Potential Mechanisms of Tea Polyphenols in Oily, Acne-Prone Skin: Effects of EGCG on Sebum Production, Lipid Peroxidation, and Inflammatory Responses
Potential Mechanisms of Tea Polyphenols in Oily, Acne-Prone Skin: Effects of EGCG on Sebum Production, Lipid Peroxidation, and Inflammatory Responses
1 Tea Polyphenol Raw Materials and Their Core Active Constituents
1.1 Tea Polyphenols Are a Group of Polyphenolic Compounds
Tea polyphenols are a collective term for various phenolic compounds found in tea leaves rather than a single chemical substance with one defined structure. The principal active constituents of green tea polyphenols belong to the catechin family and include:
① Epigallocatechin-3-gallate, or EGCG;
② Epigallocatechin, or EGC;
③ Epicatechin gallate, or ECG;
④ Epicatechin, or EC.
The actual proportions of different catechins vary according to the tea variety, harvesting season, extraction solvent, purification method, and storage conditions. “Tea polyphenol content,” “total catechin content,” and “EGCG content” stated in raw-material specifications are different analytical parameters and cannot be directly converted into one another.
Raw-Material Parameter | What It Represents | Significance for Formulation Development |
Total tea polyphenol content | The sum of multiple phenolic compounds | Reflects the overall polyphenol level of the extract |
Total catechin content | The combined amount of catechins such as EGCG, EGC, ECG, and EC | Reflects the concentration of catechin-type constituents |
EGCG content | The actual mass fraction of EGCG in the raw material | Used to calculate the actual amount of EGCG added |
Caffeine content | Residual caffeine in the extract | Reflects the composition and degree of decaffeination of the extract and affects batch consistency and quality control |
Moisture, heavy metals, and residual solvents | Indicators of raw-material purity and safety | Affect stability, color, and batch-to-batch consistency |
1.2 The Molecular Structure of EGCG Determines Both Its Activity and Instability
The molecular formula of EGCG is C₂₂H₁₈O₁₁, and its relative molecular mass is approximately 458.37. Its structure consists of a flavan-3-ol backbone, a B ring bearing three phenolic hydroxyl groups, and a gallate ester moiety, with a total of eight phenolic hydroxyl groups.
EGCG contains two sets of adjacent or consecutively arranged polyphenolic hydroxyl groups:
① A pyrogallol structure on the B ring;
② A pyrogallol structure within the gallate ester moiety.
These phenolic hydroxyl groups can donate hydrogen atoms or electrons, converting lipid peroxyl radicals into less reactive lipid hydroperoxides. The resulting EGCG phenoxyl radicals acquire a degree of stability through resonance delocalization, thereby slowing the propagation of free-radical chain reactions.
The simplified reaction is as follows:
EGCG—OH + LOO· → EGCG—O· + LOOH
Where:
① LOO· represents a lipid peroxyl radical;
② LOOH represents a lipid hydroperoxide;
③ EGCG—O· represents a resonance-stabilized EGCG phenoxyl radical.
It should be noted that although LOOH is no longer a free radical, it is not an inert end product. Under conditions involving metal ions, heat, or light, it may continue to decompose and form new radicals and secondary oxidation products such as aldehydes and ketones.
At the same time, the polyphenolic hydroxyl groups increase the likelihood that EGCG itself will be oxidized. In the presence of oxygen, light, elevated temperatures, metal ions, and neutral or alkaline conditions, EGCG may undergo autoxidation, conversion to quinone species, dimerization, and epimerization.
The antioxidant activity and chemical instability of EGCG arise from the same structural basis: EGCG can preferentially participate in redox reactions, but it is also consumed during those reactions.
2 Sebum Imbalance in Oily, Acne-Prone Skin
2.1 Major Components of Sebum
Human sebum is released by sebocytes through holocrine secretion. The table below lists its commonly reported approximate composition. Variations may occur depending on the analytical method, age, anatomical site, and level of sebum secretion. After sebum reaches the skin surface, triglycerides may be hydrolyzed by lipases to form diglycerides and free fatty acids. Consequently, the composition of newly secreted sebum may differ from that of samples collected from the skin surface.
