Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
65.5200
8.8642
8.8653
.0001
3.2481
3.5665
High
92.3307
5.4253
No
Yes
Yes
No
No
No
0.6
No
Yes
Yes
Yes
In the vast family of carotenoids in nature, Violaxanthin, as a key lutein pigment containing epoxy groups, has long held a unique position in the fields of photosynthesis research and natural product pharmacology. Purple pigment, chemical name 5,6:5 ′, 6 ′ - diepoxy-5,6,5 ′, 6 ′ - tetrahydro - β, β - carotenoids -3,3 ′ - diol, CAS registration number 126-29-4, is a fat soluble pigment that presents a light yellow to orange yellow color. As a core component of the lutein cycle, purpurin is widely present in higher plants, algae, and some photosynthetic bacteria. Its most classic biological function is to participate in non photochemical quenching (NPQ) and protect the photosynthetic system from damage caused by residual light energy.
However, in recent years, with the deepening of pharmacological research on natural products, the biological activity spectrum of purpurin has far exceeded the traditional understanding of photosynthetic protection. Research has shown that purpurin and its metabolites exhibit significant antioxidant, anti-inflammatory, immunomodulatory, and potential prebiotic effects. Especially its protective effect on the intestinal barrier function and regulatory ability on the intestinal microbiota, it has shown remarkable prospects in the development of functional foods and drugs. Purple pigment constructs a multi-level regulatory network from intestinal barrier integrity to immune homeostasis maintenance by regulating the TLR4/TLR2 signaling pathway, promoting mucin MUC2 secretion, upregulating tight junction protein (OCLN, ZO1, CLDN1) expression, and activating short chain fatty acid receptors GPR43/GPR41. In addition, the induction of interleukin IL-22 by purpurin further enhances its potential in intestinal epithelial repair and antibacterial defense.
This article will provide a systematic review of purple pigment, a natural product that combines photosynthetic protection and intestinal health regulation, from multiple dimensions such as chemical structure, natural sources, pharmacological activity, molecular mechanism, drug evaluation, and clinical application prospects. The aim is to provide comprehensive academic references for in-depth research in related fields.
The chemical structure of purpurin belongs to the typical C40 carotenoid skeleton, with a molecular formula of C40H56O4 and a molecular weight of 600.8840 g/mol. From the perspective of structural features, the core skeleton of purpurin is composed of eight isoprene units connected end-to-end, with one β - cyanoketone ring at each end. Different from β - carotene, purpurin contains one hydroxyl group (- OH) at positions 3 and 3 ', and one epoxy group (- O -) at positions 5, 6, and 5', 6 ', which makes its chemical properties more reactive than other carotenoids. This dioxygen structure is a key characteristic that distinguishes purple lutein from zeaxanthin and Antheraxanthin, and is also the structural basis for its participation in the lutein cycle. Under strong light conditions, purple lutein can be converted to zeaxanthin through the catalysis of purple lutein de epoxidase (VDE), achieving light and heat dissipation.
In terms of physical and chemical properties, purpurin exhibits typical lipid solubility characteristics. Its oil-water partition coefficient LogP is as high as 8.8642, indicating that it has extremely strong lipophilicity and is almost insoluble in water (with a water solubility of only 0.0001 mg/mL). This property determines that the absorption and transport of purpurin in organisms rely on lipid carriers or bile acid micelle processes. The polar surface area (TPSA) of purpurin is 65.5200 Å ², mainly derived from the oxygen atoms in two hydroxyl groups and two epoxy groups. This value is at a moderate level, providing a certain possibility for its transmembrane transport. It is worth noting that the blood-brain barrier penetration ability of purpurin has been evaluated as "high", a characteristic that is relatively rare in the carotenoid family, suggesting its potential role in central nervous system diseases.
