Safflower flowers (
The demand for natural compounds used in the key branches of economy is increasing in connection with the growing awareness of consumers. However, producers are forced to follow economic considerations and use cheaper equivalents of certain ingredients. For this reason, safflower (
Saffron is known for its rich chemical composition: simple and complex sugars, amino acids, proteins, lipids, cellulose, mineral compounds, and vitamins, including thiamine and riboflavin, low amounts of
The difference in the price of saffron and safflower as an industrial raw material depends on the crop yield. Commercial saffron (spice) accounts for only 8% of the total flower yield. One plant produces a maximum of 9 pistil stigmas (up to 3 flowers, each with 3 stigmas) [
The purpose of the study is to review the current information (mainly published in 2018-2020) on the chemical composition of the substances present in the flowers and green parts of safflower (
Safflower (
Safflower is resistant to wind, drought [
The quality of raw material obtained from safflower depends on the conditions prevailing in the cultivation area: air temperature and humidity, soil moisture, insolation, and soil fertility [
The above-ground parts exhibit high content of carbon (42.7–49.1% d.w.) and relatively low nitrogen (0.36–1.23%) [
The chemical composition of flowers is interesting and rich (Table
The main components of the safflower flower extract.
Compound | Structure | Molecular formula | Molecular weight (g/mol) | Color (and form) | Source of information |
---|---|---|---|---|---|
Carthamine (syn. cartamin) | C43H42O22 | 910.8 | Red powder | [ | |
Precarthamine | C44H44O24 | 956.83 | Yellow | [ | |
Carthamidin | C15H12O6 | 288.25 | Yellow | [ | |
Carthamusin A | C24H28O8 | 444.474 | White crystals | [ | |
Cartormin | C27H29NO13 | 575.5 | Yellow crystals | [ | |
Isocartormin | C27H29NO13 | 575.5 | Yellow needle crystals | [ | |
Hydroxysafflor yellow A (HSYA) | C27H32O16 | 612.5 | Yellow | [ | |
Anhydrosafflor yellow B (AHSYB) | C48H52O26 | 1044.9 | Yellow | [ | |
Safflomin C | C30H30O14 | 614.5 | Yellow powder | [ | |
Isosafflomin C | C30H30O14 | 614.5 | Yellow | [ | |
Safflor yellow A | C27H30O16 | 610.5 | Yellow | [ | |
Safflor yellow B (syn. safflomin B) | C48H54O27 | 1062.9 | Yellow | [ | |
Saffloroside | C22H22O12 | 478.403 | Yellow crystals | [ | |
Azaleatin | C16H12O7 | 316.26 | Yellow crystals | [ | |
Cinaroside | С21Н20О11 | 448.377 | Light-yellow crystals | [ | |
Guanosine | C10H13N5O5 | 283.24 | White crystalline powder | [ | |
Kaempferol | C15H10O6 | 286.24 | Light yellow powder | [ | |
Kaempferol 3- | C27H30O15 | 594.5 | Yellow, powder or crystals | [ | |
Luteolin | С15Н10О6 | 286.2 | Yellow crystals | [ | |
Luteolin 5-methyl ether (syn. 5-O-methylluteolin) | C16H12O6 | 300.3 | Yellow powder | [ | |
Quercetin | C15H10O7 | 302.2 | Yellow needle crystals | [ | |
Stigmasterol | C29H48O | 412.7 | White powder | [ | |
Syringin | C17H24O9 | 372.4 | White crystals | [ | |
Tinctormine | C27H31NO14 | 593.5 | Yellow powder | [ | |
C35H60O6 | 576.8 | White powder | [ | ||
6-Hydroxykaempferol 3-O- | C27H30O16 | 610.5 | Yellow powder | [ | |
6-Hydroxykaempferol-3- | C27H28O17 | 624.5 | Yellow | [ |
Most of the pigments found in flower petals are flavonoids of the C-glucosylquinochalcone group. The best known are carthamine (also known as safflower yellow, carthamus red, or carthamine) and carthamidin (synonyms include carthamic acid). Carthamine (C43H42O22), red pigment, is flavonoid compound consisting of two chalkonoids. It is formed as a result of oxidation with precarthamine. It is insoluble in water and it usually constitutes 3–6% of petal composition; however, in some flower parts, the content is below 1% [
Aqueous extract of flowers also contained isocartormin, new semiquinonechalcone C-glycoside, which is a cartormin isomer [
There is a correlation between the content of active substances and the intensity of flower’s color. Among the active substances, hydroxysafflor A has always been predominant (independently of the degree in which flowers are colored); however, flowers with more intense coloration (vivid red and bright yellow or bright orange) were characterized by higher content of HSYA, anhydrosafflor yellow B, kaempferol, quercetin, safflomin C, kaempferol-3-O-rutinoside, and 6-hydroxykaempferol-3–0-
Studies showed the presence of 20 [
Substances isolated from safflower flowers have been used in medicine (summarized in Figure
Bioactive effect of the safflower substances.
