10-Hydroxy-2-decenoic acid (10-HDA) is an orally active unsaturated medium-chain fatty acid with various physiological activities. 10-Hydroxy-2-decenoic acid induces ROS-mediated apoptosis in A549 cells. 10-Hydroxy-2-decenoic acid inhibits VEGF-induced angiogenesis in human venous endothelial cells. 10-Hydroxy-2-decenoic acid alleviates non-alcoholic fatty liver disease (NAFLD) by activating the AMPK-α signaling pathway. 10-Hydroxy-2-decenoic acid protects against bone loss by inhibiting NF-κB signaling downstream of FFAR4. 10-Hydroxy-2-decenoic acid is an antibiotic against many bacteria and fungi, such as Neurospora sitophila, molds and Staphylococcus aureus. 10-Hydroxy-2-decenoic acid has longevity-promoting effects in C. elegans. 10-Hydroxy-2-decenoic acid prevents osteoarthritis by targeting aspartyl β hydroxylase and inhibiting chondrocyte senescence[1][2][3][4][5][6][7][8][9][10].
Promoted the mRNA levels of CDK1, CDK2, CDK4, CDK6, cyclin A1, cyclin B1, cyclin D1, cyclin E1, proliferating cell nuclear antigen (PCNA), SRY-box transcription factor 9 (SOX9), COL2 and aggrecan (ACAN).
Inhibited the mRNA levels of COL1A1, COL1A2, COL3A1, α-SMA, FMOD, and FNDC1.
Increased the mRNA levels of CDK1, CDK2, CDK4, CDK6, cyclinA1, cyclinB1, cyclinD1, cyclinE1, and PCNA, SOX9, COL2, and ACAN, while inhibiting the expression of MMP13 and IL6 in the presence of IL-1β (10 ng/mL, 48 h).
Increased numbers of early and late apoptotic cells, loss of mitochondrial membrane potential (MMP), increased proportion of depolarized cells.
Downregulated Bcl-2, and upregulated BAX, cyto-c, caspase-3, and PARP.
Upregulated p-p38, p-JNK, and I-κB and downregulated p-ERK, p-STAT3, and NF-κB.
Inhibited cell migration, reduced the expression levels of TGF-β1, SNAI1, GSK-3β, N-cadherin and vimentin, and increased the expression level of E-cadherin.
Had no influence on the expression of Tnfrsf11a (encodes RANK), Csf1r (encodes M-CSFR), Fos, and Mitf.
Decreased osteoclastogenesis Nfatc1 and its downstream elements, without affecting the expression of Irf8 and Mafb.
IA injection, twice a week for 6 weeks; p.o., three times a week for 7 weeks
Result:
Increased the number of chondrocytes, improved knee cartilage erosion and superficial cartilage loss, inhibited cartilage degradation, increased the protein and mRNA levels of Col2 and Acan, and reduced the protein and mRNA levels of Mmp13.
Reduced pain-related behaviors associated with OA and DMM surgery.
Was not associated with any significant toxicity in oral administration group.
Inhibited the OA-induced down-regulation of ASPH expression.
Reduced p16 and p21 protein levels.
IA injection, twice a week for 8 weeks; p.o., three times a week for 8 weeks
Result:
Reduced knee joint diameter, prevented joint swelling, partially alleviated aging-related cartilage degeneration, and improved OARSI scores.
Reduced p16, p21, and Mmp13 protein levels and increased Col2 protein and ASPH expression.
Had completely prevented the development of transplantable leukemia at 1.5 mg/mL.
Animal Model:
Ascitic tumor (the 6CSHED lymphosarcoma, the TAS mammary carcinoma, and the Ehrlich carcinoma, 5-8 million tumor cells) connaught mice (Male mice, 20-22 g) model[2]
Dosage:
0.6 mg/mL, 1 mg/mL, 2.0 mg/mL
Administration:
s.c., once
Result:
Showed slight activity at a level of 0.6 mg/mL, while conferred complete protection at 1.0 mg/mL.
Animal Model:
MCD diet (5 weeks)-induced NAFLD in mice (Male C57BL/6, 6 weeks of age, weighing 20∼25 g) model[3]
Dosage:
10 mg/kg; 50 mg/kg
Administration:
p.o., once a day, 4 weeks
Result:
Inhibited weight loss, reduced fat droplets, and lowered liver TG by 32% and 60%, respectively.
Reduced hepatocyte vacuoles and ballooning, and attenuated ALT and AST levels.
Reduced TUNEL cell area, reduced BAX expression and increased BCL2 expression.
Was involved in hepatic inflammatory recruitment mainly by regulating the infiltration of macrophages and neutrophils.
Suppressed hepatic lipid accumulation by regulation lipogenesis and fatty acid β-oxidation.
Reduced feed-to-weight ratios in chickens, but had no significant effect on ADFI and ADG.
Alleviated bleeding in the duodenum, jejunum, and ileum, reduced epithelial villous damage in the jejunum and ileum, reduced serum DAO levels and CD in the jejunum, and increased VCR in the jejunum and ileum.
Reduced serum TNF-α, IL-1β, and IL-6 levels, increased serum IgA and IgG concentrations, had no significant effect on TNF-α and IL-1β levels in the 0.5% group, and increased CAT and GSH-px activities in the 0.5% group.
Downregulated the mRNA expression levels of TLR4, NF-κB, IL-1β, IL-6, TNF-α, and Caspase-3, increased Bcl2 expression, and had no significant effect on the mRNA expression levels of TLR4, IL-1β, IL-6, Bax, and Caspase-3 in the 0.5% group, increased expression levels of CAT, SOD2, ZO-1, and OCLN.
Inhibited the serum levels of C-terminal telopeptide of type I collagen (CTX-I) that contributes to osteoclast activity, without altering the serum levels of N-terminal propeptide of type I collagen (PINP).
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
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