|/China/animal||High-, medium- and low-antioxidant peptides (HCP, MCP and LCP)/silver carp skin||KM mice/5 week |
(25 ± 2 g)
|3UV-A + 1UV-B||Tg: HCP, MCP, LCP (0,200 mg/kg.bw.d)/0/1/2 weeks||1. ACPs significantly alleviated skin composition and antioxidant index abnormalities induced by UVs.|
2. HCP has the best protection effect on skin photoaging, and the difference between MCP and LCP is not obvious.
|ACPs have the potential to resist photoaging of the skin.|
|/China/animal||Gelatin (SG)and gelatin hydrolysate (SGH)/ |
|ICR male mice/ |
20 to 22 g
|UV-B||Tg: SG (100, 500 mg/kg.bw.d), SGH (100, 500 mg/kg.bw.d); Cg: Vc 100 mg/kg.bw.d/5 week||1. Antioxidant activity of SG and SGH is related to dose, molecular weight and amino acid composition.|
2. SG and SGH alleviate oxidative damage by enhancing antioxidant enzyme activity and thymus index
|SGH has the potential to be used as an antioxidant in health products and cosmetics.|
|/Korea/animal||Collagen peptide (CP)/ |
|SKH–1 hairless mice/|
6 weeks old
|UV-B||Tg:CP (0,500, 1000 mg/kg.bw.d) Cg: N–acetyl glucosamine (1000 mg/kg.bw.d)/ |
|1. Oral CP increased skin hydration, reduced wrinkle formation, changed the expression of HAS–1,–2, and maintained the stability of HA.|
2. CP regulate the expression of skin moisturizing factor filagglutinin and total chain protein
|CP can be used as a nutrient to relieve UV-B-induced skin wrinkles, dehydration and water loss.|
|/Brazil/cell||Collagen Hydrolysate (CH)/cow||HDFs || ||Cg:CH (0.5, 1.0, 2.5 and 5.0 mg/mL)/48 h||1. CH regulates cell metabolism without cytotoxicity.|
2. CH maintains intracellular protein stability by inhibiting the activity of MMP 1 and 2.
|This CH has protective effects on skin cells and has the potential to become a food supplement.|
| /Korea/clinical||Low-molecular-weight Collagen peptide (LMWCP)/|
|Women/40–60 years old||Age||Tg:LMWCP; 1000 mg/d. Cg: placebo; (0/6/12) weeks||Oral LMWCP protects photoaged skin by improving skin wrinkles, hydration and elasticity||LMWCP can be used as a functional food ingredient to relieve skin photoaging.|
|/China/animal||Collagen hydrolysates (CHs)/Nile tilapia skin||ICRmice/38 ± 4 g, 9-month-old||Age||Tg:CHs (0%, 2.5%, 5%, 10%); Ng: weaned mice; Cg: (WC, 10%|
whey protein hydrolysates)/180 days
|1. CHs significantly improves skin visual appearance, tissue structure and matrix homeostasis.|
2. CHs alleviates oxidative stress by increasing skin antioxidant activity
|CHs can be used as a functional nutritional food against skin aging, but its molecular mechanism is not clear.|
|/China/animal||Elastin peptides (EH)/bovine arteries||Female mice/ (20 ± 2 g)||UV||Nc:vehicle-treated mice; Mg:vehicle-treated + UV. EH group:UV + EH (100 mg/kg.bw.d)/8 weeks||EH can significantly reduce UV-induced epidermal hyperplasia and fibroblast apoptosis, and increase skin hydroxyproline and water content||EH has the potential to prevent and regulate skin photoaging|
|/China/animal||Collagen peptides (CPs)/silver|
|Mice/(8, 13-month-old (28 ± 2, 45 ± 5 g)||Age||Cg: young mice (normal saline); Tg: old mice (CPs: 400 mg/kg.bw.d); Mg: Old mice (normal saline)/2 months||1. CPs promotes skin collagen synthesis by regulating cytokines in skin and serum.|
2. Intake of CPs inhibited platelet release.
|CPs has the potential to be an anti-aging, anti-|
cancer and anti-
cardiovascular health product
|/Canada/cell||Collagen peptides (CPs)/Chicken meat||HDFs cells/|
|DCF-DA||Tg: Two peptides, hydrolyzed by two enzymes (0, 2.5 mg/mL)/24 h||Two chicken collagen peptides have significant effects on inflammatory changes, oxidative stress, type I collagen synthesis, and cell proliferation in skin HDFs||CPs hydrolyzed by different enzymes have different protective and regulatory effects on skin fibroblasts|
|/Canada/cell||Collagen peptides (CPs)/porcine/|
|UV-A||Tg: Four kinds of collagen peptides (0, 0.5, 1, 2, 4 mg/mL)/24 h||1. Bovine CH inhibits the MMP–1 production.|