Sebum Component | Common Approximate Proportion | Physiological Characteristics |
Triglycerides and their hydrolysis products, including free fatty acids and small amounts of diglycerides | Approximately 57%–57.5% | Constitute the main body of sebum and may be affected by microbial lipases |
Wax esters | Approximately 26% | Characteristic lipids of human sebum that contribute to lubrication and formation of the surface lipid film |
Squalene | Approximately 12% | Contains six carbon–carbon double bonds and is readily oxidized |
Cholesterol and cholesteryl esters | Approximately 2%–4.5% | Contribute to the structure of surface lipids and skin-barrier function |
2.2 Molecular Basis of Increased Sebum Synthesis
Insulin-like growth factor 1, or IGF-1, can activate phosphoinositide 3-kinase/protein kinase B signaling, or the PI3K/Akt pathway. This signaling pathway can increase the expression of sterol regulatory element-binding protein 1, or SREBP-1.
SREBP-1 is a lipogenesis-related transcription factor that promotes the expression of genes involved in lipid synthesis, including fatty acid synthase and acetyl-CoA carboxylase, thereby increasing lipid accumulation within sebocytes.
This process can be simplified as follows:
IGF-1 → PI3K/Akt activation → Increased SREBP-1 expression → Increased synthesis of fatty acids and neutral lipids → Increased sebum production
When increased sebum production occurs together with abnormal shedding of keratinocytes in the follicular duct, sebum and keratinous material accumulate within the follicle and form microcomedones. The hypoxic, lipid-rich environment of the occluded follicle may further alter the interaction between Cutibacterium acnes and the host immune system.
3 Squalene Oxidation and the Amplification Cycle of Acne
3.1 Why Squalene Is Readily Oxidized
Squalene is an unsaturated triterpene hydrocarbon containing six carbon–carbon double bonds. Its high degree of unsaturation makes it susceptible to attack by singlet oxygen, ozone, ultraviolet-associated reactive oxygen species, and free radicals.
Squalene oxidation can occur through two major pathways:
1. Photooxidation involving singlet oxygen;
2. Free-radical lipid peroxidation chain reactions.
The simplified free-radical oxidation process is as follows:
LH + R· → L· + RH
L· + O₂ → LOO·
LOO· + LH → LOOH + L·
Here, LH represents an unoxidized lipid, L· represents a lipid radical, LOO· represents a lipid peroxyl radical, and LOOH represents a lipid hydroperoxide. The newly formed L· can continue to attack other lipid molecules, allowing the oxidation reaction to propagate.
The multiple double bonds in squalene provide multiple sites for oxidation. Compared with squalane, which is fully hydrogenated and structurally saturated, squalene has lower oxidative stability.
3.2 What Is Squalene Monohydroperoxide?
Following oxidation, squalene can form squalene monohydroperoxide, abbreviated as SQOOH or Sq-OOH.
The simplified reaction can be expressed as follows:
Squalene + Singlet oxygen or reactive oxygen species → SQOOH
SQOOH indicates that one hydroperoxide group, —OOH, has formed within the squalene molecule. Because squalene contains multiple oxidation sites, SQOOH does not represent a single structure but rather a group of positional isomers.
SQOOH is an early-stage product of lipid oxidation. It may undergo further decomposition or rearrangement to form aldehydes, ketones, epoxides, and polymerized oxidation products. Some downstream products may be more reactive than the original squalene molecule.
3.3 Biological Effects of SQOOH
Squalene monohydroperoxide, or SQOOH, is a reactive lipid-peroxidation product formed in human sebum under oxidative stress.
