Hydroxysafflor yellow ACAS# 78281-02-4 |
Quality Control & MSDS
3D structure
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| Cas No. | 78281-02-4 | SDF | Download SDF |
| PubChem ID | 6443665 | Appearance | Yellow-orange powder |
| Formula | C27H32O16 | M.Wt | 612.53 |
| Type of Compound | Chalcones | Storage | Desiccate at -20°C |
| Synonyms | Safflomin A; HSYA;146087-19-6 | ||
| Solubility | DMSO : ≥ 34 mg/mL (55.51 mM) H2O : 33.33 mg/mL (54.41 mM; Need ultrasonic) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | (6E)-2,5-dihydroxy-6-[(E)-1-hydroxy-3-(4-hydroxyphenyl)prop-2-enylidene]-2,4-bis[(2S,3R,4R,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]cyclohex-4-ene-1,3-dione | ||
| SMILES | C1=CC(=CC=C1C=CC(=C2C(=C(C(=O)C(C2=O)(C3C(C(C(C(O3)CO)O)O)O)O)C4C(C(C(C(O4)CO)O)O)O)O)O)O | ||
| Standard InChIKey | IAVUBSCVWHLRGE-UXEKTNMQSA-N | ||
| Standard InChI | InChI=1S/C27H32O16/c28-7-12-16(32)19(35)21(37)23(42-12)15-18(34)14(11(31)6-3-9-1-4-10(30)5-2-9)24(39)27(41,25(15)40)26-22(38)20(36)17(33)13(8-29)43-26/h1-6,12-13,16-17,19-23,26,28-38,41H,7-8H2/b6-3+,14-11+/t12-,13-,16-,17-,19+,20+,21-,22-,23+,26-,27?/m1/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. |
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| 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. |
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| 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. | ||
| Description | Hydroxysafflor yellow A(H-A) possesses hepatoprotective, anti-inflammatory, and anti-tumor activities, it can effectively protect the liver of rats from long-term alcohol injury, which relates with the enhanced antioxidant capacity of liver tissues and inhibition of TGF-β1 expression, it also inhibited angiogenesis of hepatocellular carcinoma via blocking ERK/MAPK and NF-κB signaling pathway in H22 tumor-bearing mice. H-A also can provide protection to H9c2 cardiomyocytes against A/R-induced apoptosis by the upregulation of HO-1 expression through the PI3K/Akt/Nrf2 signaling pathway. |
| Targets | TGF-β/Smad | ERK | Raf | p38MAPK | NF-kB | p65 | IkB | VEGFR | ROS | IL Receptor | TNF-α | TLR | JNK | PI3K | Akt | Nrf2 | Bcl-2/Bax | HIF | IKK | HO-1 |
| In vitro | Upregulation of heme oxygenase-1 expression by hydroxysafflor yellow A conferring protection from anoxia/reoxygenation-induced apoptosis in H9c2 cardiomyocytes.[Pubmed: 21497407 ]Int J Cardiol. 2012 Oct 4;160(2):95-101.Reperfusion therapy is widely utilized for acute myocardial infarction (AMI), so ischemia/reperfusion (I/R) of the heart is frequently encountered in clinical practice. The curative effects of reperfusion therapy for AMI are favourable in most cases, but reperfusion can also cause harmful effect to cardiomyocytes. Hydroxysafflor yellow A (HSYA) is an effective therapeutic agent to alleviate I/R injury, but the mechanisms underlying this therapeutic effect are unknown.
