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编 号：F757635
分子式：C33H35FN2O5.1/2Ca.3H2O
分子量：632.73
分子式：C33H35FN2O5.1/2Ca.3H2O
分子量：632.73
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CAS No: 344920-08-7
产品详情
生物活性：
Atorvastatin hemicalcium trihydrate is an orally active HMG-CoA reductase inhibitor, has the ability to effectively decrease blood lipids. Atorvastatin hemicalcium trihydrate inhibits human SV-SMC proliferation and invasion with IC50s of 0.39 μM and 2.39 μM, respectively.
体内研究：
Atorvastatin (20-30 mg/kg; oral gavage; once a day; for 28 days; ApoE?/? mice) hemicalcium trihydrate treatment significantly reduces endoplasmic reticulum (ER) stress signaling proteins, the number of apoptotic cells, and the activation of Caspase12 and Bax in the Ang II-induced ApoE-/- mice. Proinflammatory cytokines such as IL-6, IL-8, IL-1β are all remarkably inhibited after Atorvastatin treatment.Animal Model:Forty 8-week-old ApoE?/? mice induced with angiotensin II (Ang II)
Dosage:20 mg/kg, 30 mg/kg
Administration:Oral gavage; once a day; for 28 days
Result:Significantly reduced ER stress signaling proteins, the number of apoptotic cells, and the activation of Caspase12 and Bax in the Ang II-induced ApoE?/? mice. Proinflammatory cytokines such as IL-6, IL-8, IL-1β were all remarkably inhibited.
体外研究：
Atorvastatin hemicalcium trihydrate treatment decreases apoptosis of myocardial cells by down-regulating GRP78, caspase-12 and CHOP expression in myocardial cells after myocardial infarction, and the endoplasmic reticulum (ER) stress is activated in response to heart failure and angiotensin II (Ang II) stimulation.
Atorvastatin hemicalcium trihydrate is an orally active HMG-CoA reductase inhibitor, has the ability to effectively decrease blood lipids. Atorvastatin hemicalcium trihydrate inhibits human SV-SMC proliferation and invasion with IC50s of 0.39 μM and 2.39 μM, respectively.
体内研究：
Atorvastatin (20-30 mg/kg; oral gavage; once a day; for 28 days; ApoE?/? mice) hemicalcium trihydrate treatment significantly reduces endoplasmic reticulum (ER) stress signaling proteins, the number of apoptotic cells, and the activation of Caspase12 and Bax in the Ang II-induced ApoE-/- mice. Proinflammatory cytokines such as IL-6, IL-8, IL-1β are all remarkably inhibited after Atorvastatin treatment.Animal Model:Forty 8-week-old ApoE?/? mice induced with angiotensin II (Ang II)
Dosage:20 mg/kg, 30 mg/kg
Administration:Oral gavage; once a day; for 28 days
Result:Significantly reduced ER stress signaling proteins, the number of apoptotic cells, and the activation of Caspase12 and Bax in the Ang II-induced ApoE?/? mice. Proinflammatory cytokines such as IL-6, IL-8, IL-1β were all remarkably inhibited.
体外研究：
Atorvastatin hemicalcium trihydrate treatment decreases apoptosis of myocardial cells by down-regulating GRP78, caspase-12 and CHOP expression in myocardial cells after myocardial infarction, and the endoplasmic reticulum (ER) stress is activated in response to heart failure and angiotensin II (Ang II) stimulation.
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