Animal and cell-based studies indicate that SQOOH and peroxidized squalene may have the following effects:
① Depletion of cellular antioxidants such as glutathione;
② Increased oxidative stress in keratinocytes;
③ Activation of nuclear factor kappa B signaling;
④ Increased expression of inflammatory mediators such as interleukin-6;
⑤ Promotion of abnormal keratinocyte proliferation;
⑥ Induction of comedone-like changes in the rabbit-ear model.
Nuclear factor kappa B is abbreviated as NF-κB. NF-κB participates in the transcription of numerous inflammation-related genes. Following treatment of keratinocytes with peroxidized squalene, increased NF-κB activation and interleukin-6 release have been observed.
The rabbit-ear comedogenicity model can be used to investigate comedone-promoting mechanisms, but it cannot be considered directly equivalent to human facial acne. Current evidence supports the pro-inflammatory and comedogenic potential of SQOOH, but SQOOH cannot yet be regarded as the sole determinant of human acne.
3.4 The Lipid-Oxidation Cycle in Acne
The relevant processes in oily, acne-prone skin can be summarized as follows:
Increased sebum synthesis → Increased lipid load within the follicle → Abnormal keratinization of the follicular duct and microcomedone formation → Altered local microbial metabolism and immune responses → Increased reactive oxygen species and inflammatory mediators → Formation of SQOOH and other squalene oxidation products → Increased keratinocyte inflammation and proliferation → Further follicular obstruction and inflammation
This cycle indicates that the management of oily, acne-prone skin should consider both the amount of sebum produced and the oxidative state of the sebum. Simply removing oil from the skin surface cannot directly influence SREBP-1-mediated lipogenic signaling within the follicle, nor can it sufficiently reduce squalene oxidation and inflammation induced by oxidized lipids.
4 Multifaceted Sebum-Regulating Mechanisms of EGCG
4.1 Activation of AMPK and Inhibition of SREBP-1
AMP-activated protein kinase, or AMPK, is an important sensor of cellular energy status.
Once activated, AMPK can inhibit multiple energy-intensive anabolic processes and reduce the maturation, transcriptional activity, or expression of SREBP-1. Studies in sebocytes have shown that EGCG can activate AMPK and reduce SREBP-1 expression, thereby decreasing the intracellular accumulation of neutral lipids.
This pathway can be expressed as follows:
EGCG → AMPK activation → SREBP-1 inhibition → Reduced expression of lipogenic enzymes → Reduced lipid accumulation in sebocytes
This mechanism occurs at the level of lipid metabolism within sebocytes and differs from that of physical oil-absorbing ingredients such as silica and starch. Physical oil absorbers mainly reduce surface shine, whereas EGCG research involves the modulation of signaling pathways associated with sebum production.
The effects of EGCG on sebocytes are concentration-dependent. Higher experimental concentrations may also inhibit cell proliferation or induce apoptosis. In formulation development, the concentration should be determined according to skin tolerability, stability, and the amount actually delivered to the skin. Concentrations used in cell-based experiments should not be directly converted into finished-product inclusion levels.
4.2 Inhibition of IGF-1-Induced Lipogenesis and Inflammation
Another study using human SZ95 sebocytes showed that EGCG inhibited IGF-1-induced cell proliferation and lipid synthesis while reducing the expression of certain inflammatory factors.
These effects involve two main areas:
Area of Action | Associated Changes |
Lipid metabolism | Reduced IGF-1-induced lipogenesis and intracellular lipid accumulation |
Inflammation regulation | Reduced inflammation-related signaling involving interleukin-1, interleukin-6, interleukin-8, and other mediators |
Sebaceous glands not only synthesize sebum but can also produce inflammatory mediators. The simultaneous regulation of IGF-1-associated lipid synthesis and cytokine expression means that the effects of EGCG are not limited to reducing the amount of oil.
4.3 Interrupting the Sebum-Peroxidation Chain
EGCG can donate hydrogen atoms to lipid peroxyl radicals, thereby reducing the ability of those radicals to abstract hydrogen atoms from other lipid molecules.