Hydroxysafflor yellow A enhances survival of vascular endothelial cells under hypoxia via upregulation of the HIF-1 alpha-VEGF pathway and regulation of Bcl-2/Bax.[Pubmed: 18670359 ]J Cardiovasc Pharmacol. 2008 Aug;52(2):191-202.Hydroxysafflor yellow A (HSYA) is a component of the flower Carthamus tinctorius L. The present investigation determines whether HSYA can modify the effects of hypoxia on vascular endothelial cells (EC) and its mechanisms.
|
| In vivo | Protective effects of hydroxysafflor yellow A (HSYA) on alcohol-induced liver injury in rats.[Pubmed: 25626885]J Physiol Biochem. 2015 Mar;71(1):69-78.Hydroxysafflor yellow A (HSYA), the main active natural constituent extracted from Carthamus tinctorius L., has been widely used for the treatment of cerebrovascular and cardiovascular diseases.
|
| Kinase Assay | Hydroxysafflor yellow A inhibits angiogenesis of hepatocellular carcinoma via blocking ERK/MAPK and NF-κB signaling pathway in H22 tumor-bearing mice.[Pubmed: 25720342]Eur J Pharmacol. 2015 May 5;754:105-14.Hydroxysafflor yellow A (HSYA), a flavonoid derived and isolated from traditional Chinese medicine Carthamus tinctorius L., possesses anti-tumor activity. However, its effects on hepatocellular carcinoma (HCC) have not been investigated.
|
| Cell Research | Hydroxysafflor yellow A (HYSA) inhibited the proliferation and differentiation of 3T3-L1 preadipocytes.[Pubmed: 25749912]Cytotechnology. 2015 Oct;67(5):885-92.Hydroxysafflor yellow A (HSYA), a main component of safflor yellow, has been demonstrated to prevent steroid-induced avascular necrosis of femoral head by inhibiting primary bone marrow-derived mesenchymal stromal cells adipogenic differentiation induced by steroid. |
| Animal Research | Hydroxysafflor yellow A ameliorates lipopolysaccharide-induced acute lung injury in mice via modulating toll-like receptor 4 signaling pathways.[Pubmed: 25466274]Int Immunopharmacol. 2014 Dec;23(2):649-57.Hydroxysafflor yellow A (HSYA) is a main bio-active compound important of a traditional Chinese medicine named Carthamus tinctorius L. and has been shown to possess various effects, especially anti-inflammatory benefits and potential protections against acute lung injury (ALI) in previous studies.
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Hydroxysafflor yellow A Dilution Calculator
Hydroxysafflor yellow A Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.6326 mL | 8.1629 mL | 16.3257 mL | 32.6515 mL | 40.8143 mL |
| 5 mM | 0.3265 mL | 1.6326 mL | 3.2651 mL | 6.5303 mL | 8.1629 mL |
| 10 mM | 0.1633 mL | 0.8163 mL | 1.6326 mL | 3.2651 mL | 4.0814 mL |
| 50 mM | 0.0327 mL | 0.1633 mL | 0.3265 mL | 0.653 mL | 0.8163 mL |
| 100 mM | 0.0163 mL | 0.0816 mL | 0.1633 mL | 0.3265 mL | 0.4081 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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Hydroxysafflor yellow A is a flavonoid derived and isolated from traditional Chinese medicine Carthamus tinctorius L., possesses anti-tumor activity. IC50 value: Target: in vitro: HYSA could inhibit LPS-induced VSMCs proliferation and migration, accompanied by the downregulated levels of several key pro-inflammatory cytokines, including TNF-α, IL-6, and IL-8. We further showed that HYSA inhibited LPS-induced upregulation of TLR-4 expression as well as the activation of Rac1/Akt pathway [1]. HSYA protected EC viability against LPS-induced injury (P<0.05). LPS-induced NF-κB p65 subunit DNA binding (P<0.01) and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor -α (I-κB-α) phosphorylation was inhibited by HSYA. HSYA attenuated LPS triggered ICAM-1 and E-selectin mRNA levels elevation and phosphorylation of p38 MAPK or c-Jun N-terminal kinase MAPK [2]. HSYA inhibited the proliferation of 3T3-L1 preadipocytes and cell viability greatly decreased in a dose and time dependent manner. HSYA (1 mg/l) notably reduced the amount of intracellular lipid and triglyceride content in adipocytes by 21.3 % (2.13 ± 0.36 vs 2.71 ± 0.40, P < 0.01) and 22.6 % (1.33 ± 0.07 vs 1.72 ± 0.07, P < 0.01) on days 8 following the differentiation, respectively [3]. in vivo: HSYA treatment ameliorated serum biochemical indicators by reducing the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronan (HA), laminin (LN), and type III precollagen (III-C) in rats [4].
