Vitamin D3

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

胆钙化醇是维生素 D 的天然形式。据报道，代谢激活后，胆钙化醇可诱导细胞分化并防止 Y 细胞增殖。

Cholecalciferol is a naturally occuring form of vitamin D. Reported that upon metabolic activation, Cholecalciferol induces cell differentiation and prevents proliferation of Y cells.(In Vitro):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) occurrs 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.(In Vivo):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.

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. Cell Viability Assay Cell Line:EC cell lines from EEC, Ishikawa 3-H-12(IK), RL-95/2, and HEC-1-A cells Concentration:2-10 μM Incubation Time:24-72 hours Result:Reduced viability in response to VD3 in a dose- and time-dependent manner.Indicated that the conversion of VD3 to 25(OH)D is an essential step for the reduced cell viability effect. Cell Viability Assay Cell Line:EC cell lines from EEC, Ishikawa 3-H-12(IK) cells Concentration:10 μM Incubation Time:24-48 hours Result:Improved nuclear VDR content in IK cells.

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.

Cholecalciferol | NSC 375571

Others

VD

vitamin D receptor

Cancer

——

67-97-0

384.64

C27H44O

>98% (HPLC)

10 mM in DMSO

C[C@H](CCCC(C)C)[C@H]1CC[C@@H]\2[C@@]1(CCC/C2=C\C=C/3\C[C@H](CCC3=C)O)C

(S,Z)-3-(2-((1R,3aS,7aR,E)-7a-methyl-1-((R)-6-methylheptan-2-yl)octahydro-4H-inden-4-ylidene)ethylidene)-4-methylenecyclohexan-1-ol

(-20℃)

With Ice Pack

≥ 2 years