10-Hydroxy-2-decenoic acid
10-Hydroxy-2-decenoic acid is a potential HDACI which inhibits the proliferation of FLS cells by PI3K-AKT pathway; it exerts an inhibitory effect on VEGF-induced angiogenesis, partly by inhibiting both cell proliferation and migration. 10-Hydroxy-2-decenoic acid activates AMPK, and insulin independently enhances glucose uptake following translocation of Glut4 to PM; it also can prevent UVA-induced damage and inhibit MMP-1 and MMP-3 expressions.
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J Eur Acad Dermatol Venereol. 2013 Oct;27(10):1269-77.
10-Hydroxy-2-decenoic acid prevents ultraviolet A-induced damage and matrix metalloproteinases expression in human dermal fibroblasts.[Pubmed:
23030720]
10-Hydroxy-2-decenoic acid (10-HDA) is a major fatty acid component of royal jelly, which has been reported to have a variety of beneficial pharmacological characteristics. However, the effects of 10-HDA on skin photoageing and its potential mechanism of action are unclear.
We investigated the protective effects of 10-HDA on ultraviolet (UV) A-induced damage in human dermal fibroblasts (HDFs). We then explored the inhibitory effects of 10-HDA on UVA-induced matrix metalloproteinases (MMPs) expression and elucidated the signalling pathways controlling MMPs inhibition.
METHODS AND RESULTS:
Primary human dermal fibroblasts were exposed to UVA. Cell proliferation, cellular senescent state and collagen content were analysed using CCK-8, senescence-associated β-galactosidase staining and Sircol collagen assay, respectively. Fluorometric assays were performed to detect the formation of reactive oxygen species (ROS) in the cells. The mRNA levels of MMP-1, MMP-3 and type I (α1) collagen were determined by quantitative real-time PCR. Western blot was applied to detect the expression of MMP-1, MMP-3, JNK and p38 MAPK.
HDFs treated with 10-HDA were significantly protected from UVA-induced cytotoxicity, ROS, cellular senescence and stimulated collagen production. Moreover, 10-HDA suppressed the UVA-induced expression of MMP-1 and MMP-3 at both the transcriptional and protein levels. Treatment with 10-HDA also reduced the UVA-induced activation of the JNK and p38 MAPK pathways.
CONCLUSIONS:
The data obtained in this study provide evidence that 10-HDA could prevent UVA-induced damage and inhibit MMP-1 and MMP-3 expressions. Therefore, 10-HDA may be a potential agent for the prevention and treatment of skin photoageing.
Evid Based Complement Alternat Med. 2009 Dec;6(4):489-94.
10-Hydroxy-2-decenoic acid, a major fatty acid from royal jelly, inhibits VEGF-induced angiogenesis in human umbilical vein endothelial cells.[Pubmed:
18955252]
10-Hydroxy-2-decenoic acid (10HDA), a major fatty acid component of RJ, is known to have various pharmacological effects; its antitumor activity being especially noteworthy. However, the mechanism underlying this effect is unclear.
METHODS AND RESULTS:
We examined the effect of 10-Hydroxy-2-decenoic acid on VEGF-induced proliferation, migration and tube formation in human umbilical vein endothelial cells (HUVECs). Our findings showed that, 10-Hydroxy-2-decenoic acid at 20 microM or more significantly inhibited such proliferation, migration and tube formation. Similarly, 10 microM GM6001, a matrix metalloprotease inhibitor, prevented VEGF-induced migration and tube formation.
CONCLUSIONS:
These findings indicate that 10-Hydroxy-2-decenoic acid exerts an inhibitory effect on VEGF-induced angiogenesis, partly by inhibiting both cell proliferation and migration.
Mol Nutr Food Res. 2013 Oct;57(10):1794-802.
10-Hydroxy-2-decenoic acid, a unique medium-chain fatty acid, activates 5'-AMP-activated protein kinase in L6 myotubes and mice.[Pubmed:
23754629]
10-Hydroxy-2-decenoic acid (10H2DA) is one of the unique medium-chain fatty acids (MCFAs) specifically found in royal jelly. We hypothesize that 10-Hydroxy-2-decenoic acid has multiple biological functions and may aid in 5'-AMP-activated protein kinase (AMPK) activation and affect the glucose transport system in skeletal muscle.
METHODS AND RESULTS:
We examined whether various MCFAs present in royal jelly activated AMPKα. Treatment of L6 myotubes with various MCFAs showed that 10-Hydroxy-2-decenoic acid administration resulted in a significant increase in phosphorylated AMPKα. 10-Hydroxy-2-decenoic acid activates AMPK independently of insulin and significantly increased glucose uptake into L6 myotubes following translocation of glucose transporter 4 (Glut4) to the plasma membrane (PM).Oral administration of 10-Hydroxy-2-decenoic acid significantly stimulated phosphorylation of AMPK and Glut4 translocation to the PM in mouse skeletal muscle.
CONCLUSIONS:
These findings indicate that (i) 10-Hydroxy-2-decenoic acid activates AMPK, and insulin independently enhances glucose uptake following translocation of Glut4 to PM, (ii) activation of AMPKα by 10-Hydroxy-2-decenoic acid is mediated via extracellular Ca2⁺-dependent Ca2⁺/calmodulin-dependent kinase kinase β, without alteration in the AMP:ATP ratio, and liver kinase B1 was not involved in the activation.
Int Immunopharmacol. 2015 Jun 4.
10-Hydroxy-2-decenoic acid inhibiting the proliferation of fibroblast-like synoviocytes by PI3K-AKT pathway.[Pubmed:
26050632]
To reveal the mechanism of 10-Hydroxy-2-decenoic acid inhibiting the proliferation of fibroblast-like synoviocytes (FLSs) of RA patients.
METHODS AND RESULTS:
Cell proliferation, HDAC activity and histone acetylation level of FLS cells treated with 10-Hydroxy-2-decenoic acid were detected by MTT assay, Colorimetric HDAC Activity Assay and Western-blot. Different genes in FLS cells from RA patients were primary cultured and treated with 10-Hydroxy-2-decenoic acid. They were then screened by Human Transcriptome 1.0 ST microarrays and verified by real-time PCR. The results showed dose-dependent and time-dependent decreases in cell viability and HDAC activity in FLSs treated with 10-Hydroxy-2-decenoic acid, and time-dependent induction in the acetylation of H3 and H4 at the same time.
CONCLUSIONS:
These results imply that 10-Hydroxy-2-decenoic acid is a potential HDACI which inhibits the proliferation of FLS cells by PI3K-AKT pathway.