References:
[1]. Yang G, et al. Hydroxysafflor yellow A inhibits lipopolysaccharide-induced proliferation and migration of vascular smooth muscle cells via Toll-like receptor-4 pathway. Int J Clin Exp Med. 2015 Apr 15;8(4):5295-302.
[2]. Zhu HJ, et al. Hydroxysafflor yellow A (HYSA) inhibited the proliferation and differentiation of 3T3-L1 preadipocytes. Cytotechnology. 2015 Mar 7.
[3]. He Y, et al. Protective effects of hydroxysafflor yellow A (HSYA) on alcohol-induced liver injury in rats. J Physiol Biochem. 2015 Mar;71(1):69-78.
[4]. Jin M, et al. Hydroxysafflor yellow A attenuate lipopolysaccharide-induced endothelium inflammatory injury. Chin J Integr Med. 2015 May 27.
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Hydroxysafflor yellow A ameliorates lipopolysaccharide-induced acute lung injury in mice via modulating toll-like receptor 4 signaling pathways.[Pubmed:25466274]
Int Immunopharmacol. 2014 Dec;23(2):649-57.
Hydroxysafflor yellow A (HSYA) is a main bio-active compound important of a traditional Chinese medicine named Carthamus tinctorius L. and has been shown to possess various effects, especially anti-inflammatory benefits and potential protections against acute lung injury (ALI) in previous studies. Therefore, in this present study, we aimed to evaluating effects of HSYA on lipopolysaccharide (LPS)-induced ALI in mice. ALI was induced by intratracheal instillation of LPS into lung, and dexamethasone was used as a positive control. Results demonstrated that HSYA abated LPS-induced pathological change and attenuated lung vascular permeability and edema. HSYA down-regulated both the ability of myeloperoxidase (MPO) in lung tissues and levels of inflammatory mediators including tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6 and IFN(interferon)-beta in serum. Moreover, HSYA prevented toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and TIR-domain-containing adapter-inducing interferon-beta (TRIF) protein up-expressions. In addition, the activations of mitogen-activated protein kinases including p38, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) were blocked by HSYA. And also, the phosphorylations of interferon regulatory factor 3 (IRF3), translocation of nuclear factor kappa B (NF-kappaB)/p65 and inhibitory kappa B (IkappaB)-alpha were inhibited by HSYA. In conclusion, HSYA attenuated inflammatory response in ALI mice through inhibition of TLR 4-dependent signaling pathways.
Synergistic neuroprotective effects of Danshensu and hydroxysafflor yellow A on cerebral ischemia-reperfusion injury in rats.[Pubmed:29383171]
Oncotarget. 2017 Dec 15;8(70):115434-115443.
Ischemic stroke is a common cerebrovascular disease with substantial morbidity and mortality worldwide. However, therapeutic options to minimize the cerebral ischemia-reperfusion (I/R) injury are limited. In China, combination of herb Danshen (Salvia miltiorrhiza Bge) and Honghua (Carthamus tinctorius L.) is effective for stroke treatment in patients but its underlying mechanism requires further investigation. Our study was conducted to evaluate and explore the synergistic effects of two herb ingredients Danshensu and Hydroxysafflor yellow A (HSYA) on cerebral ischemia-reperfusion (I/R) injury in rats. Rats were randomly assigned to the following five groups: sham group, model group, Danshensu group, HSYA group, and Danshensu+HSYA group. Under our experimental conditions in vitro, oxygen-glucose deprivation (OGD) model was established to determine the synergistic neuroprotective effects of Danshensu and HSYA. With such methods as neurological deficits scoring, TTC, HE and TUNEL staining, and ELISA detection, the results demonstrated that administration of either Danshensu or HSYA improved neurological defects and alleviated pro-inflammatory and oxidative stress reactions. Notably, combination of Danshensu and HSYA exerted more effective results than that used alone. Furthermore, western blot analysis results showed that Danshensu and HSYA combination displayed synergistic regulation on TLR4/NF-kappaB and Nrf2/HO-1 pathways. Consistently, Danshensu +HSYA group exhibits better neuroprotection in primary neurons with OGD model compared with Danshensu or HSYA group. Taken together, we found for the first time that Danshensu plus HSYA could achieve remarkable synergistic neuroprotective effects on I/R injury, which is related to the anti-inflammatory and antioxidant pathways.
