Rosuvastatin (ZD4522) is an inhibitor of HMG-CoA reductase (HMGCR) (IC50=11 nM), selective and competitive. Rosuvastatin has hypolipidemic and antiatherosclerotic effects.

HMG-CoA:11 nM

METHODS: Microglia cultures subDIV were treated with Rosuvastatin (1 µM) and LPS (20 ng/mL) for 24 h, and cell counts were measured by Bürker chamber.
RESULTS: After the 24 h treatment period, Rosuvastatin significantly inhibited cell proliferation in unchallenged and LPS-challenged cultures by 47.8% and 68.9%, respectively. [1]
METHODS: Nthy-ori 3-1 and B-CPAP cells were treated with Rosuvastatin (12.5-200 µM) for 48-72 h. Apoptosis was detected by TUNEL assay.
RESULTS: The number of apoptotic cells increased in both Nthy ori 3-1 and B-CPAP cells after Rosuvastatin treatment. 12.5 µM concentration of Rosuvastatin treatment resulted in an increase in Apoptotic Index of Nthy ori 3-1 and B-CPAP cells after 48 h. The results were summarized as follows. [2]

METHODS: To investigate the anti-atherosclerotic effects, Rosuvastatin (5 mg/kg) and candesartan (2.5 mg/kg) were administered by gavage to streptozotocin-induced diabetic Apoe-/- mice once daily for 20 weeks.
RESULTS: In the absence of lipid-lowering effects, Rosuvastatin attenuated plaque area in diabetic mice.The anti-atherosclerotic effect of Rosuvastatin was comparable to that of candesartan. Dual therapy had similar beneficial effects, although it was not superior to monotherapy. [3]