The simplified process is as follows:
Lipid peroxyl radical + EGCG → Lipid hydroperoxide + A relatively more stable EGCG radical
EGCG can also form complexes with transition-metal ions such as iron and copper, reducing the likelihood that some metal ions will participate in radical-generating reactions. However, this effect is system-dependent. Under certain conditions involving pH, oxygen, and metal ions, EGCG may also undergo autoxidation and generate hydrogen peroxide. Metal chelation therefore cannot be assumed to result invariably in antioxidant activity.
The effects of EGCG on sebum oxidation may be divided into two stages:
1. Capturing lipid peroxyl radicals during the chain-propagation stage;
2. Reducing the likelihood of highly reactive radical formation catalyzed by metal ions.
This chemical mechanism supports the potential of EGCG to help reduce oxidative stress in sebum. However, large-scale clinical trials using facial SQOOH levels as the primary endpoint are still lacking. Product efficacy should therefore be further evaluated using sebum-peroxidation markers, the squalene-to-SQOOH ratio, or other lipidomics-based methods.
4.4 Modulation of Inflammation-Related Signaling
In sebocytes and acne-related experimental models, EGCG has been shown to inhibit NF-κB and activator protein 1, or AP-1, signaling.
NF-κB and AP-1 participate in the transcription of inflammatory cytokines, chemokines, and certain matrix-degrading enzymes. By reducing the activity of these signaling pathways, EGCG may decrease the release of inflammatory mediators within the pilosebaceous unit.
EGCG has also been shown to reduce the viability of acne-associated bacteria in vitro. The currently accepted scientific name of the acne-associated bacterium is Cutibacterium acnes. Evidence for this effect is derived mainly from laboratory studies. Actual antimicrobial performance in a formulation will depend on the EGCG concentration, stability, contact time, and overall product system.
Current cell-based, animal, and preliminary human studies suggest that EGCG may act through the following pathways:
Reduced lipogenic signaling + Reduced lipid peroxidation + Modulation of inflammatory responses + Reduced microbe-related stimulation
5 EGCG Raw-Material Purity and Effective Content
5.1 The Main Value of High Purity Is Improved Controllability
There is currently no consistent human clinical evidence demonstrating that an EGCG raw material must reach a particular purity before it produces a sebum-regulating effect. Raw-material purity is not a fixed efficacy threshold.
The primary advantages of high-purity raw materials include:
① More accurate calculation of the actual EGCG content in a formulation;
② Reduced batch variation caused by other catechins, caffeine, and pigments;
③ Reduced effects of unidentified impurities on color, odor, and stability;
④ Easier establishment of quantitative analytical methods for both raw materials and finished products.
When EGCG is used as the principal research constituent, raw materials with a high EGCG content, a complete high-performance liquid chromatography chromatogram, and adequate impurity-control documentation may be selected according to the research objectives and quality-control requirements. For example, an EGCG content above 95% may further improve the consistency of dose calculations and quality control. However, this value is a raw-material development recommendation and does not represent a medically effective concentration.
5.2 Raw-Material Purity and Finished-Product Concentration Must Be Calculated Separately
Assuming that a raw material containing 95% EGCG is added at a concentration of 1%, the theoretical EGCG concentration is:
1% × 95% = 0.95%
This value represents the theoretical content at the initial stage of manufacture. Exposure to light, oxygen, elevated temperatures, metal ions, and prolonged storage may reduce the EGCG content. The actual amount present when the consumer uses the product will also depend on its retention throughout the shelf life.
5.3 Human Evidence for Topical Concentrations
In an eight-week randomized, double-blind, split-face study involving 35 subjects with acne, a 1% or 5% EGCG solution was applied twice daily to one side of the face, while a vehicle containing 3% ethanol was applied to the other side. Improvements in both inflammatory and non-inflammatory lesions were observed, and overall tolerability was reported to be good.
This study provides preliminary human evidence for topical EGCG concentrations of 1% and 5%. However, it was limited by its relatively small sample size, short study duration, and simple formulation format.
