Cholesterol is the primary sterol in mammals, accounting for approximately 20–25% of the plasma membrane structure. It plays a key role in regulating membrane fluidity, permeability, and protein function. As an endogenous agonist of estrogen-related receptor α (ERRα), cholesterol is widely involved in metabolic regulation and serves as a precursor for the synthesis of hormones and bile acids. It is commonly used in experimental models of hyperlipidemia.

METHODS: CD4+ T lymphocytes were incubated with 7-KC (17.5-70 µM) and Cholesterol-MβCD (17.5-70 µM) for 10 min, and T cell membrane order and disorder were assessed using di-4 ANEPPDHQ fluorescent dye.
RESULTS: After exposure to 7-KC, T cell membrane order was altered in a dose-dependent manner, with significant reconstitution of membrane order observed only in cells treated with 35 µM Cholesterol, while reconstitution with l7.5 µM Cholesterol induced minimal effects. [1]
METHODS: Human gastric cancer cells SNU601, SNU638 and SNU216 were treated with Cholesterol (25-100 µM) for 48 h and cell viability was measured using MTT Assay.
RESULTS: Cholesterol caused a dose-dependent decrease in cell viability in all three cell lines. [2]

METHODS: To induce hypercholesterolemia, STD:ddY mice were fed a high cholesterol diet (1% cholesterol, 0.5% cholic acid, 0.5% olive oil and 93% standard mouse chow).
RESULTS: Cholesterol can be used to construct a mouse model of hypercholesterolemia. [3]
METHODS: To induce hyperlipidemia, CD-1 mice were fed a high cholesterol diet (2% cholesterol and 0.6% sodium deoxycholate).
RESULTS: Cholesterol can be used to construct a mouse model of hyperlipidemia. [4]