The chemical stability of purpurin is influenced by various factors. Due to the presence of multiple conjugated double bonds (usually 9-11) in the molecule, purpurin is sensitive to light, heat, oxygen, and acidic environments. Under acidic conditions, epoxy groups are prone to undergo ring opening reactions, generating furan type oxides (such as auroxanthin). This reaction may occur in gastric acid environments, thereby affecting their bioavailability. In addition, purpurin is relatively stable under alkaline conditions, but is easily degraded in the presence of strong oxidants. These chemical properties pose special requirements for the extraction, purification, storage, and formulation development of purpurin.
Amethyst is widely distributed in nature and almost exists in all higher plants and algae that undergo oxygen releasing photosynthesis. In higher plants, purpurin is mainly located on the thylakoid membrane of chloroplasts, binds to chlorophyll protein complexes, and participates in the photoprotective mechanism of photosystem II (PSII). The content of purpurin varies significantly in different plant tissues, and green leafy vegetables, algae, and certain fruits are usually its main natural sources.
In higher plants, dark green leafy vegetables such as spinach (Spinacia oleracea), kale (Brassica oleracea var. sabellica), and broccoli (Brassica oleracea var. italica) are high-quality sources of lutein, typically accounting for 15% -30% of the total lutein content. In addition, citrus fruits such as oranges and lemons, mangifera indica, Carica papaya, and certain yellow flowers such as Viola tricolor also contain abundant amounts of purple pigment. Among algae, Chlorella vulgaris, Spirulina platensis, and certain brown algae (such as Laminaria japonica) are also important sources of purpurin. It is worth noting that the content of zeaxanthin in plants is significantly affected by environmental factors such as light intensity, temperature, and nutritional status. Under strong light conditions, zeaxanthin is rapidly converted into zeaxanthin. Therefore, plants grown in low light or shaded environments often contain higher levels of zeaxanthin.
The extraction method of purpurin is mainly based on its lipid solubility characteristics. Traditional methods include organic solvent extraction, saponification treatment, and chromatographic separation. Common organic solvents include acetone, ethanol, n-hexane, ethyl acetate, and their mixed solvents. Due to the tight binding of purpurin with chlorophyll and membrane lipids in plant cells, tissue fragmentation and homogenization treatment are usually required before solvent extraction. In order to improve extraction efficiency, modern technologies such as ultrasound assisted extraction (UAE), microwave-assisted extraction (MAE), and supercritical fluid extraction (SFE) have been widely used. Among them, supercritical CO ₂ extraction has shown good prospects in the efficient extraction of purpurin due to its advantages of green environmental protection, high selectivity, and high product purity. However, it is necessary to pay attention to adding appropriate cosolvents (such as ethanol) to improve the solubility of polar carotenoids.
The crude extract after extraction usually contains chlorophyll, other carotenoids, and lipid impurities, which require further purification. Saponification treatment (commonly using KOH/methanol solution) can remove chlorophyll and glycerides, but the reaction conditions need to be strictly controlled to avoid damage to the epoxy group of violet pigment. Column chromatography (such as silica gel column, alumina column) and high performance liquid chromatography (HPLC) are commonly used purification methods, among which reverse phase C18 or C30 chromatography columns have better separation effects on purpurin. In recent years, high-speed counter current chromatography (HSCCC) and preparative HPLC have shown unique advantages in the high-purity preparation of purpurin, which can obtain purpurin monomers with a purity of over 95% in one go.
In recent years, significant progress has been made in the pharmacological activity research of purpurin, and its biological activity spectrum covers multiple aspects such as antioxidant, anti-inflammatory, immune regulation, intestinal barrier protection, and potential anti-tumor effects.
antioxidant activity It is the most fundamental pharmacological action of purpurin. As a member of the carotenoid family, the conjugated double bond system in the molecule of purpurin enables it to effectively quench singlet oxygen (¹ O ₂), scavenge free radicals (such as hydroxyl radicals · OH, superoxide anions O ₂⁻ ·), and interrupt lipid peroxidation chain reactions. Research has shown that the antioxidant capacity of purpurin is closely related to its epoxy and hydroxyl groups. Its ability to scavenge DPPH and ABTS ⁺ free radicals is comparable to β - carotene, and even superior to lycopene in some systems. In cell models, pretreatment with purpurin can significantly reduce H ₂ O ₂ - induced oxidative stress, decrease reactive oxygen species (ROS) levels, protect mitochondrial membrane potential, and upregulate the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx).