Selected studies of antioxidant activity of substances present in safflower flowers.
Substance | Research object | Type of test | Parameter determined | Tested concentrations | Results | Authors |
---|---|---|---|---|---|---|
HSYA | Tyrosinase activity assay | Change in absorbance per min at 475 nm | 0, 0.5, 1.5, and 2.5 mM HSYA | Inhibition of l-DOPA oxidation, reduction of tyrosinase activity | [ | |
HSYA | CAT kit | CAT mRNA level | 800 mM HSYA | Increase of SOD, GSH-Px, and CAT levels; decrease of ROS and MDA levels | [ | |
GSH-Px kit | GSH-Px mRNA level | |||||
SOD kit | SOD mRNA level | |||||
MDA kit | MDA level | |||||
HSYA | Lipid peroxidation MDA assay kit | MDA level | 3.5 mg kg-1 HSYA in 0.1 ml; injection | Control: approx. 21 nmol/mg; DHEA+ HSYA = approx. 22 nmol/mg | [ | |
GSH and GSSG assay kit | GSH/GSSG ratio | Control: approx. 7.7; DHEA+ HSYA = approx. 6.4 | ||||
SOD assay kit | SOD activities | Control: approx. 246 U/mg; DHEA+ HSYA = approx. 200 U/mg | ||||
GSH-Px assay kit | Activities of GSH-Px | Control: approx. 600 mU/mg; DHEA+ HSYA = approx. 500 mU/mg | ||||
CAT assay kit | Activities of CAT | Control: approx. 59 U/mg; DHEA+ HSYA = approx. 38 U/mg | ||||
HSYA | Commercial assay kits, fluorescence spectrophotometry | 5 mg/kg HSYA; intraperitoneally injected | [ | |||
Content of MDA | ||||||
HSYA, carthamine | MDA assay kit | MDA level | 200 mg/kg/d SY or HSYA; injection | Increase of SOD activity and MDA level (in a high-fat diet group) | [ | |
SOD assay kit | SOD activities | |||||
HSYC | Antioxidative effects against H2O2-induced cytotoxicity | Cell viability | 60 | 71% of control; control: vitamin C (1.1 mg/ml) | [ | |
Methanol extract of safflower flowers | FRAP | Optical density at 700 nm | 20 mg/ml, 40 mg/ml, and 80 mg/ml | 0.749; 1.155; 1.532 (respectively) | [ | |
DPPH | Absorbance at 517 nm; IC50 | 0.1 ml solution of different concentrations of extract | ||||
Safflower flower extract, HSYA, SYA | ORAC | Fluorescence emission intensity at 530 nm | Water extract (5%), HYSA, SYA | Total antioxidant activity | [ | |
DPPH | Absorbance at 517 nm; IC50 | IC50 |
Studies on the use of HSYA for medical purposes (from 2018 to 2020).
