Atorvastatin hemicalcium trihydrate

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CAS NO:	344920-08-7
规格:	≥98%

理化性质和储存条件

Molecular Formula: C33H35FN2O5.1/2Ca.3H2O;

Molecular Weight: 632.73

In Vitro	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[4].
In Vivo	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[5]. Animal Model: Forty 8-week-old ApoE–/– mice induced with angiotensin II (Ang II)[5] 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.

In Vitro

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[4].

In Vivo

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[5]. Animal Model: Forty 8-week-old ApoE–/– mice induced with angiotensin II (Ang II)[5] 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.