In addition, all of the treated mice lose the normal righting reflex which suggests a myorelaxant action of the flavonoid. The presence in P. coerulea of benzodiazepine-like compounds was also confirmed.

Preparing Stock Solutions of Chrysin

	1 mg	5 mg	10 mg	20 mg	25 mg
1 mM	3.9339 mL	19.6696 mL	39.3391 mL	78.6782 mL	98.3478 mL
5 mM	0.7868 mL	3.9339 mL	7.8678 mL	15.7356 mL	19.6696 mL
10 mM	0.3934 mL	1.967 mL	3.9339 mL	7.8678 mL	9.8348 mL
50 mM	0.0787 mL	0.3934 mL	0.7868 mL	1.5736 mL	1.967 mL
100 mM	0.0393 mL	0.1967 mL	0.3934 mL	0.7868 mL	0.9835 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.

References on Chrysin

Chrysin, an anti-inflammatory molecule, abrogates renal dysfunction in type 2 diabetic rats.[Pubmed:24848621]

Toxicol Appl Pharmacol. 2014 Aug 15;279(1):1-7.

Diabetic nepropathy (DN) is considered as the leading cause of end-stage renal disease (ESRD) worldwide, but the current available treatments are limited. Recent experimental evidences support the role of chronic microinflammation in the development of DN. Therefore, the tumor necrosis factor-alpha (TNF-alpha) pathway has emerged as a new therapeutic target for the treatment of DN. We investigated the nephroprotective effects of Chrysin (5, 7-dihydroxyflavone) in a high fat diet/streptozotocin (HFD/STZ)-induced type 2 diabetic Wistar albino rat model. Chrysin is a potent anti-inflammatory compound that is abundantly found in plant extracts, honey and bee propolis. The treatment with Chrysin for 16weeks post induction of diabetes significantly abrogated renal dysfunction and oxidative stress. Chrysin treatment considerably reduced renal TNF-alpha expression and inhibited the nuclear transcription factor-kappa B (NF-small ka, CyrillicB) activation. Furthermore, Chrysin treatment improved renal pathology and suppressed transforming growth factor-beta (TGF-beta), fibronectin and collagen-IV protein expressions in renal tissues. Chrysin also significantly reduced the serum levels of pro-inflammatory cytokines, interleukin-1beta (IL-1beta) and IL-6. Moreover, there were no appreciable differences in fasting blood glucose and serum insulin levels between the Chrysin treated groups compared to the HFD/STZ-treated group. Hence, our results suggest that Chrysin prevents the development of DN in HFD/STZ-induced type 2 diabetic rats through anti-inflammatory effects in the kidney by specifically targeting the TNF-alpha pathway.

Chrysin (5,7-di-OH-flavone), a naturally-occurring ligand for benzodiazepine receptors, with anticonvulsant properties.[Pubmed:2173925]

Biochem Pharmacol. 1990 Nov 15;40(10):2227-31.

Chrysin (5,7-di-OH-flavone) was identified in Passiflora coerulea L., a plant used as a sedative in folkloric medicine. Chrysin was found to be a ligand for the benzodiazepine receptors, both central (Ki = 3 microM, competitive mechanism) and peripheral (Ki = 13 microM, mixed-type mechanism). Administered to mice by the intracerebroventricular route, Chrysin was able to prevent the expression of tonic-clonic seizures induced by pentylenetertrazol. Ro 15-1788, a central benzodiazepine receptor antagonist, abolished this effect. In addition, all of the treated mice lose the normal righting reflex which suggests a myorelaxant action of the flavonoid. The presence in P. coerulea of benzodiazepine-like compounds was also confirmed.

Chrysin suppresses renal carcinogenesis via amelioration of hyperproliferation, oxidative stress and inflammation: plausible role of NF-kappaB.[Pubmed:23194824]

Toxicol Lett. 2013 Feb 4;216(2-3):146-58.

Flavonoid family is a rich source of polyphenolic compounds and hence possess strong antioxidant and anti inflammatory properties. The aim of this study was to determine the efficacy of Chrysin; a bio-active flavonoid as an anticancer agent. Renal cancer was initiated by single intraperitoneal (i.p.) injection of N-nitrosodiethylamine (DEN 200 mg/kg BW body weight) and promoted by twice weekly administration of ferric nitrilotriacetate (Fe-NTA) 9 mg Fe/kg BW for 16 wk. In the present study, we report the chemopreventive effects of Chrysin against (Fe-NTA) induced renal oxidative stress, inflammation, hyperproliferative response, and two-stage renal carcinogenesis. To ascertain the molecular mechanism implicated in the antitumor promoting activity of Chrysin, its effect was investigated on markers of tumor promotion and inflammation: ornithine decarboxylase (ODC) activity, proliferating cell nuclear antigen (PCNA), inducible nitric oxide synthase (iNOS) and cyclo-oxygenase-2 (COX-2) expression, and on levels of proinflammatory cytokines interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and prostaglandin E(2) (PGE(2)). Pretreatment of animals with Chrysin at both doses (20 and 40 mg/kg body weight) markedly inhibited all. Further, Fe-NTA enhances renal lipid peroxidation, with concomitant reduction in reduced glutathione content (GSH), antioxidant enzymes, and phase II metabolizing enzymes. It induces serum toxicity markers, viz., blood urea nitrogen (BUN), creatinine and lactate dehydrogenase (LDH). Prophylactic treatment of animals with Chrysin before the administration of Fe-NTA was effective in modulating oxidative and renal injury markers and resulted in the diminution of Fe-NTA mediated injury. These results suggest Chrysin as an effective chemopreventive agent having the capability to obstruct DEN initiated and Fe-NTA promoted renal cancer in the rat model.

