Tsugaric acid A
Tsugaric acid A can significantly inhibit superoxide anion formation in fMLP/CB-stimulated rat neutrophils, it is also able to protect human keratinocytes against damage induced by ultraviolet B (UV B) light, indicates that tsugaric acid A can protect keratinocytes from photodamage.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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Separations2023, 10(4), 231.
Journal of Ginseng Research2021, 3 June.
Appl Biochem Biotechnol.2022, s12010-022-04166-2.
J Clin Med.2019, 8(10):E1664
Biomed Pharmacother.2024, 174:116598.
Applied Biological Chemistry2022, 65(12)
Chemistr of plant2016, 2016021195
J Chromatogr B Analyt Technol Biomed Life Sci.2019, 1124:323-330
Metab Eng.2022, 75:143-152.
Food Funct.2023, 14(9):4354-4367.
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Phytochemistry. 2008 Jan;69(1):234-9.
Antiinflammatory triterpenoids and steroids from Ganoderma lucidum and G. tsugae.[Pubmed:
17655889 ]
The antiinflammatory properties of triterpenoids and steroids from both Ganoderma lucidum and Ganoderma tsugae were studied.
METHODS AND RESULTS:
Twelve compounds, including ergosta-7,22-dien-3beta-ol (1), ergosta-7,22-dien-3beta-yl palmitate (2), ergosta-7,22-dien-3-one (3), ergosta-7,22-dien-2beta,3alpha,9alpha-triol (4), 5alpha,8alpha-epidioxyergosta-6,22-dien-3beta-ol (5), ganoderal A (6), ganoderal B (7), ganoderic aldehyde A (8), Tsugaric acid A (9), 3-oxo-5alpha-lanosta-8,24-dien-21-oic acid (10), 3alpha-acetoxy-5alpha-lanosta-8,24-dien-21-oic acid ester beta-d-glucoside (11), and tsugaric acid B (12), were assessed in vitro by determining their inhibitory effects on the chemical mediators released from mast cells, neutrophils, and macrophages.
CONCLUSIONS:
Compound 10 showed a significant inhibitory effect on the release of beta-glucuronidase from rat neutrophils stimulated with formyl-Met-Leu-Phe (fMLP)/cytochalasin B (CB) whereas compound 9 significantly inhibited superoxide anion formation in fMLP/CB-stimulated rat neutrophils. Compound 10 also exhibited a potent inhibitory effect on NO production in lipopolysaccharide (LPS)/interferon-gamma (IFN-gamma)-stimulated N9 microglial cells. Moreover, compound 9 was also able to protect human keratinocytes against damage induced by ultraviolet B (UV B) light, which indicated 9 could protect keratinocytes from photodamage.
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