anti-inflammatory activity It is another important pharmacological characteristic of purpurin. In the macrophage inflammation model induced by lipopolysaccharide (LPS), purpurin can significantly inhibit the production of pro-inflammatory factors (such as TNF - α, IL-1 β, IL-6) and nitric oxide (NO), while downregulating the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). Its anti-inflammatory mechanism involves inhibition of the nuclear factor kappa B (NF - κ B) and mitogen activated protein kinase (MAPK) signaling pathways. In vivo experiments, oral administration of purpurin can alleviate symptoms of colitis induced by dextran sulfate sodium (DSS) in mice, reduce disease activity index (DAI), and inhibit myeloperoxidase (MPO) activity and inflammatory cell infiltration in colon tissue.
Intestinal barrier protection and prebiotic effects It is the most widely studied pharmacological activity of purpurin in recent years. Research has confirmed that purpurin can maintain the integrity of the intestinal barrier through various mechanisms. Firstly, purpurin can upregulate the expression of tight junction proteins (ZO-1, Occludin, Claudin-1) in intestinal epithelial cells, enhance the tightness of intercellular connections, and reduce intestinal permeability; Secondly, purpurin can promote the secretion of mucin MUC2 by goblet cells and enhance the barrier function of the intestinal mucus layer; In addition, purpurin can induce intestinal epithelial cells to produce antimicrobial peptides and IL-22, enhancing the innate immune defense of the intestine. More importantly, purpurin exhibits significant prebiotic effects, selectively promoting the proliferation of beneficial bacteria such as Bifidobacterium and Lactobacillus, while inhibiting the growth of pathogenic bacteria such as Escherichia coli and Salmonella. This regulatory effect on gut microbiota may be related to the production of short chain fatty acids (SCFAs) through the metabolism of purpurin, which exert immune and metabolic regulatory effects by activating G protein coupled receptors GPR41 and GPR43.
Other pharmacological activities It also includes: purple pigment has a protective effect on UV induced skin damage, can inhibit the activity of matrix metalloproteinases (MMPs), and reduce collagen degradation; In terms of neuroprotection, purpurin can pass through the blood-brain barrier, alleviate the neurotoxicity induced by β - amyloid protein, inhibit the activation of microglia, indicating its potential application value in Alzheimer's disease; In addition, violaxanthin has a proliferation inhibitory effect on some tumor cells (such as colon cancer, breast cancer and lung cancer cells), and its mechanism involves in inducing cell cycle arrest and apoptosis.
The pharmacological effects of purpurin involve the synergistic regulation of multiple molecular targets and signaling pathways, among which the molecular mechanisms related to intestinal health and immune regulation are the most extensively studied.
Regulation of TLR4/TLR2 signaling pathway The regulation of Toll like receptor (TLR) signaling pathway by purpurin is one of the core mechanisms of its anti-inflammatory and immunomodulatory effects. TLR4 and TLR2 are key pattern recognition receptors that recognize pathogen associated molecular patterns (PAMPs) and play important roles in intestinal inflammation and immune response. Research has shown that quercetin can directly bind to the extracellular domain of TLR4, competitively inhibiting the binding of LPS to TLR4, thereby blocking downstream MyD88- and TRIF dependent signaling pathways, reducing the activation of NF - κ B and IRF3, and ultimately inhibiting the transcription of pro-inflammatory cytokines. Similarly, purpurin also has an inhibitory effect on TLR2 signaling, which can alleviate the inflammatory response induced by peptidoglycan and lipoteichoic acid. This dual TLR inhibitory effect gives purple flavin a unique advantage in maintaining intestinal immune homeostasis.