Test organism | Type of test/parameter | Concentration/dose | Authors |
---|---|---|---|
Intracellular Ca2+ mobilization assay/imaging with excitation at 488 nm | 50 | [ | |
MTT assay (cell viability assay)/absorbance at 490 nm | 1 | ||
50 | |||
ELISA kits (human chemokine array kits)/measurements of cytokines (levels of TNF- | |||
LC-ESI-MS/MS (liquid chromatography-electrospray ionization-tandem mass spectrometry)/histamine release assay | |||
Western blot analysis (ECL kit)/protein expression (transillumination) | |||
Hindpaw swelling and extravasation assay/optical density at 620 nm | 0, 2.5 mg/kg, 5 mg/kg, 10 mg/kg HSYA in saline | ||
ELISA kits/assay the levels of testosterone, estradiol, progesterone, luteinizing hormone, follicle-stimulating hormone, anti-Müllerian hormone (AMH) | 3.5 mg kg-1 HSYA in 0.1 ml, injection | [ | |
Cell viability assay/absorbance at 570 nm | 200 | [ | |
Western blot analysis/protein expression (transillumination, band densities) | 800 | ||
Insulin ELISA kit/glucose stimulated insulin secretion | |||
Anthrone method/hepatic glycogen in the liver | 120 mg/kg, for 8 weeks | [ | |
WST-8 method/glycogen synthase | |||
Fasting blood glucose/glucometer test | |||
Oral glucose tolerance test/glucometer test (0, 30, 60, and 120 minutes after oral administration with glucose solution) | |||
Assay kits/fasting blood insulin, triglycerides, total serum cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol in serum | |||
Western blot analysis/protein expression | |||
Western blot analysis/protein expression | 10 mg/ml HSYA | [ | |
Cellular immunofluorescence assay/photographing (fluorescent inverted microscope) | |||
ELISA kit/interleukin-6 levels, tumor necrosis factor- | Doses of 10 mg/kg daily, intragastrically, for 6 weeks | ||
RT-qPCR assay (PCR)/relative expression level of miRNA-140-5p | |||
BCA method (based on T-AOC and MDA kit)/protein concentrations | |||
MTT assay/cell viability | 5 | [ | |
Total mRNA (amount and purity)/absorbance at 260/280 nm | 10 | ||
Western blot/protein expression | |||
Immunofluorescence assay/immunofluorescence (confocal microscopy) | 20 | ||
Therapeutic effect in vivo/infarct area, ratio of infarct volume to whole brain tissue | 10 mg/kg, 20 mg/kg | ||
CCK-8 assay/absorbance at 450 nm | 1 | [ | |
EdU assay/cell proliferation rate | |||
Cell apoptosis/BD FACSCalibur flow cytometry | |||
Western blot analysis/protein expression | |||
Hanging wire test/hanging time | 20 mg/kg/d, for 28 days | [ | |
Western blot analysis/protein expression | |||
IPGTT (intraperitoneal glucose tolerance test), IPITT (intraperitoneal insulin tolerance test)/glucose and insulin tolerance tests | 200 mg/kg/d HSYA, for 10 weeks | [ | |
2−DDCt method/expression of antioxidant enzymes in the liver and adipose tissue | |||
2−DDCt method/expression of antioxidant enzymes | 3T3-L1 adipocytes: 10, 50, and 100 mg/l HSYA for 24 h; HepG2 cells: 10, 50, and 100 mg/l SY | ||
ALP activity assay/percentage of ALP activity | |||
Caspase colorimetric assay kit/caspase-3 activity assay | |||
Annexin V-FITC/IP staining kit/percentage of apoptotic cells | |||
Western blot analysis/protein expression | |||
HOP | |||
ELISA kits/concentrations of inflammatory cytokines (IL-6, IL-1 | 9, 27, and 81 mmol/l | [ | |
Western blot analysis/protein expression | |||
Calcium-sensitive fluorescent probe Fluo-3/AM/intracellular calcium ion concentration | |||
Dual-luciferase reporter assay/transcriptional activities of NF- | |||
Double-staining method (with Tcc and Evans blue stains)/infarct size | 5 mg/kg HSYA; intraperitoneally injected | [ | |
ELISA kits/cTnI, IL-6, and LdH levels | |||
Flow cytometry analysis, TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling)/apoptosis level | |||
ELISA/caspase-3 activity | 20 | ||
CCK-8/cell viability | |||
Western blot analysis/protein expression | |||
Span diagnostic reagent kit/serum glutamic oxaloacetic transaminase | |||
Span diagnostic reagent kit/serum alkaline phosphatase | |||
