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生物来源
cod liver oil
质量水平
检测方案
≥95%
形式
waxy solid
官能团
carboxylic acid
脂质类型
omega FAs
运输
ambient
储存温度
−20°C
SMILES字符串
CC/C=C\C/C=C\C/C=C\C/C=C\C/C=C\C/C=C\CCC(O[Na])=O
InChI
1S/C22H32O2.Na/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-20-21-22(23)24;/h3-4,6-7,9-10,12-13,15-16,18-19H,2,5,8,11,14,17,20-21H2,1H3,(H,23,24);/q;+1/p-1/b4-3-,7-6-,10-9-,13-12-,16-15-,19-18-;
InChI key
SNNDEWVSGZRIFE-FPYKSTABSA-M
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
个人防护装备
Eyeshields, Gloves, type N95 (US)
Wei Cai et al.
Translational stroke research, 9(6), 669-680 (2018-09-12)
Systemic docosahexaenoic acid (DHA) has been explored as a clinically feasible protectant in stroke models. However, the mechanism for DHA-afforded neuroprotection remains elusive. Transient middle cerebral artery occlusion (tMCAO) was induced for 1 h. DHA (i.p., 10 mg/kg) was administered immediately after
Christel Björk et al.
Nutrition & metabolism, 13, 4-4 (2016-01-21)
Previous studies suggest that intake of specific bioactive compounds may have beneficial clinical effects on adipose tissue partly due to their anti-inflammatory and insulin-sensitizing properties. With the overall aim to contribute to better understanding of the mechanisms of selected bioactive
Yong-Ping Zhang et al.
Prostaglandins, leukotrienes, and essential fatty acids, 136, 85-94 (2017-08-06)
Omega-3 polyunsaturated fatty acids (n-3 PUFAs), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), have been reported to prevent neurodegenerative diseases such as Alzheimer's disease (AD) in both experimental and clinical/epidemiological studies. However, whether DHA and EPA from natural products exert
Shurong Huang et al.
Journal of lipid research, 53(9), 2002-2013 (2012-07-07)
Toll-like receptor 4 (TLR4) and TLR2 were shown to be activated by saturated fatty acids (SFAs) but inhibited by docosahexaenoic acid (DHA). However, one report suggested that SFA-induced TLR activation in cell culture systems is due to contaminants in BSA
Ryan G Snodgrass et al.
Journal of immunology (Baltimore, Md. : 1950), 191(8), 4337-4347 (2013-09-18)
Many studies have shown that TLR4- and TLR2-deficient mice are protected from high-fat diet-induced inflammation and insulin resistance, suggesting that saturated fatty acids derived from the high-fat diet activate TLR-mediated proinflammatory signaling pathways and induce insulin resistance. However, evidence that
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