2. Tilapia CH promotes cell viability and type I collagen generation, while inhibiting ROS and MMP–3 generation.
3. Hen CH promotes collagen production and reduces ROS, MMP–1 and 9 generation and the expression of apoptotic genes.
|Hen CH protects HDFs from UV-A-induced damage better than pigs, cattle and tilapia.|
|/China/animal||High, low molecular weight collagen hydrolysates (HMCH/LMCH)/Silver Carp||Mice/5weeks (25 ± 2 g)||UV-A + UV-B||Tg1:UV + LMCH (HMCH)(50, 100, 200 mg/kg.bw.d)/6 weeks; Tg2:UV+LMCH (HMCH) (200 mg/kg.bw.d)/|
|1. Both HMCH and LMCH increase skin components and antioxidant enzyme activity in skin and serum.|
2. LMCH is more effective than HMCH.
3. Skin hydroxyproline, HA, and moisture content depend on peptide dose.
|LMCH extracted from silver carp skin can be used as a dietary supplement to prevent skin aging.|
|High, low purity collagen hydrolysate (H-CP/L- CP)/fish gelatin||Female/(35–55 years old)||Age||H-CP group: 5 g/d; L-CP group: 5 g/d; Cp: placebo; 0/4/8 weeks.||H-CP is more significant than L-CP in improving facial skin moisture, elasticity, wrinkles, and roughness.||L-CP and H-CP are both effective dietary supplements to improve skin conditions.|
|Collagen hydrolysate (HC)/Lates calcarifer skin||HDFs/human; Wistar rats (214 ± 26 g)|| ||Mice Tg: (0,2000,5000 mg/kg.bw.d)/15d;|
Cell Tg: (50, 100, 150 and 200 µg/mL)/24 h.
|1. Animal and cell experiments prove that HC is non-toxic.|
2. HC can promote the growth of fibroblasts and the synthesis of cellular collagen, but not as effective as HC combined with VC.
|Single HC or HC combined with VC can be used as nutritional health products for skin care.|
|Gelatin hydrolysates (CGH)/Cod skin||HDF cells/ |
|UV-B||Tg: CGH (0, 0.001, 0.01, 0.1,1, 10) mg/mL|
|1. CGH inhibits the expression of MMP–1 in fibroblasts induced by UV-B.|
2. Purified MMP–1 inhibitory peptides have significant inhibitory effects on MMP–1, p-ER and p-p38.
|CGH can be used as a functional supplement for skin care.|
|High, medium, low antioxidant peptide (HCP/|
MCP/LCP)/Silver carp skin; Serum collagen
|SD rat (8 week); ESF cells/skin ||UV-A||Rats Tg (HCP, MCP and LCP)/(2.4 g/kg.bw.d)/2 h; Cell Tg: (SHCP, SMCP and SLCP)/(0, 50, 200 µM/mL)/24 h.||1. SCP is the active component of serum metabolites, which shows repair effect by removing ROS. |
2. SCP promotes collagen synthesis and inhibits its degradation by activating TGF-β/Smad3 pathway and inhibiting the expression of AP–1 and MMP–1,3,SHCP is the best one.
|CP promotes photoaging skin repair by activating the TGF- TGF/Smad pathway and inhibiting collagen reduction.|
Collagenase Collagen peptide (ACP/CCP)/
|Mice/(8, 13-month-old (28 ± 2, 45 ± 5 g)||Age||Cg: young mice (normal saline); Tg: old mice/ACP (200, 400, and 800 mg/kg.bw.d), CCP (400 mg/kg.bw.d)/8 weeks||Oral CPs improve skin relaxation, increase collagen content and antioxidant enzyme activity, repair collagen fibers, and normalize the ratio of skin collagen. ACP is better than CCP.||CP can alleviate the chronological aging of the skin and has the potential to become an anti-aging functional food.|
|Collagen peptide NS (CPNS)/fish scale||HDF cells |
Mice/8 weeks old (25–30 g)
|UV-B||Cell Tg: CPNS (0, 50, 100, 250, 500 µg/mL)/24 h; Mice Tg: CPNS (300, 500 mg/kg.bw.d)/12weeks||1. CPNS treatment reduced the production of MMP–1 and increased the synthesis of type 1 procollagen in HFD cells. |
2. Oral CPNS significantly reduced skin wrinkle formation, epidermal water loss, epidermal thickness, and increased hydration.