In skincare formulation development, 1% active EGCG may serve as one starting reference concentration for subsequent efficacy studies. However, it does not represent an established minimum effective concentration, a universal recommended concentration, or an equivalent concentration across different dosage forms. Lower concentrations should be assessed in combination with finished-product stability, skin delivery, and human efficacy data. A 5% concentration may increase development challenges related to raw-material cost, color, oxidative stability, and tolerability assessment.
6 Stability Design for EGCG in Skincare Formulations
6.1 Major Degradation Pathways of EGCG
The principal changes that may occur to EGCG in aqueous systems include the following:
1. Autoxidation
Phenolic hydroxyl groups may be oxidized into semiquinone or quinone structures, potentially forming hydrogen peroxide and oxidized dimers.
2. Epimerization
EGCG may be converted into gallocatechin gallate, or GCG.
3. Photodegradation
Ultraviolet and visible light can accelerate EGCG oxidation and structural changes.
4. Metal-Catalyzed Oxidation
Trace amounts of iron and copper may accelerate free-radical reactions.
5. Polymerization and Color Changes
Oxidation products may undergo further coupling reactions, causing the formulation to become yellow or brown or to form precipitates.
The degradation rate of EGCG is affected by pH, temperature, oxygen partial pressure, raw-material concentration, and formulation composition. Acidic conditions are generally more favorable for maintaining EGCG stability than neutral or alkaline conditions. Higher temperatures and increased oxygen exposure accelerate degradation.
6.2 Key Considerations in Formulation-System Design
Design Parameter | Recommended Approach | Mechanistic Basis |
EGCG inclusion level | Calculate the actual active content according to the assayed purity of the raw material | Prevents the raw-material inclusion level from being treated as equivalent to the EGCG content |
System pH | Use a mildly acidic system that has been validated for stability | Reduces autoxidation under neutral and alkaline conditions |
Processing temperature | Add EGCG during a lower-temperature processing stage | Reduces thermal degradation and epimerization |
Metal-ion control | Use purified water, equipment with low metal-ion contact, and suitable chelating agents | Reduces oxidation catalyzed by iron and copper |
Oxygen control | Minimize prolonged high-speed mixing and air entrainment | Reduces oxidation caused by dissolved oxygen |
Packaging | Use light-protective, low-oxygen-permeability packaging that minimizes air re-entry | Reduces degradation caused by light exposure and repeated contact with air |
Supporting antioxidant system | Evaluate co-antioxidant systems, such as vitamin C and α-lipoic acid, that have been validated in the target formulation | Some studies indicate improved EGCG photostability, although the effects of different co-antioxidants are system-dependent |
Content determination | Use high-performance liquid chromatography to quantify EGCG | Color and total antioxidant capacity cannot replace direct determination of active content |
A model cream study showed that 1% EGCG underwent substantial photodegradation under simulated sunlight. The addition of vitamin C or α-lipoic acid reduced the extent of EGCG photodegradation.
The effects of co-antioxidants depend on their concentration, solubilization state, pH, and the emulsion system and must therefore be determined experimentally in the actual formulation.
6.3 Formulation Framework for an EGCG Sebum-Control Serum
The following formulation illustrates a possible framework for applying EGCG. Specific proportions should be adjusted according to preservative requirements, stability testing, and skin testing.
