S-Space College of Medicine/School of Medicine (의과대학/대학원) Dept. of Medicine (의학과) Theses (Ph.D. / Sc.D._의학과)
Post-ischemic administration of pravastatin reduces neuronal injury by inhibiting Bax protein expression after transient forebrain ischemia in rats
백서의 일과성 전뇌허혈 모델에서 허혈 후 프라바스타틴 투여로 인한 Bax 단백질 발현 억제에 의한 신경 세포 손상 감소
- 의과대학 의학과
- Issue Date
- 서울대학교 대학원
- 학위논문 (박사)-- 서울대학교 대학원 : 의학과, 2016. 8. 전영태.
- 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.