目的　研究二苯乙烯苷（tetrahydroxy stilbene glucoside, TSG）对脑缺血/再灌注（ischemia/reperfusion, I/R）沙鼠脑海马损伤的保护作用及可能机制。  方法    采用结扎沙鼠双侧颈动脉缺血30 min，再灌注5 d复制沙鼠全脑I/R模型。沙鼠随机分为6组，假手术组、模型对照组、TSG大、中、小剂量（6、3、1.5 mg/kg）组和阳性对照药依达拉奉注射组（3 mg/kg）。5 d后通过Morris水迷宫测定沙鼠学习记忆功能；Nissl染色观察沙鼠大脑海马CA1区神经元结构和数量的变化；TUNEL染色法观察沙鼠大脑海马CA1区神经元凋亡的变化；Western blot法检测脑组织active-caspase-3的表达。  结果　与假手术组相比，I/R组沙鼠学习记忆能力明显降低，海马CA1区神经元大量丢失，结构紊乱。同时，I/R组沙鼠CA1区神经元凋亡数量明显增加，脑组织中caspase-3显著活化。TSG中、高（3、6 mg/kg）剂量组和依达拉奉阳性对照组均可以显著改善I/R引发的沙鼠学习记忆能力的降低，抑制海马CA1区神经元的丢失，改善神经元结构；抑制CA1区神经元的凋亡以及caspase-3的活化。而TSG低剂量组对上述变化均没有明显的治疗作用。   结论　TSG对于I/R引发的脑损伤，尤其是海马区神经元迟发性凋亡具有明显的治疗作用，这种作用与其抑制caspase-3的活化相关。

Objective　To investigate the protective effects of tetrahydroxy stilbene glucoside (TSG) on ischemia-reperfusion (I/R)-induced hippocampal injury and the underlying mechanisms in gerbils.　Methods Gerbil global I/R model was established by clamping bilateral carotid arteries for 30 min followed by reperfusion for 5 days. Animals were divided into 6 groups randomly: Sham, I/R, I/R+TSG high, middle, low (6, 3, 1.5 mg/kg) and edaravone injection group (3 mg/kg). The functions of learning and memory were detected by Morris water maze 5 days after reperfusion. The number and structure of neurons and neuronal apoptosis in hippocampal CA1 region were evaluated by Nissl and TUNEL staining, respectively. In addition, the expression of active-caspase-3 in cerebral tissues was measured by Western blot.　Results　Compared to Sham group, learning and memory capacity of gerbils in I/R group declined significantly, the number of functional neurons in hippocampal CA1 region decreased dramatically. Furthermore, the apoptotic neurons indicated by TUNEL staining as well as caspase-3 activation increased remarkably. TSG administration at middle and high dose (3, 6 mg/kg) and edaravone injection significantly reversed aforementioned changes induced by I/R. In contrast, TSG administration at low dose (1.5 mg/kg) had no effect.　Conclusion　TSG had therapeutic effects on I/R induced cerebral injury, especially on delayed neuron apoptosis in hippocampal CA1 region, which may be related to its suppression effect on caspase-3 activation.