Formulation Ingredient | Reference Use Level | Primary Function |
High-purity EGCG raw material | Approximately 1.0% calculated as active EGCG | Used to evaluate sebum-regulating, antioxidant, and anti-inflammatory-related efficacy |
Glycerin | 2.0%–3.0% | Provides moisturization and reduces the drying sensation associated with sebum-control products |
1,3-Propanediol | 3.0%–5.0% | Solvent and humectant |
Betaine | 0.5%–1.5% | Provides moisturization and improves skin feel |
Panthenol | 0.3%–0.8% | Provides soothing effects and supports barrier function |
Sodium phytate or another suitable chelating agent | 0.03%–0.10% | Controls trace metal ions |
Nonionic thickener | As required | Establishes a low-irritation aqueous gel system |
Buffer system | As required | Maintains a validated mildly acidic pH |
Preservative system | Selected according to the formulation and applicable regulations | Controls microbial contamination |
Deionized water | Quantity sufficient to 100% | Continuous phase |
7 Representative Chemicals Related to Research on the Mechanisms by Which Tea Polyphenols Regulate Sebum Synthesis and Lipid Oxidation
Table 1. Core Tea Polyphenol Constituents and Catechin Analytical Standards
Category | CAS No. | Aladdin Item No. | Name | Specification or Purity | Product Features and Applications |
Core tea polyphenol raw material | 84650-60-2 | Tea Polyphenols | Moligand™, TP98% | High-content tea polyphenol raw material; used for screening sebum-control and antioxidant formulations for oily, acne-prone skin, evaluating total polyphenol content, and analyzing catechin composition | |
Core active catechin | 989-51-5 | (−)-Epigallocatechin Gallate | Analytical standard, Moligand™ | Core active constituent used in research on the sebum-regulating effects of tea polyphenols; used for content determination, stability evaluation, studies of lipid synthesis in sebocytes, and inhibition of lipid peroxidation | |
Non-esterified catechin | 970-74-1 | (−)-Epigallocatechin (EGC) | Analytical standard, Moligand™, ≥98% | Non-gallate catechin standard; used for quantitative analysis of tea polyphenol composition and comparative studies of the effects of ester-group structure on antioxidant activity | |
Esterified catechin | 1257-08-5 | (−)-Epicatechin Gallate | Analytical standard, Moligand™, ≥98% | Gallate ester catechin standard; used for catechin quantification and for investigating associations between gallate ester structure, free-radical scavenging, and inhibition of lipid oxidation | |
Non-esterified catechin | 490-46-0 | Epicatechin (EC) | Analytical standard, Moligand™, ≥98% (HPLC) | Major non-esterified catechin standard in tea polyphenols; used for chromatographic quantification, raw-material fingerprint analysis, and comparative structure–activity studies of catechins | |
Catechin reference standard | 154-23-4 | (+)-Catechin | Analytical standard, ≥97% | Reference material representing the basic catechin structure; used for identification of tea polyphenol constituents, development of chromatographic methods, and comparison of stereochemistry-related activities | |
Epimerization product | 4233-96-9 | (−)-Gallocatechin Gallate (GCG) | Analytical standard, Moligand™ | Important heat-induced epimerization product of epigallocatechin gallate; used for evaluating stability during processing, storage, and formulation development | |
Esterified catechin | 130405-40-2 | (−)-Catechin Gallate | ≥98% (HPLC) | Reference material for catechin gallate constituents; used for analysis of minor tea polyphenol components, chromatographic separation, and comparison of the activities of esterified catechins | |
Non-esterified catechin | 3371-27-5 | (−)-Gallocatechin | ≥98% | Gallocatechin reference material; used for catechin composition analysis, epimerization monitoring, and studies of the structure–activity relationships of polyphenolic hydroxyl groups | |
Polyphenolic structural unit | 149-91-7 | Gallic Acid | Moligand™, ≥99% | Structural reference compound for the gallate ester moiety; used for degradation-product analysis, comparison of antioxidant capacity, and validation of chromatographic methods |
