Post-ischemic administration of pravastatin reduces neuronal injury by inhibiting Bax protein expression after transient forebrain ischemia in rats

NEUROSCIENCE LETTERS

卷:594

Article

Jung, Yoo Sun¹  Oh, Ah-Young²  Park, Hee-Pyoung¹  Hwang, Jung-Won²  Lim, Young-Jin¹  Jeon, Young-Tae² 

[1] Seoul Natl Univ Hosp, Dept Anesthesiol & Pain Med, Seoul 110744, South Korea

[2] Seoul Natl Univ, Bundang Hosp, Dept Anesthesiol & Pain Med, Songnam, South Korea

关键词: Apoptosis;    Bax protein;    Brain ischemia;    Pravastatin;   

DOI  :  10.1016/j.neulet.2015.03.038

来源: Elsevier

【 摘 要 】

This study investigated the neuroprotective effect of pravastatin administration after forebrain ischemia in rats. Forebrain ischemia was induced by bilateral common carotid artery occlusion and systemic hypotension for 8 min. Pravastatin at 1 mg/kg (pravastatin group, n = 10), or an identical volume of normal saline (control group, n = 10), was injected 10 min, and 1-4 days after reperfusion. Arterial blood gas was analyzed 10 min before ischemia onset and 10 min after ischemia completion. Viable and apoptotic neuronal cells were evaluated 7 days after ischemia by hematoxylin and eosin (H&E) staining and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuracil triphosphate biotin in situ nick-end labeling (TUNEL) staining of the hippocampal Cornu Ammonis area (CM). Expression of Bcl-2 and Bax proteins was quantified by Western blot analysis. The proportion of viable neuronal cells after ischemia was greater in the pravastatin vs. control group (p < 0.01), with greater expression of apoptotic cells in the control vs. pravastatin group (p < 0.05). Bax protein expression was significantly decreased in the pravastatin group (p < 0.05), whereas, Bcl-2 expression was increased, but not significantly (p > 0.05). Our findings suggest that pravastatin administration after forebrain ischemia confers neuroprotection in rats by inhibiting Bax protein expression. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

【 授权许可】

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