|CPNS are a potential food supplement to prevent skin aging.|
|Gelatin/Amur sturgeon swim bladder||Female |
SD rat/6 months old
|Age||Cg (8% whey protein); Tg (8%, 4%, 2%)/12 months.||1. Oral administration of 3.85 g/kg.bw.d gelatin significantly improved skin histological structure and collagen ratio. |
2. Skin antioxidant activity increased.
|The gelatin improves the foundation for the development of anti-aging foods.|
|Protein hydrolysate (WPH)/Walnut ||SD rats/|
|UV-A + UV-B||Cg:( distilled water); Tg: UV-R + WPH (0, 0.32, 0.98, 2.88 g/L)/18 weeks||1. WPH significantly enhances skin elasticity and promotes the biosynthesis of Col I, Hyp, and HA.|
2. WPH inhibits MMP–1 activity and repairs skin damage.
3. WPH repair effect becomes dose dependent, high dose is best.
|WPH has potential as a functional food ingredient against photoaging.|
|Effects of Oral Polyphenol on Skin Aging|
|Polyphenol extract (HPE)/hawthorn ||HDFs and HaCaT/human; mice/5–6 weeks old||UV-B||Cell Tg: HPE (0, 5, 10 µg/mL)/24 h; Mice |
Tg: HPE (0, 100, 300 mg/kg.bw.day)/12 weeks
|1. HPE treatment can promote cell proliferation, increase intracellular collagen and reduce MMP–1 production.|
2. Oral HPE reduces UV-B-induced skin damage by eliminating ROS, reducing DNA damage and inhibiting p53 expression.
|HPE can be used as an anti-aging food or cosmetic ingredient.|
|Products rich in polyphenol (NutroxsunTM)/rosemary and citrus||Adult female||UV-B + UV-A||Long-term: NutroxsunTM (250 mg/day)/|
2 weeks; Short-term: NutroxsunTM (100, 250 mg/day)/24, 48 h
|1. Dietary NutroxsunTM reduces UV- induced skin changes, wrinkles and elasticity improvements. |
2. The improvement effect between two doses is not obvious.
|Long-term oral NutroxsunTM can be used as a nutritional supplement to improve skin conditions.|
rich extract (SSE and SSW)/Spatholobus Suberectus stem
|HaCaT/Human skin||UV-B||Tg1: SSE (0, 3, 10, 30, 300 µg/mL); Tg2: SSW (0, 3, 10, 30, 300 µg/mL)/24 h||1. SSE and SSW inhibited ROS production and cell damage.|
2. SSE repairs skin by upregulating the expression of enzymes and proteins in cells, blocking UV-B-induced MAPKs phosphorylation and its downstream transcription factor.
|SSE can be used as a natural biomaterial to inhibit UV-B-induced photoaging.|
|Rambutan peel phenolics (RPP)/Nephelium lappaceum; Leu-Ser-Gly-Tyr-Gly-Pro|
|Male BALB/c nude mice/20–22 g ||UV-B||Single group: RPP (100 mg/kg.bw. d), SGYGP (100 mg/kg.bw.d); Composite group: (50 RPP+ 50 LSGYGP) mg/kg.bw.d, (100 RPP + 100 LSGYGP)mg/kg.bw.d/10 weeks||1. RPP and LSGYGP improve skin biochemical indicators, tissue structure and collagen levels.|
2. RPP enhances the regulation of oxidative stress and inflammatory factor levels.
3. LSGYGP significantly affects skin collagen and HA content.
|Oral RPP and LSGYGP can alleviate UV-B- induced skin aging.|
|Polyphenols/Flavonoid hesperidin exerts||Male hairless mice/6-|
|UV-B||Cg: water; Tg: UV-B + hesperidin (0, 100 mg/kg.bw.d)/12 weeks||1. Oral hesperidin inhibited UV-B-induced skin thickening and wrinkle formation.|
2. Hesperidin inhibited UV-B-induced expression of MMP–9 and cytokines, and protected collagen fiber loss.
|Oral hesperidin regulates MMP–9 expression by inhibiting MAPK-|
dependent signaling pathways to relieve skin photo-aging.