Upregulation of heme oxygenase-1 expression by hydroxysafflor yellow A conferring protection from anoxia/reoxygenation-induced apoptosis in H9c2 cardiomyocytes.[Pubmed:21497407]
Int J Cardiol. 2012 Oct 4;160(2):95-101.
BACKGROUND: Reperfusion therapy is widely utilized for acute myocardial infarction (AMI), so ischemia/reperfusion (I/R) of the heart is frequently encountered in clinical practice. The curative effects of reperfusion therapy for AMI are favourable in most cases, but reperfusion can also cause harmful effect to cardiomyocytes. Hydroxysafflor yellow A (HSYA) is an effective therapeutic agent to alleviate I/R injury, but the mechanisms underlying this therapeutic effect are unknown. METHODS AND RESULTS: The H9c2 cardiomyocyte cell line was incubated with or without HSYA during hypoxia, then it was reoxygenated. In the presence of HSYA, reoxygenation resulted in the upregulated expression and activity of heme oxygenase-1 (HO-1), phosphorylation of Akt, translocation of nuclear factor Nrf2, and most importantly, a reduction in A/R-induced apoptosis. An HO-1 inhibitor completely suppressed HO-1 enzymatic activity upregulated by HSYA and notably diminished the anti-apoptotic effect of HSYA. An inhibitor of PI3K, completely blocked Akt phosphorylation induced by HSYA and partly negated HSYA-induced upregulation of HO-1, translocation of nuclear factor Nrf2 and suppression of apoptosis in the H9c2 cardiomyocytes. CONCLUSIONS: Our study suggests that HSYA can provide protection to H9c2 cardiomyocytes against A/R-induced apoptosis. This protective effect largely depends on the upregulation of HO-1 expression through the PI3K/Akt/Nrf2 signaling pathway.
Protective effect of hydroxysafflor yellow A on bleomycin- induced pulmonary inflammation and fibrosis in rats.[Pubmed:29294256]
Chin J Integr Med. 2018 Jan;24(1):32-39.