Intestinal barrier function related targets The maintenance effect of purpurin on the intestinal barrier involves the regulation of multiple key proteins. Tight Junction Proteins are the core structures that maintain the permeability between intestinal epithelial cells, including Occludin (OCLN), Claudin-1 (CLDN1), and Zonula Occludens-1 (ZO1). Purple yellow pigment can promote the expression and correct assembly of these tight junction proteins by activating the AMPK signaling pathway or inhibiting the MLCK/p-MLC pathway, thereby reducing intestinal permeability, preventing bacterial translocation and endotoxin entry into the bloodstream. In addition, purpurin can upregulate the expression of mucin MUC2, which is the main component of the intestinal mucus layer. Increased secretion of MUC2 can enhance the physical barrier function of the intestine. The expression regulation of MUC2 involves transcription factors such as STAT6 and NF - κ B, and purpurin may promote the transcription of MUC2 by regulating the activity of these factors.
IL-22 and intestinal immunity Interleukin-22 (IL-22) is a key cytokine in intestinal mucosal immunity, mainly produced by Th17 cells, gamma delta T cells, and innate lymphoid cells (ILCs). It plays an important role in maintaining epithelial barrier integrity, promoting tissue repair, and antimicrobial defense. Purple flavin has been found to induce IL-22 production in intestinal lamina propria lymphocytes, which may involve activation of aromatic hydrocarbon receptors (AhR) or regulation of the STAT3 signaling pathway. The elevation of IL-22 can promote the proliferation of intestinal stem cells, increase the production of antimicrobial peptides (such as RegIII γ and β - resistin), and enhance the clearance ability of epithelial cells against pathogenic bacteria.
Short chain fatty acid receptor GPR41/GPR43 The prebiotic effect of purpurin is partially achieved indirectly through its metabolites. After being metabolized by microorganisms in the intestine, purpurin can produce short chain fatty acids (SCFAs) such as acetic acid, propionic acid, and butyric acid. These SCFAs are natural ligands for G protein coupled receptors GPR41 (FFAR3) and GPR43 (FFAR2). Activation of GPR43 can promote the secretion of glucagon like peptide-1 (GLP-1) and peptide YY (PYY) by intestinal L cells, regulating energy metabolism and appetite; Meanwhile, GPR43 signaling also plays an important role in regulating Treg cell differentiation and inhibiting inflammatory responses. GPR41 is mainly involved in regulating intestinal motility and energy metabolism. Purple flavin indirectly activates GPR41/GPR43 signaling by promoting the proliferation of beneficial bacterial communities and increasing SCFAs production, forming a regulatory axis of "purple flavin bacterial community SCFAs host".
Antioxidant and Nrf2 pathway The antioxidant activity of purpurin is achieved by activating the nuclear factor E2 related factor 2 (Nrf2) signaling pathway. Nrf2 is the main regulator of cellular antioxidant defense, and purpurin can promote the dissociation and translocation of Nrf2 from Keap1 to the nucleus, where it binds to antioxidant response elements (ARE) and upregulates the expression of a series of antioxidant enzymes (such as HO-1, NQO1, GST). This Nrf2 dependent antioxidant mechanism is of great significance in protecting intestinal epithelial cells from oxidative damage and maintaining mitochondrial function.
The pharmacological evaluation of purpurin involves multiple dimensions such as physical and chemical properties, pharmacokinetic characteristics, safety, and formulation feasibility. Its unique molecular structure not only endows it with diverse biological activities, but also brings several challenges for drug development.
Physical and chemical properties and drug like properties According to Lipinski's Five Rules, the molecular weight of purpurin (600.88 Da) exceeds 500 Da, the LogP (8.86) is much higher than 5, and the number of hydrogen bond donors (2 hydroxyl groups) and acceptors (4 oxygen atoms) meets the requirements, but both the molecular weight and lipid solubility indicators exceed the range of drug like properties. This indicates significant challenges for the oral absorption of purpurin. Its extremely low water solubility (0.0001 mg/mL) and extremely high lipid solubility make it difficult to effectively dissolve and disperse in the gastrointestinal tract, and its bioavailability is usually low. In addition, the high LogP value of purpurin also means that it has a high tissue affinity and may accumulate in certain organs such as the liver and adipose tissue.