|Polyphenols/3,5,6,7,8,3,4-heptam-ethoxy flavone (HMF)/C. unshiu peels ||HDFn cells/human dermal ||UV-B||HMF (0, 50, 100, 200 µg/mL)/24 h||1. HMF protects UV-induced HDFn cell damage by inhibiting MMP–1 expression through phosphorylated MAPK signals.|
2. HMF regulates the expression of Smad3 and Smad7 proteins in a dose-dependent manner.
|HMF has the potential to be an anti-aging cosmetic or food supplement.|
Belamcanda chinensis L
|HaCaT cells/human||UV-B||Tg: Tectorigenin (0,|
0.1, 1,10 µM); Cg: VC (200 µM)/24 h
|1. Tectorigenin lowers ROS levels by increasing intracellular antioxidant enzymes.|
2. Tectorigenin reduces mmp–1 and inhibits collagen degradation.
3. Tectorigenin inhibits apoptosis by regulating the levels of caspase–3 and bcl–2 related proteins.
|Tectorigenin alleviates skin damage by inhibiting UV-B-induced cellular oxidation, apoptosis and collagen degradation.|
|Effects of Oral Polysaccharides on Skin Aging|
|SD rats/6~7 weeks old (180–220 g)||UV-A + UV-B||Cg: no irradiation; |
Tg group: UV + TP (0, 100, 200, 300 mg/kg.bw.d)/12 weeks
|Oral TP can alleviate UV-induced skin structural changes, repair collagen damage, maintain the I/III collagen ratio and enhance skin antioxidant enzyme activity.||TP has the potential to become a skin-protective functional food additive.|
|Polysaccharide (HFPS)/Hizikia fusiforme||HDF cells||UV-B||Cg: no irradiation;|
Tp: UV + HFPS (0, 25, 50, 100 µg/mL)/24 h
|1. HFPS significantly reduces cell ROS and increases the pure activity rate. 2.HFPS inhibits UV-induced skin damage by regulating NF-κB, ap–1 and MAPKs signaling pathways.||HFPS has a strong anti-ultraviolet effect and is a potential pharmaceutical, food, and cosmetic ingredient.|
|HaCaT cells||UV-B||Tg1: LBP (0, 50, 100, 300, 600, 1500, 3000 µg/mL)|
24 h; Tp2: UV-B + LBP (0, 300 µg/mL)/24 h
|LBP mainly eliminates ROS and reduces DNA damage. In part, the Nrf2/ARE pathway is activated to inhibit the p38 MAP pathway, thereby inhibiting the activation of caspase–3 and the expression of mmp–9 to protect the aging cells.||LBP may be used as a protective agent or food additive against skin oxidative damage.|
|Fibroblast/men foreskin||UV-B||Tg: UV-B + GL-PS (0, 10, 20, 40 µg/mL) 24 h; Tg: no UV-B and GL-PS/24 h||After GL-PS treatment, cell activity increased, senescent cells decreased, CICP protein expression increased, MMP–1 protein expression decreased, and cell ROS level decreased.||GL-PS protects UV-B- induced cell photoaging by eliminating intracellular ROS, which will provide strategies for subsequent studies.|
|Polysaccharide (SFP)/Sargassum fusiforme||Female KM mice/7 weeks old (20–25 g)||UV-B||Cg: UV-B + sodium hyaluronate (400 mg/kg. bw/d); SFP Tg: UV-B + SFP (0, 200, 400, 600 mg/kg.bw/d)/9 weeks||1. SFP regulates mouse chest, spleen index and skin water content.|
2. SFP increases skin antioxidant enzyme activity, reduces ROS, and reduces oxidative damage.3.SFP inhibits MMP–1 and 9 levels in the skin.
