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

Abstract

Introduction: This study investigated the neuroprotective effect of pravastatin administration after forebrain ischemia in rats. Materials and Methods: 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 (CA1). Expression of Bcl-2 and Bax proteins was quantified by Western blot analysis. Results: 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). Conclusions: Our findings suggest that pravastatin administration after forebrain ischemia confers neuroprotection in rats by inhibiting Bax protein expression.