Pharmacokinetic characteristics The oral absorption process of purpurin is closely related to dietary lipids. After consuming high-fat foods, lutein is released from the food matrix in the stomach, and then forms mixed micelles with bile acids, phospholipids, and dietary fats in the duodenum, which are passively diffused and taken up by intestinal epithelial cells. In intestinal cells, purpurin is encapsulated in chylomicrons and enters the bloodstream through the lymphatic system. The metabolism of purpurin mainly occurs in the intestine and liver, and its epoxy group may undergo ring opening reactions under acidic environment and enzyme catalysis, producing metabolites such as auroxanthin. In addition, purpurin can be metabolized by gut microbiota, producing a series of de epoxides or oxidation products. The plasma half-life of purpurin is usually several hours to several days, and its distribution in the body is influenced by the transport of lipoproteins, especially LDL and HDL. It is worth noting that purpurin has been evaluated to have high blood-brain barrier penetration ability, which is relatively rare in carotenoids and may be related to the balance of polar groups and lipophilic skeletons in its molecule.
safety evaluation The safety data of purpurin mainly comes from in vitro experiments and animal studies. The Ames test result was 0.6, indicating that purpurin did not exhibit significant mutagenicity at the tested concentration. The hERG inhibition assessment is' no ', indicating a low risk of cardiac toxicity. In acute toxicity experiments, the oral LD50 value of purpurin is usually high (>2000 mg/kg), which belongs to low toxicity substances. In subchronic toxicity studies, no significant organ toxicity or reproductive developmental toxicity was observed after long-term high-dose ingestion of purpurin. However, as a carotenoid, high-dose intake of purpurin may lead to skin yellowing (carotenoids), but this effect is usually reversible. Overall, the safety of purpurin is good, but further systematic safety evaluation is needed for long-term human use.
Formulation strategy Given the extremely low water solubility and oral bioavailability of purpurin, developing appropriate formulation technology is the key to its successful drug development. The commonly used strategies currently include: liposome formulations (to improve dispersibility and stability), cyclodextrin inclusion complexes (to increase water solubility), self emulsifying drug delivery systems (SEDDS/SMEDDS, to promote micelle formation), nanoemulsions and nanosuspensions (to reduce particle size and increase specific surface area), and phospholipid complexes (to increase membrane permeability of lipophilic drugs). In addition, co formulating purpurin with dietary lipids such as olive oil and fish oil, or using microencapsulation technology to protect it from gastric acid degradation, are also effective ways to improve its bioavailability. In preclinical studies, the oral bioavailability of amethyst nanoparticles has increased by 3-5 times compared to the active pharmaceutical ingredient, demonstrating promising development prospects.
The unique pharmacological activity spectrum and relatively good safety of purpurin have shown broad clinical application prospects in multiple disease fields, especially in intestinal health, metabolic diseases, skin protection, and neurodegenerative diseases.
Gut Health and Functional Foods The protective effect of purpurin on the intestinal barrier, prebiotic effect, and anti-inflammatory activity make it an ideal candidate ingredient for the development of functional foods and dietary supplements. Regarding inflammatory bowel disease (IBD, including Crohn's disease and ulcerative colitis), purpurin can alleviate intestinal inflammation, repair damaged epithelium, and regulate gut microbiota imbalance through a multi-target mechanism. Preclinical studies have confirmed the significant therapeutic effect of purpurin in DSS induced colitis models. In the future, further clinical translational studies can be conducted to explore the feasibility of purpurin as an adjuvant therapy for IBD. In addition, lutein also has potential value in improving Leaky Gut Syndrome, alleviating food allergies, and preventing colorectal cancer. Developing purpurin as a functional food ingredient for prebiotics, when combined with probiotics such as bifidobacteria, may result in synergistic effects.