|SFP can be a potential functional food additive for skin protection.|
|Purified, crude polysaccharide (TLH–3,TLH)/|
|HELF cells/human; Mice/8 weeks|
(23 ± 2 g)
|t-BHP/D-galactose||Cell Tg: TLH–3 (0, 50, 100, 200, 400 µg/mL), Pc: Vc (50 ug/mL)/24 h; Mice Tg: TLH–3 and TLH (200 mg/kg. bw/d),Pc: Vc (100 mg/kg. bw/d)/5 weeks||1. TLH–3 relieves cell senescence by regulating the expression of bcl–2, bax, caspase–3 proteins, inhibiting senescence-related enzyme levels.|
2. TLH–3 reduced skin pathological lesions by reducing IL–6, LPF, AGEs, and enhanced MAO activity.
|TLH–3 is an active polysaccharide that protects cells and mice from oxidative stress aging.|
|Effects of Oral Vitamins on Skin Aging|
|Vitamin Coenzyme Q10 (CoQ10)||ESF and HaCaT cells/|
|UV-A, UV-B||Cg: ESF, HaCat (CoQ10 (0, 0.5, 1, 2 µM))/24 h; Tg: ESF, HaCat (UV-A or UV-B + CoQ10 (0, 1, 5, 10 µM))/24 h||1. CoQ10 treatment promoted ESF cell proliferation, type IV collagen and elastin gene expression.|
2. CoQ10 treatment inhibited UV-induced IL–1a production in HaCaT cells.
|CoQ10 has anti-aging effect on chronological aging and photo-aging and can be used in food and cosmetics.|
|VC, VE, and Astaxanthin (AX)||Female/(mean age 37.26 years)||-||Tg1:AX (6 mg) + VC (1000 mg) + VE (10 mg)/d; Tg2:VC (1000 mg) + VE (10 mg)/d/20 weeks||Tg 1 significantly improved skin moisture content, skin elasticity and wrinkles; Tg 2 did not improve the|
|Oral formulations containing astaxanthin and vitamin C and E have skin-improving effects.|
|Balb/C mice/6 weeks old (30 ± 2 g)||UV-B||Cg: Silymarin (100),VC|
(40 mg/kg.bw/d)/; Tg: UV-B + Silymarin (0, 100 mg/kg.bw/d), UV-B + VC: (0, 40 mg/kg.bw/d)/4 weeks.
|Oral VC enhances skin antioxidant enzyme activity, reduces skin wrinkle formation and thickness increase in mice induced by UV-B.||Salicylic acid and vitamin C can be used as food or cosmetic ingredients to resist skin photo-aging.|
|Niacinamide (NIA) ||HaCaT/|
|PM2.5||Cg: NIA (0, 12.5, 25, 50, 100, or 200 µM); Tg: NIA (0, 12.5, 25, 50, 100, or 200 µM) + PM2.5 (50 µM)/24 h||NIA treatment can inhibit the oxidation of lipid, protein, DNA and other molecules induced by PM 2.5, as well as inhibit apoptosis and ROS production.||NIA protects cells from PM 2.5-induced oxidative stress and cell damage.|
|Effects of Oral Fatty Acids on Skin Aging|
|0live oil ||Swiss mice/8–12 weeks age||Rotational stress||Stress group: stress + olive (1.5 g/kg.bw. d), Cg: olive (1.5 g/kg. bw/d)/29 d||Olive inhibited skin ROS, lipid peroxidation, protein carbonylation, phenolamine synthesis, MMP–8 expression and promotes collagen deposition in mice through NF-κB and NRF2 pathways.||Oral administration of olive oil can reduce mice skin aging induced by stress.|
|7-MEGATM500/> 50% of palmitoleic acid containing fish oil, omega–7||H–1 mice/5-week old (18–20 g) ||UV-B||Cg: 30% EtOH; Tp: 7-MEGATM500 (50, 100, 200 mg/kg.bw/d)/4 weeks||1.7-MEGATM 500 improves skin histological indicators and significantly down-regulated the expression levels of MMP–3 and c-jun genes and proteins in the skin.||7-MEGATM500 can alleviate UV-B induced skin photoaging in mice|
Fish Oil (FFO)
Tp:PM2.5 + FFO (0,
20 µg/mL)/24 h
|FFO can inhibit PM 2.5-induced intracellular ROS, Ca 2+ levels and MMPs–1,2,9 production, and block the MAPK/AP–1 pathway.||FFO can alleviate PM 2.5 induced skin aging.|
|Coconut oil||Female mice/(6 weeks old) ||DNFB||Cg: Coconut or soybean oil (4%)/2 months; Tg: Coconut or soybean oil (4%)/after 2 months + DNFB||Oral coconut oil improves BDFB-induced skin inflammation in mice. Mechanistically related to elevated mead acid in serum inhibiting directional migration of neutrophils.||Dietary coconut oil improved skin contact allergies in mice by producing midic acid.|