OBJECTIVE: To observe the effect of Hydroxysafflor yellow A (HSYA), an active ingredient of a traditional Chinese herbal medicine Carthamus tinctorius L., on lung inflflammation and pulmonary fibrosis induced by bleomycin (BLM) in rats. METHODS: Animals were divided into 6 groups including normal group, model group, three HSYA groups and dexamethasone (DXM) group. Three doses of HSYA (35.6, 53.3, and 80.0 mg*kg(-1)*day(-1)) were intraperitoneally (i.p.) injected in rats for 3 weeks after BLM administration and DXM was used as the positive control (n=8 or 12). Arterial blood gas was assayed and morphological changes were observed. Lung mRNA expressions of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6 and some cytokines in lung tissue were detected by real-time polymerase chain reaction. Nuclear factor-kappaB p65 or alpha-smooth muscle actin (alpha-SMA) protein distribution in rat lung tissue was observed by immunohistochemistry. RESULTS: On the 7th day after BLM administration, lung tissue showed serious inflammation. Treatment with HSYA or DXM ameliorated lung inflammation. After treatment with HSYA or DXM, oxygen partial pressure (PaO2) increased (HSYA 80.0 mg*kg(-1), P<0.01) and CO2 partial pressure (PaCO2) decreased (HSYA 53.3, 80.0 mg*kg(-1), P<0.05). Moreover, the mRNA expression of TNF-alpha, IL-1beta, and IL-6; and the number of NF-kappaB p65 positive cells was lower in HSYA 53.3 and 80.0 mg*kg(-1) groups than those in the model group (all P<0.05). Twenty-one days after BLM administration, HSYA or DXM treatment ameliorated fibrosis, increased PaO2 (HSYA 53.3, 80.0 mg*kg-1, P<0.01), and decreased PaCO2 (53.3 and 80.0 mg*kg-1, P<0.05). Further, the mRNA expression of TGF-beta1, alpha-SMA, and collagen I as well as the number of alpha-SMA positive cells increased in the model group and HSYA can attenuate these changes (53.3, 80.0 mg*kg(-1), P<0.05). Hematoxylin and eosin and Masson's trichrome staining indicated that the fibrosis and collagen deposition were ameliorated in HSYA groups (53.3, 80.0 mg*kg(-1), P<0.05). CONCLUSION: HSYA could alleviate acute lung inflflammation and chronic pulmonary fibrosis induced by BLM in rats.
Buyang Huanwu Decoction ameliorates ischemic stroke by modulating multiple targets with multiple components: In vitro evidences.[Pubmed:29576055]
Chin J Nat Med. 2018 Mar;16(3):194-202.
Buyang Huanwu Decoction (BYHWD) is a well-known traditional Chinese medicine prescription which is used to treat ischaemic stroke and stroke-induced disabilities. However, the exact mechanism underlying BYHWD's amelioration of ischaemic stroke and its effective constituents remain unclear. The present study aimed to identify the effective constituents of BYHWD and to further explore its action mechanisms in the amelioration of ischaemic stroke by testing the activities of 15 absorbable chemical constituents of BYHWD with the same methods under the same conditions. The following actions of these 15 compounds were revealed: 1) Ferulic acid, calycosin, formononetin, astrapterocarpan-3-O-beta-D-glucoside, paeonol, calycosin-7-O-beta-D-glucoside, astraisoflavan-7-O-beta-D-glucoside, ligustrazine, and propyl gallate significantly suppressed concanavalin A (Con A)-induced T lymphocyte proliferation; 2) Propyl gallate, calycosin-7-O-beta-D-glucoside, paeonol, and ferulic acid markedly inhibited LPS-induced apoptosis in RAW264.7 cells; 3) Propyl gallate and formononetin significantly inhibited LPS-induced NO release; 4) Hydroxysafflor yellow A and inosine protected PC12 cells against the injuries caused by glutamate; and 5) Formononetin, astragaloside IV, astraisoflavan-7-O-beta-D-glucoside, inosine, paeoniflorin, ononin, paeonol, propyl gallate, ligustrazine, and ferulic acid significantly suppressed the constriction of the thoracic aorta induced by KCl in rats. In conclusion, the results from the present study suggest that BYHWD exerts its ischaemic stroke ameliorating activities by modulating multiple targets with multiple components.
Hydroxysafflor yellow A enhances survival of vascular endothelial cells under hypoxia via upregulation of the HIF-1 alpha-VEGF pathway and regulation of Bcl-2/Bax.[Pubmed:18670359]
J Cardiovasc Pharmacol. 2008 Aug;52(2):191-202.