Agappe diagnostic kit/serum total bilirubin | |||
SP kit (MMP-2, MMP-9, and COX-2)/immunohistochemical analysis | 1.125 mg/kg, 2.25 mg/kg, intraperitoneally, for 14 days | [ | |
Growth inhibition assay—CCK-8/rate of growth inhibition (IC50 80 | 40, 60, 80, 120, and 160 | ||
Western blot analysis/protein expression | |||
Clonogenic assay/optical density at 570 nm | |||
Wound healing assay/cell migration, via Image-Pro Plus | |||
CCK-8 assay/proliferative activity (optical density of cells) | 0,1, 1, 10, 20, and 50 | [ | |
Microscopic measurement of the number of cells/cell invasion and cell migration assays | 20 | ||
Flow cytometric analysis of cell apoptosis/apoptotic rate of cells | |||
Western blot analysis/protein expression | |||
Serum levels of AFP, ALT, TBIL, and ALB/automatic analyzer | |||
Cytotoxicity assay (CCK-8)/cell survival rates | 1 mg/ml | [ | |
RTCA test (real-time cellular analysis)/monitoring cell proliferation | |||
Flow cytometry (Guava EasyCyte Plus)/evaluation of apoptosis | 1 mg/ml, for 24 | ||
Electronic digital caliper/weekly measurement of tumor size and volume | 1.1 g/kg body weight; once every three days, for five weeks | ||
Western blot analysis/protein expression | |||
Cell proliferation assay kit/cell proliferation | 10, 20, 50, 100, and 150 mg/l, for 72 h | [ | |
CellTiter-Blue Cell Viability kit/cell viability assay | 10, 20, 50, 100, and 150 mg/l, for 48 h | ||
Western blot analysis (protein concentration assay kit)/protein expression | 10, 20, 50, 100, and 150 mg/l |
n.d.: no date; SY: carthamine; HOP: hydroxyproline; HOM: hexosamine; CCK-8: cell counting kit.
Studies on the use of the substances contained in safflower flowers, except HSYA, for medical purposes (from 2018 to 2020).
Substance or plant | Test organism | Type of test/parameter | Concentration/dose | Authors |
---|---|---|---|---|
Safflower yellow (SY) | Transwell and tube formation assay/migration and angiogenesis of HUVEC-12 cells | 4.5, 9.0, and 18 | [ | |
Western blot analysis/protein expression | ||||
Polysaccharides isolated from safflower | MTT assay/cell proliferation (percentage of cell viability) | 25, 50, and 100 | [ | |
ALP activity assay/percentage of ALP activity | ||||
Caspase colorimetric assay kit/caspase-3 activity assay | ||||
Annexin V-FITC/IP staining kit/percentage of apoptotic cells | ||||
Western blot analysis/protein expression | ||||
(1→3)-linked | Western blot analysis/protein expression | 25, 100, and 200 mg/kg, for 60 days | [ | |
HOP (hydroxyproline) and HOM (hexosamine) concentration in serum | ||||
Methanol extract of flowers | Histological studies/examination of pancreatic tissue | Doses 200 mg/kg daily, intraperitoneally, for 4 weeks | [ | |
Methanol extract of | Span diagnostic reagent kit/serum glutamic pyruvic transaminase level | 100, 200, and 400 mg/kg body, for 24 days; oral route | [ | |
Span diagnostic reagent kit/serum glutamic oxaloacetic transaminase | ||||
Span diagnostic reagent kit/serum alkaline phosphatase | ||||
Agappe diagnostic kit/serum total bilirubin | ||||
LDF (Chinese herbal formula) | Overall survival and time to progression | 100 ml/time, three times a day | [ | |
Serum levels of AFP, ALT, TBIL, and ALB/automatic analyzer | ||||
Minimum inhibitory concentration (MIC)/the minimum inhibitory concentration | Extract: 1.0 mg/ml, 2.0 mg/ml, 3.0 mg/ml, 4.0 mg/ml, and 5.0 mg/ml | [ | ||
Well diffusion method/zone of inhibition against pathogens growth | 200 | |||
Castor oil-induced diarrhea; magnesium sulfate-induced diarrhea/% inhibition of defecation, latency | Methanol extract: 200 mg/kg, 400 mg/kg | |||
WST-8 method/glycogen synthase | ||||
Fasting blood glucose/glucometer test | ||||
Oral glucose tolerance test/glucometer test (0, 30, 60, and 120 minutes after oral administration with glucose solution) | ||||
Assay kits/fasting blood insulin, triglycerides, total serum cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol in serum | ||||
Western blot analysis/protein expression |
Action mechanisms by safflower substances.
