产品
编 号：F424408
分子式：C27H44O
分子量：384.64
分子式：C27H44O
分子量：384.64
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价格
是否有货
100mg
440
In-stock
1g
960
In-stock
5g
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CAS No: 67-97-0
产品详情
生物活性：
Vitamin D3 (Cholecalciferol; Colecalciferol) is a naturally occuring form of vitamin D. Vitamin D3 induces cell differentiation and prevents proliferation of cancer cells.
体内研究：
Cholecalciferol (oral gavage; 5 mg/kg; 7 days) potentiates the CCl4 toxicity only in the liver, as indicated by plasma levels of ALT and AST, biochemical markers of hepatic damage. It significantly increases renal calcium levels in mice, but renal calcium content does not differ significantly between mice.Animal Model:Male ddY mice on CCl4?toxicity
Dosage:5 mg/kg
Administration:Oral gavage; 5 mg/kg; 7 days
Result:Potentiated CCl4-induced hepatotoxicity and enhanced mouse mortality, without increasing renal toxicity and generation of liver fibrosis.
体外研究：
Vitamin D3 is an inactive vitamin D molecule in vivo. Vitamin D3 undergoes two hydroxylation processes to activate it. Vitamin D3 is first hydroxylated in the liver to form the circulating prohormone 25-hydroxy vitamin D3 [25(OH)D3] by the enzyme 25-hydroxylase (CYP27A1) and probably also by other enzymes (e.g., CYP2R1).The second hydroxylation occurs in the kidneys via the enzyme 1-alpha-hydroxylase, yielding 1,25- dihydroxycholecalciferol (calcitriol), which is the biologically active form of vitamin D.Vitamin D3 (2-10 μM; 24-48 hours) exhibits anti-proliferative effects in a dose- and time-dependent manner. Maximal reduction of viability post-treatment of 62% (IK), 52% (RL-95-2), and 55% (Hec-1A) occurs by 72 h of treatment with 10 μM Vitamin D3. but 24-hour exposure lacks significant reduction in viable cells.Cholecalciferol (10 μM; 24-48 hours) shows marked increases in nuclear VDR staining and produces local VDR activation in IK cells.
Vitamin D3 (Cholecalciferol; Colecalciferol) is a naturally occuring form of vitamin D. Vitamin D3 induces cell differentiation and prevents proliferation of cancer cells.
体内研究：
Cholecalciferol (oral gavage; 5 mg/kg; 7 days) potentiates the CCl4 toxicity only in the liver, as indicated by plasma levels of ALT and AST, biochemical markers of hepatic damage. It significantly increases renal calcium levels in mice, but renal calcium content does not differ significantly between mice.Animal Model:Male ddY mice on CCl4?toxicity
Dosage:5 mg/kg
Administration:Oral gavage; 5 mg/kg; 7 days
Result:Potentiated CCl4-induced hepatotoxicity and enhanced mouse mortality, without increasing renal toxicity and generation of liver fibrosis.
体外研究：
Vitamin D3 is an inactive vitamin D molecule in vivo. Vitamin D3 undergoes two hydroxylation processes to activate it. Vitamin D3 is first hydroxylated in the liver to form the circulating prohormone 25-hydroxy vitamin D3 [25(OH)D3] by the enzyme 25-hydroxylase (CYP27A1) and probably also by other enzymes (e.g., CYP2R1).The second hydroxylation occurs in the kidneys via the enzyme 1-alpha-hydroxylase, yielding 1,25- dihydroxycholecalciferol (calcitriol), which is the biologically active form of vitamin D.Vitamin D3 (2-10 μM; 24-48 hours) exhibits anti-proliferative effects in a dose- and time-dependent manner. Maximal reduction of viability post-treatment of 62% (IK), 52% (RL-95-2), and 55% (Hec-1A) occurs by 72 h of treatment with 10 μM Vitamin D3. but 24-hour exposure lacks significant reduction in viable cells.Cholecalciferol (10 μM; 24-48 hours) shows marked increases in nuclear VDR staining and produces local VDR activation in IK cells.
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