Table 2. Substances Used in Studies of Human Sebum Composition and Lipid Oxidation
Category | CAS No. | Aladdin Item No. | Name | Specification or Purity | Product Features and Applications |
Squalene oxidation model | 111-02-4 | Squalene | Moligand™, ≥98% | Characteristic unsaturated lipid in human sebum; used in studies of squalene oxidation, squalene hydroperoxide formation, and the inhibition of lipid peroxidation by tea polyphenols | |
Saturated lipid control | 111-01-3 | Squalane | ≥98% | Saturated structural control obtained by complete hydrogenation of squalene; used to compare the effects of unsaturation on oxidative stability and formulation tolerability | |
Sebum wax ester model | 540-10-3 | Cetyl Palmitate | ≥98% | Representative wax ester in artificial sebum systems; used to simulate the physical properties and viscosity of sebum and the discharge behavior of follicular contents | |
Sebum triglyceride model | 122-32-7 | Glyceryl Trioleate | ≥99% | Representative triglyceride in artificial sebum; used to construct models of lipase hydrolysis, free-fatty-acid formation, and sebum oxidation | |
Characteristic sebum fatty acid | 17004-51-2 | cis-6-Hexadecenoic Acid | ≥99% | Characteristic monounsaturated fatty acid in human sebum; used in studies of sebum fatty-acid composition, Cutibacterium acnes metabolism, and inflammatory responses | |
Monounsaturated fatty acid | 112-80-1 | Oleic Acid | European Pharmacopoeia (Ph. Eur.), ≥65% | Component of artificial sebum and cellular lipid-loading models; used to investigate unsaturated fatty-acid oxidation, changes in membrane lipids, and keratinocyte responses | |
Polyunsaturated fatty acid | 60-33-3 | Linoleic Acid | Analytical standard, Moligand™, ≥99% (GC) | Lipid-peroxidation-sensitive substrate and sebum fatty-acid standard; used in studies of oxidative chain reactions, follicular lipid composition, and inflammatory markers | |
Saturated fatty acid | 57-10-3 | Palmitic Acid | BioReagent, ≥99% | Common saturated fatty acid in human sebum; used for artificial sebum preparation, sebocyte lipid-accumulation studies, and saturated fatty-acid control experiments | |
Saturated fatty acid | 57-11-4 | Stearic Acid | Moligand™, C18: 98% | Long-chain saturated fatty-acid model compound; used in studies of artificial sebum composition, lipid phase behavior, and control experiments involving oxidation of unsaturated lipids | |
Cholesterol component | 57-88-5 | Cholesterol | Animal-origin-free, low endotoxin, suitable for cell culture, ≥99% | Component of artificial sebum and cell-membrane lipid systems; used in studies of sebum cholesterol composition, lipid homeostasis, and cell culture | |
Cholesteryl ester component | 303-43-5 | Cholesteryl Oleate | ≥98% (HPLC) | Representative cholesteryl ester; used for construction of artificial sebum systems, sebum lipidomic analysis, and studies of cholesteryl ester oxidation | |
Lipid-peroxidation product | 75899-68-2 | 4-Hydroxynonenal (4-HNE) | Moligand™, ≥97% | Reactive aldehyde formed through lipid peroxidation; used in models of keratinocyte oxidative stress, inflammatory signaling, and cellular injury | |
Lipid-peroxidation marker | 542-78-9 | Malondialdehyde | 1,000 μg/mL in H₂O | Standard for lipid-peroxidation assays; used for malondialdehyde quantification, oxidative-damage assessment, and methodological validation of tea polyphenol antioxidant experiments |
Table 3. Reagents Used in Studies of Sebum Synthesis and Inflammatory Signaling Pathways
Category | CAS No. | Aladdin Item No. | Name | Specification or Purity | Product Features and Applications |
Sebum-synthesis stimulant | 67763-96-6 | Recombinant Human IGF-1 Protein | Animal-origin-free, carrier-free, biologically active, ActiBioPure™, high-performance, ≥95% (SDS-PAGE) | Used to induce lipid synthesis and inflammatory-factor expression in sebocytes and to establish an insulin-like growth factor 1-mediated sebum-production model | |