Activity | Result of mechanism | Mechanism | Authors |
---|---|---|---|
Prevention of anaphylaxis | (i) Inhibition of mast cell degranulation | (i) Inhibition of Ca2+ flow | [ |
Alleviation of polycystic ovary syndrome | (i) Reduction of cysts | (i) Reversion of the expression of genes Star, Hsd3b1, Cyp11a1 (increase), and Cyp19a1 (reduction) | [ |
Antitumor effects | (i) Induction of cisplatin sensitivity by JNK and P38 MAPK signaling pathway | (i) Increase in P-JNK and P-38 levels | [ |
(i) Inhibition of cancer cell proliferation | (i) Inhibition of Skov3 cell proliferation | [ | |
(i) Inhibition of cancer cell proliferation | (i) Inhibition of the MCF-7 cell cycle at the S phase | [ | |
(i) Inhibition of tumor angiogenesis | (i) Inhibition of p38 MAPK phosphorylation | [ | |
(i) Induction of autophagy in cancer cells by regulating Beclin 1 and ERK expression | (i) Increase in Beclin 1 and LC3-II expression in tumor cells | [ | |
(i) Induction of apoptosis of tumor cells by regulating the NF- | (i) Inhibition of the expression of ICAM1, MMP9, TNF- | [ | |
Alleviation of damage and brain injuries | (i) Inhibition of the activation of the pyroptotic pathway and apoptosis of injured nerves | (i) Reduction of cytokine expression (NLRP3, ASC, caspase-1, GSDMD, IL-1 | [ |
(i) Reduction of the apoptosis and autophagy of neural stem cells by modulation of the p38/MAPK/MK2/Hsp27-78 signaling pathway | (i) Reduction of p38 and Hsp27-78 phosphorylation and MK-2, Bax, cleaved caspase-3, LC3-II, and mTOR phosphorylation expression | [ | |
(i) Inhibition of dopamine synthesis | (i) Increase in the formation of autophagosomes | [ | |
Alleviation of diabetes complications | (i) Inhibition of JNK/c-Jun signaling pathway | (i) Inhibition of p-JNK and p-c-Jun activation | [ |
(i) Promotion of PI3K and Akt activation | (i) Increase of PI3K, AKT, and p-AKT expressions | [ | |
(i) Reduction of renal fibrosis | (i) Increase of miRNA-140-5p mRNA, BG, 24 h UP, TC, TG, T-AOC, MDA, IL-6, TNF- | [ | |
Protection of the digestive system | (i) Protection of the liver and other organs against aging | (i) Increase of CAT, GSH-Px, MDA, and SOD activities | [ |
(i) Protection of the liver against damage | (i) Reduction of ALT, ALP, AST, and total bilirubin levels | [ | |
Protection and treatment of cardiovascular diseases | (i) Change in platelet activation pathway | (i) Regulation of core genes: PRKACA, PIK3R1, MAPK1, PPP1CC, PIK3CA, and SYK | [ |
(i) Inhibition of activation of the JAK2/STAT1 pathway | (i) Inhibition of caspase-3 activity (reduction of H/R-induced apoptosis) | [ | |
(i) Effect on vasodilation | (i) Inhibition of the PKA and NO production | [ | |
Protection of skeletal system | (i) Regulation of pVHL/HIF-1 | (i) Increase of ALP, Ang-2 (Angiopoietin-2), HIF-1 | [ |
(i) Increase in osteoblast differentiation | (i) Inhibition of caspase-3 activity (change in caspase-3-dependent signaling pathway) | [ | |
Protection of the respiratory system | (i) Inhibition of the platelet activating factor in the airway epithelium | (i) Changes in the expression of interleukin- (IL-) 1 | [ |
Reduction of overweight and obesity | (i) Change in the composition of intestinal microflora | (i) Changes in pathways of sphingolipid and glycerophospholipid metabolisms | [ |
(i) Increase in the synthesis of antioxidant enzymes in adipose tissue and in the liver | (i) Increase of expression of antioxidant enzymes and Nrf2 in adipocytes, liver tissue, and HepG2 cells | [ |
Hydroxysafflor yellow A has an antioxidant effect, enabling cells to survive oxidative stress [
Products containing HSYA have enabled preventing acute anaphylaxis in mice. Anaphylaxis may appear in response to contact with allergen or drug, and it is associated with a rapid activation of mediators (i.e., tumor necrosis factor, histamine,