Hydroxysafflor yellow A (HSYA) is a component of the flower Carthamus tinctorius L. The present investigation determines whether HSYA can modify the effects of hypoxia on vascular endothelial cells (EC) and its mechanisms. Human EC line (EAhy926) viability was determined using the MTT assay. EC cycle phase distribution was done with PI staining and flow cytometric analysis, and EC apoptosis was done by AnnexinV-FITC detection and the TUNEL assay. The protein levels of VEGF, Bcl-2, Bax, and HIF-1 alpha were determined by ELISA or Western blot analysis, and the mRNA expression of these genes by RT-PCR analysis. HIF-1 alpha transcriptional activity was measured using a reporter gene assay. HSYA improved cell viability under hypoxia in a concentration-dependent manner by attenuating its cycle arrest and inhibiting its apoptosis. HSYA upregulated the bcl-2/bax ratio, which is downregulated under hypoxia, increased VEGF protein concentration and VEGF mRNA expression and enhanced HIF-1 alpha protein accumulation and its transcriptional activity. In conclusion, HSAY could enhance the survival of ECs under hypoxia, which may be correlated with its effect of upregulating the bcl-2/bax ratio and promoting HIF-1 alpha protein accumulation, which increases VEGF. These findings provide evidence for the mechanisms by which HSYA maintains EC survival under hypoxia.
Hydroxysafflor yellow A (HYSA) inhibited the proliferation and differentiation of 3T3-L1 preadipocytes.[Pubmed:25749912]
Cytotechnology. 2015 Oct;67(5):885-92.
Hydroxysafflor yellow A (HSYA), a main component of safflor yellow, has been demonstrated to prevent steroid-induced avascular necrosis of femoral head by inhibiting primary bone marrow-derived mesenchymal stromal cells adipogenic differentiation induced by steroid. In this study, we investigate the effect of HSYA on the proliferation and adipogenesis of mouse 3T3-L1 preadipocytes. The effects of HSYA on proliferation and differentiation of 3T3-L1 cells and its possible mechanism were studied by 3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyl tetrazolium bromide spectrophotometry, Oil Red O staining, intracellular triglyceride assays, real-time quantitative RT-PCR, transient transfection and dual luciferase reporter gene methods. HSYA inhibited the proliferation of 3T3-L1 preadipocytes and cell viability greatly decreased in a dose and time dependent manner. HSYA (1 mg/l) notably reduced the amount of intracellular lipid and triglyceride content in adipocytes by 21.3 % (2.13 +/- 0.36 vs 2.71 +/- 0.40, P < 0.01) and 22.6 % (1.33 +/- 0.07 vs 1.72 +/- 0.07, P < 0.01) on days 8 following the differentiation, respectively. HSYA (1 mg/l) significantly increased hormone-sensitive lipase (HSL) mRNA expression and promoter activities by 2.4- and 1.55-fold, respectively (P < 0.01), in differentiated 3T3-L1 adipocytes. HSYA inhibits the proliferation and adipogenesis of 3T3-L1 preadipocytes. The inhibitory action of HYSA on adipogenesis may be due to the promotion of lipolytic-specific enzyme HSL expression by increasing HSL promoter activity.
Topical application of Hydroxysafflor Yellow A accelerates the wound healing in streptozotocin induced T1DM rats.[Pubmed:29408092]
Eur J Pharmacol. 2018 Mar 15;823:72-78.
To investigate the effects of Hydroxysafflor yellow A (HSYA), which is derived from safflower, on the proliferation, migration and angiogenesis of cells in vitro and its potential efficacy in vivo when topically applied to a diabetic wound. Human umbilical vein endothelial cells (HUVECs) and mouse macrophage cells (RAW264.7) were used to evaluate angiogenesis and anti-inflammatory activities, respectively. The influence of HSYA on the wound scratch assay was investigated in keratinocytes. A splinted excisional wound model in rats with TIDM induced by streptozotocin was used to assess the effects of wound healing. Collagen disposition and secretion of vascular growth factors (VEGF) as well as transforming growth factor-beta1 (TGF-beta1) were evaluated by an ELISA assay and histological staining. The in vitro results showed that HSYA could significantly enhance both the neovascularization of HUVECs and the migration of keratinocytes. It showed the significant inhibitory effect on nitric oxide production, indicating the anti-inflammatory activity of HSYA. In vivo, the topical application of HSYA significantly enhanced the wound closure rate, and the time to complete wound closure was 17 days, whereas 30 days were needed with PBS treatment. Further, treatment with HSYA exhibited significant granulation tissue formation with higher collagen content, re-epithelialization and angiogenesis according to Masson's trichrome staining evaluation, VEGE and TGF-beta1 ELISA measurement. In conclusion, HSYA application could be considered a promising therapeutic strategy for treating chronic non-healing diabetic foot ulcers.