Chrysin inhibits cell invasion by inhibition of Recepteur d'origine Nantais via suppressing early growth response-1 and NF-kappaB transcription factor activities in gastric cancer cells.[Pubmed:25625479]

Int J Oncol. 2015 Apr;46(4):1835-43.

Cell invasion is one of crucial reasons for cancer metastasis and malignancy. Recepteur d'origine Nantais (RON) has been reported to play an important role in the cancer cell invasion process. High accumulation and activation of RON has been implicated in gastric adenocarcinoma AGS cells. Chrysin is a naturally occurring phytochemical, a type of flavonoid, which has been reported to suppress tumor metastasis. However, the effects of Chrysin on RON expression in gastric cancer are not well studied. In the present study, we examined whether Chrysin affects RON expression in gastric cancer, and if so, its underlying mechanism. We examined the effect of Chrysin on RON expression and activity, via RT-PCR, promoter study, and western blotting in human gastric cancer AGS cells. Chrysin significantly inhibited endogenous and inducible RON expression in a dose-dependent manner. After demonstrating that Egr-1 and NF-kappaB are the critically required transcription factors for RON expression, we discovered that Chrysin suppressed Egr-1 and NF-kappaB transcription factor activities. Additionally, the phorbol-12-myristate-13-acetate- (PMA) induced cell invasion was partially abrogated by Chrysin and an RON antibody. Our results suggest that Chrysin has anticancer effects at least by suppressing RON expression through blocking Egr-1 and NF-kappaB in gastric cancer AGS cells.

Chrysin-induced apoptosis is mediated through caspase activation and Akt inactivation in U937 leukemia cells.[Pubmed:15555556]

Biochem Biophys Res Commun. 2004 Dec 24;325(4):1215-22.

Chrysin is a natural, biologically active compound extracted from many plants, honey, and propolis. It possesses potent anti-inflammation, anti-cancer, and anti-oxidation properties. The mechanism by which Chrysin initiates apoptosis remains poorly understood. In the present report, we investigated the effect of Chrysin on the apoptotic pathway in U937 human promonocytic cells. We show that Chrysin induces apoptosis in association with the activation of caspase 3 and that Akt signal pathway plays a crucial role in Chrysin-induced apoptosis in U937 cells. Furthermore, we have shown that inhibition of Akt phosphorylation in U937 cells by the specific PI3K inhibitor, LY294002 significantly, enhanced apoptosis. Overexpression of a constitutively active Akt (myr-Akt) in U937 cells inhibited the induction of apoptosis, activation of caspase 3, and PLC-gamma1 cleavage by Chrysin. Together, these findings suggest that the Akt pathway plays a major role in regulating the apoptotic response of human leukemia cells to Chrysin and raise the possibility that combined interruption of Chrysin and PI3K/Akt-related pathways may represent a novel therapeutic strategy in hematological malignancies.

Effect of chrysin on hepatoprotective and antioxidant status in D-galactosamine-induced hepatitis in rats.[Pubmed:20056116]

Eur J Pharmacol. 2010 Apr 10;631(1-3):36-41.

Chrysin is a natural, biologically active compound present in many plants and possesses potent anti-inflammatory, anticancer and antioxidation properties. This work was designed to investigate the effect of Chrysin, on the hepatoprotective efficacy in d-galactosamine-intoxication rats. d-galactosamine-induced toxicity was manifested by the elevation of serum hepatic marker enzyme activities (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma-glutamyl transpeptidase) and the lipid peroxidation process and by decreasing the antioxidant capacity of the plasma, erythrocyte and tissues. Treatment with Chrysin (25, 50 and 100mg/kg body weight) decreased hepatic marker enzyme activities and lipid peroxidation products such as thiobarbituric acid reactive substances, lipid hydroperoxides and conjugated dienes, increased the activities of free-radical scavenging enzymes superoxide dismutase, catalase and glutathione peroxidase and the levels of non-enzymatic antioxidants reduced glutathione, vitamin C and vitamin E. These findings demonstrate that Chrysin acts as a hepatoprotective and antioxidant agent against d-galactosamine-induced hepatotoxicity.

Possible anxiolytic effects of chrysin, a central benzodiazepine receptor ligand isolated from Passiflora coerulea.[Pubmed:7906886]

Pharmacol Biochem Behav. 1994 Jan;47(1):1-4.

The pharmacological effects of 5,7-dihydroxyflavone (Chrysin), a naturally occurring monoflavonoid that displaces [3H]flunitrazepam binding to the central benzodiazepine (BDZ) receptors, were examined in mice. In the elevated plus-maze test of anxiety, diazepam (DZ, 0.3-0.6 mg/kg) or Chrysin (1 mg/kg) induced increases in the number of entries into the open arms and in the time spent on the open arms, consistent with an anxiolytic action of both compounds. The effects of Chrysin on the elevated plus-maze was abolished by pretreatment with the specific BDZ receptor antagonist Ro 15-1788 (3 mg/kg). In the holeboard, diazepam (1 mg/kg) and Chrysin (3 mg/kg) increased the time spent head-dipping. In contrast, high doses of DZ (6 mg/kg) but not of Chrysin produced a decrease in the number of head dips and in the time spent head-dipping. In the horizontal wire test, diazepam (6 mg/kg) had a myorelaxant action. In contrast, Chrysin (0.6-30 mg/kg) produced no effects in this test. These data suggest that Chrysin possesses anxiolytic actions without inducing sedation and muscle relaxation. We postulate that this natural monoflavonoid is a partial agonist of the central BDZ receptors.

Description

Chrysin is one of the most well known estrogen blockers.