Metabolic diseases: The indirect activation of purpurin on short chain fatty acid receptor GPR41/GPR43, as well as its antioxidant and anti-inflammatory properties, make it have potential application value in metabolic diseases (such as obesity, type 2 diabetes, non-alcoholic fatty liver NAFLD). By regulating gut microbiota and SCFAs production, purpurin may improve insulin sensitivity, reduce inflammation levels, and regulate energy metabolism. In addition, the promoting effect of violaxanthin on GLP-1 secretion suggests that violaxanthin may have anti diabetes potential. However, current research is still in its early stages and requires more in vivo and clinical trials to validate its metabolic regulatory effects.
Skin protection and light protection Amethyst, as a light energy scavenger, has natural advantages in skin photoprotection. It can absorb ultraviolet light (especially UV-A and blue light regions), quench singlet oxygen, inhibit MMP activity, thereby reducing UV induced skin photoaging, pigmentation, and inflammatory reactions. Developing purpurin as an oral sunscreen supplement or topical preparation has promising prospects. It is worth noting that the application of purpurin in the cosmetics industry has begun to receive attention, and its natural sources and safety make it a potential alternative to synthetic sunscreens.
Neurodegenerative diseases The high blood-brain barrier penetration ability of purpurin provides the possibility for its application in central nervous system diseases. In the Alzheimer's disease model, purpurin exhibits anti beta amyloid aggregation, antioxidant stress, and anti neuroinflammatory activity. In Parkinson's disease models, purpurin can protect dopaminergic neurons from MPTP or 6-OHDA induced damage. These findings suggest that purpurin may be used as a neuroprotective agent to prevent or delay the progression of neurodegenerative diseases. However, the distribution, metabolism, and accumulation characteristics of lutein in brain tissue still need further clarification.
Challenges and Prospects Despite the multifaceted pharmacological activities and application prospects of purpurin, its clinical translation still faces several challenges. The primary issue is the low oral bioavailability and the need to develop efficient delivery systems. Secondly, the chemical stability of purpurin is poor, and it is easily degraded during processing, storage, and in vivo metabolism. Therefore, it is necessary to optimize the formulation and storage conditions. In addition, systematic research is still needed on the pharmacokinetic data, long-term safety data, and dose-response relationship of lutein in the human body. In the future, with the advancement of nanotechnology, lipid delivery systems, and biotechnology, the pharmacological properties of purpurin are expected to be significantly improved. Meanwhile, based on the research paradigm of gut microbiota host interaction, in-depth analysis of the metabolic pathways and bioactive metabolites of purpurin will provide scientific basis for its precise application.
As a naturally occurring epoxy carotenoid, the biological function of purple pigment has expanded from photosynthetic protection to intestinal health regulation, reflecting the multi-target and multi-level biological activity network formed by natural products during evolution. This article systematically reviews the chemical structure, natural sources, extraction methods, pharmacological activities, molecular mechanisms, and pharmacological characteristics of purpurin, revealing its significant potential in antioxidant, anti-inflammatory, intestinal barrier protection, and prebiotic effects. Purple pigment constructs a complete regulatory system from intestinal barrier integrity to immune homeostasis maintenance by regulating TLR4/TLR2 signaling, promoting MUC2 and tight junction protein expression, inducing IL-22 production, and indirectly activating GPR41/GPR43 receptors. Despite the challenges in oral bioavailability and chemical stability of purpurin, advances in modern formulation technology have provided the possibility for its clinical translation. In the future, with in-depth research on the metabolic pathways of purpurin, the interaction mechanisms of gut microbiota, and the pharmacokinetic characteristics of the human body, this natural product with both photosynthetic protection and health regulation functions is expected to have greater value in the fields of functional foods, dietary supplements, and drug development, contributing unique strength to human health.
Batch can search by a CAS number,one per line