Hydroxysafflor yellow A inhibits angiogenesis of hepatocellular carcinoma via blocking ERK/MAPK and NF-kappaB signaling pathway in H22 tumor-bearing mice.[Pubmed:25720342]
Eur J Pharmacol. 2015 May 5;754:105-14.
Hydroxysafflor yellow A (HSYA), a flavonoid derived and isolated from traditional Chinese medicine Carthamus tinctorius L., possesses anti-tumor activity. However, its effects on hepatocellular carcinoma (HCC) have not been investigated. The proliferation and metastasis of HCC are dependent on angiogenesis, which also strongly links with several signal transduction pathways associated with cell proliferation and apoptosis. This study aimed to explore the effect of HSYA on vasculogenesis and to determine its molecular mechanism by investigating the expression of ERK/MAPK (p-c-Raf, c-Raf, p-ERK1/2, ERK1/2) and NF-kappaB (p65, IkappaB and p-IkappaB) signaling pathway in H22 tumor-bearing mice. The results showed that HSYA could considerably suppress tumor growth by inhibiting secretion of angiogenesis factors (vascular endothelial growth factor A, basic fibroblast growth factor) and vascular endothelial growth factor receptor1. At the moleculcould block ERK1/2 phosphorylation and then restrain the activation of NF-kappaB and its nuclear translocation by down-regulating the expression of p65 in the nucleus, up-regulating p65 level in the cytoplasm, inhibiting IkappaB phosphorylation and cytoplasmic degradation of IkappaB-alpha. Finally, we demonstrate that HSYA could suppress mRNA expression levels of cell proliferation-related genes (cyclinD1, c-myc, c-Fos) compared with negative control group. And best of all, HSYA could improve spleen/thymus indexes, which was evaluated as the marker of protective effect on the immune system. Our findings support HSYA as a promising candidate for the prevention and treatment of HCC.
Protective effects of hydroxysafflor yellow A (HSYA) on alcohol-induced liver injury in rats.[Pubmed:25626885]
J Physiol Biochem. 2015 Mar;71(1):69-78.
Hydroxysafflor yellow A (HSYA), the main active natural constituent extracted from Carthamus tinctorius L., has been widely used for the treatment of cerebrovascular and cardiovascular diseases. The aim of this study is to explore the effect of HSYA on alcohol-induced liver injury and the underlying mechanism. Male Sprague-Dawley rats were used to establish the liver injury model induced by alcohol. HSYA treatment ameliorated serum biochemical indicators by reducing the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronan (HA), laminin (LN), and type III precollagen (III-C) in rats. HSYA efficiently increased the activity and messenger RNA (mRNA) of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in rat liver tissue compared with those of model group, which was obviously reduced by alcohol. HSYA also apparently decreased the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) in rat liver tissue compared with those of model group, which was obviously enhanced by alcohol. Histological studies demonstrated that HSYA substantially reduced the number of macro- and micro-vesicular steatosis, suppressed hepatic fibrogenesis and shrunk ballooning degeneration areas, ameliorated the severity of liver damage induced by long-term drinking, and finally improved the liver architecture. In addition, immunohistochemistry study indicated that the activation of transforming growth factor beta1 (TGF-beta1) stimulated by alcohol in rat liver tissue was significantly blocked by HSYA. Collectively, these data demonstrated that HSYA can effectively protect the liver of rats from long-term alcohol injury, which relates with the enhanced antioxidant capacity of liver tissues and inhibition of TGF-beta1 expression.
