| Bioactivity | Cholestyramine (Colestyramine) is a bile acid binding resin and can inhibit intestinal bile acid absorption which results in the increasing bile acid synthesis from cholesterol. | ||||||||||||
| Invitro | Cholestyramine (0.1-50 μg/mL) produced the most dramatic results after a 24-hour exposure; an efflux rate of 65% compared with control cells. Cholestyramine is an anion-exchange resin and is insoluble in water. alcohol, chloro-form, and ether. For the assay, cholestyramine is initially wetted with a small amount of DMSO further diluting with media. A blank sample prepared with dimethylsulfoxide DMSO without cholestyramine displayed no differences from the control samples[3]. | ||||||||||||
| In Vivo | Cholestyramine (Colestyramine) is a bile acid binding resin and can inhibit intestinal bile acid absorption which results in the increasing bile acid synthesis from cholesterol[1]. Results reveal that GSPE treatment alone, and co-administration with Cholestyramine (Colestyramine), regulate BA, cholesterol and TG metabolism differently compare to Cholestyramine administration alone. Notably, GSPE decreases intestinal apical sodium-dependent bile acid transporter (Asbt) gene expression, while Cholestyramine significantly induces expression. Administration with GSPE or Cholestyramine robustly induces hepatic BA biosynthetic gene expression, especially cholesterol 7α-hydroxylase (Cyp7a1), compare to control, while co-administration further enhances expression. Treatment with Cholestyramine induces both intestinal and hepatic cholesterologenic gene expression, while co-administration with GSPE attenuates the Cholestyramine-inducing increase in the liver but not in the intestine. Cholestyramine also induces hepatic lipogenic gene expression, which is attenuated by co-administration with GSPE[2]. | ||||||||||||
| Name | Cholestyramine | ||||||||||||
| CAS | 11041-12-6 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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| Reference | [1]. Maugeais C, et al. rHDL administration increases reverse cholesterol transport in mice, but is not additive on top of ezetimibe or cholestyramine treatment. Atherosclerosis. 2013 Jul;229(1):94-101. [2]. Rebecca M. Heidker, et al. Grape Seed Procyanidins and Cholestyramine Differentially Alter Bile Acid and Cholesterol Homeostatic Gene Expression in Mouse Intestine and Liver. PLoS One. 2016; 11(4): e0154305. [3]. J M Pruckler, et al. Use of a human microvascular endothelial cell line as a model system to evaluate cholesterol uptake. Pathobiology. 1993;61(5-6):283-7. |