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19891-51-1

中文名稱(chēng) 竹柏內(nèi)酯 B
英文名稱(chēng) (1S)-1,2,3,3a,5aβ,6,10b,10cβ-Octahydro-1,2α,6α-trihydroxy-3aβ,10bα-dimethyl-7-isopropyl-4H,9H-furo[2',3',4':4,5]naphtho[2,1-c]pyran-4,9-dione
CAS 19891-51-1
分子式 C19H24O7
分子量 364.39
MOL 文件 19891-51-1.mol
19891-51-1 結(jié)構(gòu)式 19891-51-1 結(jié)構(gòu)式

基本信息

中文別名
竹柏內(nèi)酯 B
英文別名
Nagilactone B
(1S)-1,2,3,3a,5aβ,6,10b,10cβ-Octahydro-1,2α,6α-trihydroxy-3aβ,10bα-dimethyl-7-isopropyl-4H,9H-furo[2',3',4':4,5]naphtho[2,1-c]pyran-4,9-dione
4H,9H-Furo[2',3',4':4,5]naphtho[2,1-c]pyran-4,9-dione, 1,2,3,3a,5a,6,10b,10c-octahydro-1,2,6-trihydroxy-3a,10b-dimethyl-7-(1-methylethyl)-, (1S,2R,3aS,5aS,6R,10bS,10cR)-
所屬類(lèi)別
天然產(chǎn)物:萜類(lèi)

物理化學(xué)性質(zhì)

熔點(diǎn)258-261℃
沸點(diǎn)644.6±55.0 °C(Predicted)
密度1.42±0.1 g/cm3(Predicted)
儲(chǔ)存條件-20°C儲(chǔ)存
溶解度溶于二甲基亞砜
酸度系數(shù)(pKa)12.23±0.70(Predicted)
形態(tài)Solid
顏色White to off-white
竹柏內(nèi)酯 B價(jià)格(試劑級(jí))
報(bào)價(jià)日期產(chǎn)品編號(hào)產(chǎn)品名稱(chēng)CAS號(hào)包裝價(jià)格
2024/11/08HY-N3216竹柏內(nèi)酯 B
Nagilactone B
19891-51-11mg5400元

常見(jiàn)問(wèn)題列表

生物活性
Nagilactone B,是從 Podocarpus nagi 根皮中提取的,是一種肝 X 受體 (LXR) 激動(dòng)劑。
靶點(diǎn)

LXR

體外研究

RAW264.7 cells are co-incubated with oxLDL (20?μg/mL) and Nagilactone B (0.02, 0.1, and 0.5?μM) for 24?h. Oil Red O (ORO) staining reveals significant lipid accumulation and foam cell formation in RAW264.7 cells following oxLDL treatment. Nagilactone B (NLB) significantly ameliorates intracellular lipid accumulation. ORO positive areas are reduced by 30.05±7.49 (P<0.01), 47.25±5.39 (P<0.001), and 48.65±7.44% (P<0.001) in Nagilactone B (0.02, 0.1, and 0.5 μM)-treated groups, respectively. The effects of Nagilactone B are evaluated ton cholesterol efflux. Nagilactone B (0.02, 0.1, and 0.5?μM) markedly promotes cholesterol efflux to extracellular apolipoprotein A-I (apoA-I) and high density lipoprotein (HDL) with maximal 5.72- (P<0.05) and 2.34-fold (P<0.01), respectively.

體內(nèi)研究

Nagilactone B (NLB) suppresses atherosclerosis in apoE -/- mice by inducing ATP-binding cassette transporter A1 (ABCA1) and G1 (ABCG1) mediated cholesterol efflux in macrophages. Male apoE-deficient mice on C57BL/6J background receive Nagilactone B (10 and 30?mg/kg) for 12 weeks. Compared with the model group, Nagilactone B treatment (10 and 30?mg/kg) significantly reduces en face lesions of total aorta areas. Six-week-old male apoE -/- mice on an HFD are randomized to receive Atorvastatin (10 mg/kg/day), Nagilactone B (10 and 30?mg/kg/day), or CMC-Na for 12 weeks. Mice on chow diet are administered CMC-Na as the normal diet control group. En face aortic lesion areas are evaluated with Sudan IV staining and lesion areas in the aortic sinus monitored via ORO staining. Atherosclerosis developes slowly in the normal diet group, whereas lesions in the HFD model group are significantly increased in en face aortas. Nagilactone B treatment (10 and 30 mg/kg/day) significantly reduces en face aortic lesions, compared with the HFD group by 54.96±10.06% (P<0.01), 71.50±15.37% (P<0.001) in both NLB (L) and NLB (H) groups. In particular, Nagilactone B markedly attenuates atherosclerotic plaque lesion areas in the aortic arch aorta, thoracic aorta, and abdominal aorta [P<0.01 in NLB (H) group].

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