HSYA injection led to reduction of cysts on mouse ovaries with polycystic ovary syndrome, and at the same time, it regulated the hormonal balance and restored normal ovulation cycle by reducing the levels of testosterone and follicle-stimulating hormone (FSH) in the blood and increasing the level of progesterone, estradiol, and luteinizing hormone [
Untreated diabetes results in increased level of advanced glycation end products (AGEs) and methylglyoxal in the organism’s cells, which have toxic effect on cells (apoptosis), tissues (accelerated aging), and organs (destruction). In the course of diabetes, increased content of caspase-3 is observed, which is responsible for, among others, degradation of the ICAD protein (inhibitor of caspase-activated DNase), DAFF40/CAD endonuclease inhibitor. This leads to activation of endonuclease and DNA fragmentation. Lower amounts of AGEs are formed in the organism after administration of HSYA, which impedes cell apoptosis. This compound has protective effect on the microvascular endothelium in the human brain, which reduces the range of damage caused by elevated AGE level [
Furthermore, hydroxysafflor A has protective effect towards pancreatic cells. High blood glucose concentration leads to oxidative damage and apoptosis of
Favorable impact of HSYA was also observed in the treatment of kidney fibrosis associated with diabetes in rats. This substance affected the course of TLR4/NF-
Administration of methanol extract of safflower flowers containing phenolic compounds (i.e., acids: caffeic, catechin, catechol, chlorogenic, ellagic, protocatechuic, and vanillic) and flavonoids (i.e., hesperidin, kaempferol, narengin, quercetin, quercitrin, rosmarinic, rutin, and 7-hydroxyflavone) reduced symptoms of pancreas dysfunction in rats with diabetes. This extract exhibited high reducing force and antioxidative activity (DPPH+) [
As shown for rats, HSYA reduces the effects of brain injuries (contusions). It inhibited development of symptoms, favored the increase of superoxide dismutase and ATPase activity, increased the amount of tissue plasminogen activator, and resulted in reduced level of plasminogen-1 activator inhibitor in the blood plasma as well as malondialdehyde in the tissues adjacent to the injury [
HSYA has proven effective in the treatment of skin hyperpigmentation and hypopigmentation. The substance formed complexes with tyrosinase altering its activity, and as an end result, it inhibited production of melanin from tyrosine. This resulted in homogenization of the skin color [
HSYA reduces obesity in mice and rats. When administered orally, it resulted in a change of composition of the diet-dependent intestinal microflora. As a result of this, certain bacteria groups had markedly increased counts, while other reduced, which affected the course of digestive processes and enhanced the function of the digestive tract (i.e., the intestines), as well as systemic metabolism. The level of lysophosphatidylcholines (lyso PCs), L-carnitine, and sphingomyelin increased, whereas that of phosphatidylcholines decreased. This resulted in reduced amount of fat accumulated, restored glucose homeostasis, alleviation of insulin resistance, and reduced amount of inflammations in the organism [
During
HSYA produced reduction of vessel permeability, reduction of the amount of blood platelets in plasma, and reduced their aggregation in the lungs of rats with prolonged exposure to car exhaust fumes, which considerably mitigated lung injury and reduced the likelihood of other lung diseases [
In China, HSYA is recommended for the treatment of angina pectoris [
