产品
编 号：F246343
分子式：C19H24O7
分子量：364.39
分子式：C19H24O7
分子量：364.39
产品类型
规格
价格
是否有货
1mg
询价
询价
结构图
CAS No: 19891-51-1
产品详情
生物活性：
Nagilactone B is a liver X receptor (LXR) agonist.
体内研究：
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].
体外研究：
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 (PNagilactone B 相关抗体:
Nagilactone B is a liver X receptor (LXR) agonist.
体内研究：
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].
体外研究：
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 (PNagilactone B 相关抗体:
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