|A unique collection of 36 Anti-photoaging natural compounds|
|Catalog No:||C1|| Anti-photoaging Compound Library
|Size:||1mg/well * 36 Compounds|
2mg/well * 36 Compounds
1. Ganoderol A, isolated from Ganadermalucidum, has significant anti-inflammatory activity and protection against UVA damage, thus suggesting that the compound is a candidate for the development of a suitable product to protect skin from UV-induced photoaging.
2. Ganoderol A, the 70% MeOH extract of Ganoderma lucidum , has an inhibitory effect on angiotensin converting enzyme activity.
3. Ganoderol A inhibits cholesterol biosynthesis via conversion of acetate or mevalonate as a precursor of cholesterol.
1. Scoparone shows antifungal activity.
2. Scoparone has immunosuppression and vasorelaxation effects.
3. Scoparone protects against carbon tetrachloride-induced liver injury.
4. Scoparone has antianginal action.
5. Scoparone has antioxidant capabilities, it is a very efficient inhibitor of ultraviolet radiation -induced lipid peroxidation and damage.
6. Scoparone is a phytoalexin associated with resistance of citrus to Phytophthora citrophthora.
1. Carnosic acid can protect neurons both in vitro and in vivo through activation of the Keap1/Nrf2 pathway via S-alkylation of targeted cysteines on Keap1.
2. Carnosic acid has antioxidant properties, it is a powerful inhibitor of lipid peroxidation in microsomal and liposomal systems.
3. Carnosic acid, vitamin C, and vitamin E show photoprotective potential.
4. Carnosic acid is a class of lipid absorption inhibitor from sage.
5.. Carnosic acid is capable of antiproliferative action in leukemic cells and can cooperate with other natural anticancer compounds in growth-inhibitory and differentiating effects.
6. Carnosic acid has a protective effect on cisplatin induced experimental nephrotoxicity and is attributed to its potent antioxidant and antiapoptotic properties.
7. Carnosic acid has antimicrobial activity against oral pathogens.
8. Carnosic acid can inhibit adipogenesis in vitro, and it is a therapeutic agent for obesity-related non-alcoholic fatty liver disease.
1. Ginsenoside-Ro has anti-inflammatory activity, it (10, 50, and 200 mg/kg, p.o.) inhibits an increase in vascular permeability in mice induced by acetic acid and reduces an acute paw edema in rats induced by compound 48/80 or carrageenin.
2. Ginsenoside Ro inhibits the increase of connective tissue in the liver of CCl4-induced chronic hepatitic rats, it shows a stronger inhibitory effect on the GalN-induced acute hepatitic model than those of the aglycone of ginsenoside Ro, oleanolic acid, or glycyrrhizic acid and its aglycone, glycyrrhetinic acid.
3. Ginsenoside Ro enhances in vivo hair re-growth based on their inhibitory activity against 5αR in the androgenetic alopecia model.
4. Ginsenoside-Ro shows immunomodulatory effects by regulating the production and expression of Th1/Th2 cytokines in murine splenocytes.
5. Ginsenoside Ro exerts anti-apoptosis and anti-inflammation in IL-1β-induced rat chondrocytes, which might be related to NF-κB signal pathway, it might be a potential novel drug for the treatment of osteoarthritis.
6. Ginsenoside Ro has antioxidative properties against UV-B-induced oxidative stress in human dermal fibroblasts, it possesses a potential skin anti-photoaging property against UV-B radiation in fibroblasts.
1. Salidroside has anti-tumor action.
2. Salidroside has antidepressant and anxiolytic actions.
3. Salidroside has Anticancer action through inhibiting JAK2/STAT3 signaling pathway.
4. Salidroside alleviates the pulmonary symptoms of paraquat-induced acute lung injury, at least partially, by repressing inflammatory cell infiltration and the expression of TGF-β1 resulting in delayed lung fibrosis.
5. Salidroside has potent antioxidant action against oxidative stress-induced cell apoptosis, may be a potential therapeutic agent for treating or preventing neurodegenerative diseases implicated with oxidative stress.
6. Salidroside has shown cardioprotective effects in vivo, it has protective effect against hypoxia-induced cardiomyocytes necrosis and apoptosis by increasing HIF-1α expression and subsequently up-regulating VEGF levels.