Substances isolated from safflower flowers have therapeutic effect on blood pressure problems. HSYA reduced systolic pressure in the left ventricle in rats with pulmonary hypertension [
HSYA inhibited liver cell fibrosis [
HSYA inhibits the development of cancers [
HSYA reversed drug resistance to chemotherapy drugs of ovarian carcinoma cells in mice [
HSYB, an isomer of HSYA, inhibited proliferation of breast cancer cells (MCF-7) in humans and reduced survival rate and proliferation of tumor cells by blocking their cellular cycle in S phase. Increased apoptosis of tumor cells was linked to reduced level of cyclin D1, cyclin E, CDK2, p-PI3K, PI3K, AKT, and p-AKA proteins in MCF-7 cells and reduced level of Bcl-2 [
Doses up to 2000 mg/kg body weight of carthamus red are safe (no toxicity was found [
Importance of
Due to the high content of carotene, riboflavin, and vitamin C in the green parts, in India this plant is cultivated as leaf vegetable [
The use of safflower flowers and its components in food production.
Safflower flowers also carry a potentially high significance for food production, because they can constitute an ingredient enriching meals with nutrients. Flower petals contain all necessary amino acids, except tryptophan. Flowers of thornless cultivars are popular already: they have been shown to be rich in protein, sugars, calcium, iron, magnesium, and potassium. By using these properties, teas, whose main ingredient are
Thus far, mainly carthamine and carthamidin have been used in food production (Figure
The applicability of carthamidin as an ice cream dye was investigated. Addition of this pigment had positive effect on sensory evaluation and chemical composition of products. The highest sensory acceptability is characterized by ice cream containing 0.06 ml of carthamidin; increasing and decreasing the content of this substance deteriorated results of sensory evaluation, particularly for flavor, color, and texture of product. Addition of the pigment caused a slight increase in the moisture and the content of protein, lipids, carbohydrates, and ash. The authors of this study pointed to the health benefits of using this natural pigment [
However, the dyes contained in the safflower flowers have not been used in food production to take advantage of their health-promoting nature. The exception is herbal teas containing whole dried flowers. Introduction of HSYA to food production would be highly beneficial from the consumers’ standpoint. This flavonoid is widely applied in medicine, and its addition to food products at the production stage, naturally at doses lower than therapeutic, would greatly improve their health-promoting value. Such products would be of substantial significance for the reduction of oxidative stress within different tissues and organs, and they could exhibit prophylactic action towards cardiovascular diseases and neoplastic diseases, among others.
An additional aspect favoring the addition of HSYA to foods is its beneficial impact on the reduction of adipose tissue and body weight following oral administration associated with its effect on the composition of intestinal microorganisms and cellular metabolism [
Furthermore, research conducted on rats provided evidence that after intravenous administration of HSYA the presence of metabolites of the pigment was found in blood plasma, bile, urine and faeces, but these were not toxic values [
The wide commercial use of safflower means that the demand for its flowers is steadily increasing. In China, 1800–2600 MT of flowers were produced annually at the beginning of the 21st century [
The authors declare that they have no conflicts of interest.