Phosphoinositide 3-kinase pathway inhibitor | 154447-36-6 | LY294002 (2-Morpholin-4-yl-8-phenylchromen-4-one) | Moligand™, ≥98% | Used as one of the pharmacological inhibitory controls for the PI3K pathway to assist in evaluating whether IGF-1-mediated lipid synthesis and the effects of EGCG involve this pathway | |
Phosphoinositide 3-kinase pathway inhibitor | 19545-26-7 | Wortmannin | Moligand™, ≥98% | PI3K pathway-blocking reagent; used in studies of lipogenic signaling, protein kinase B activation, and pathway dependence | |
AMPK-activating tool compound | 2627-69-2 | Acadesine | Moligand™, ≥98% | Positive control for the AMP-activated protein kinase pathway; used to investigate cellular energy sensing, inhibition of lipid synthesis, and comparisons with the effects of tea polyphenols | |
AMPK-inhibiting tool compound | 866405-64-3 | Dorsomorphin | Moligand™, ≥98% | Used as one of the pharmacological AMPK-inhibitory controls to assist in evaluating whether EGCG-mediated regulation of sebum synthesis involves the AMPK pathway | |
Sterol regulatory element-binding protein pathway inhibitor | 947303-87-9 | PF-429242 | ≥96% | Site-1 protease inhibitor; used to block sterol regulatory element-binding protein maturation and investigate the regulation of lipid synthesis in sebocytes | |
Nuclear factor kappa B pathway inhibitor | 19542-67-7 | BAY 11-7082, IκBα Phosphorylation Inhibitor | Moligand™, ≥98% | Inhibitory control for inflammatory signaling pathways; used to investigate NF-κB activation, inflammatory-mediator expression, and the anti-inflammatory mechanisms of tea polyphenols |
Table 4. Antioxidants, Metal-Ion Control Agents, and Buffer Systems for Formulation Development
Category | CAS No. | Aladdin Item No. | Name | Specification or Purity | Product Features and Applications |
Mildly acidic buffer system | 77-92-9 | Anhydrous Citric Acid Powder | Anhydrous grade, UltraBio™, ≥99.5% (T) | Used to establish a mildly acidic formulation environment, adjust the pH of tea polyphenol systems, and conduct storage-stability studies of epigallocatechin gallate | |
Mildly acidic buffer system | 6132-04-3 | Trisodium Citrate Dihydrate | European Pharmacopoeia (Ph. Eur.), suitable for analysis, ACS, reagent grade | Used together with citric acid to form a buffer system, maintain formulation pH, and reduce pH drift during storage | |
Aqueous-phase antioxidant | 50-81-7 | L-Ascorbic Acid | Anhydrous grade, Moligand™, ACS, ≥99% | Water-phase reducing antioxidant; used in tea polyphenol co-antioxidant systems, photostability evaluation, and redox-cycle studies | |
Oil-phase antioxidant | 59-02-9 | D-α-Tocopherol | Moligand™, ≥97% (GC) | Lipid-phase free-radical chain terminator; used in antioxidant systems for artificial sebum and in studies of synergistic activity between tea polyphenols in the aqueous and lipid phases | |
Amphiphilic antioxidant | 1077-28-7 | DL-α-Lipoic Acid | ≥99% | Amphiphilic redox-active substance; used in tea polyphenol co-antioxidant systems, photodegradation control, and studies of antioxidant activity at interfaces between different phases | |
Metal-ion chelating agent | 6381-92-6 | Disodium Ethylenediaminetetraacetate Dihydrate | Suitable for plant cell culture, ≥99% | Chelates metal ions such as iron and copper; used to reduce metal-catalyzed autoxidation of tea polyphenols and sebum-peroxidation reactions | |
Naturally derived chelating agent | 83-86-3 | Phytic Acid Solution | 70% in H₂O | Multidentate metal-ion chelating agent; used for metal-ion control in formulations, tea polyphenol stability studies, and investigation of oxidation-catalyzing factors | |
Naturally derived chelating agent | 14306-25-3 | Sodium Phytate Hydrate | ≥75% | Water-phase metal-ion control ingredient; used in mildly acidic tea polyphenol formulations, inhibition of metal-catalyzed oxidation, and storage-stability evaluation |
Note: The products listed above are representative Aladdin products related to scientific research and formulation studies. Additional product specifications, grades, and Certificate of Analysis information can be retrieved from the Aladdin website by searching the product name, CAS number, or item number.
References
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