摘要
本实验采用沙土鼠脑缺血再灌注损伤模型，比较研究了补阳还五
汤原方和有效部位组方对脑缺血再灌注后海马CA_1区病理形态结构及
神经元凋亡、热休克蛋白70（HSP70）表达和反应性星形胶质细胞活
化的影响。结果显示：
1、对沙土鼠脑缺血再灌注后海马CA_1区神经细胞病理形态结构
的影响：于缺血15分钟再灌注后5天取脑组织观察，发现补阳还五
汤及其有效部位组方均可防止脑缺血再灌注后海马CA_1区神经元密度
的降低，对海马CA_1区神经细胞病理形态结构变化均有改善作用，且
二者作用程度相近，提示补阳还五汤原方和有效部位组方可防止脑缺
血后海马CA_1区神经元丢失，对脑缺血后海马CA_1区迟发性神经元损
伤有明显的抑制作用。
2、对沙土鼠脑缺血再灌注后海马CA_1区热休克蛋白70表达的影
响：脑缺血15分钟再灌注48小时后，脑组织HSP70mRNA和蛋白表
达显著增加，补阳还五汤及其有效部位组方可使脑缺血再灌注后
HSP70mRNA表达减少，补阳还五汤的抑制作用强于有效部位组方，
但两者对脑缺血再灌注后HSP70蛋白的表达增加无明显影响。提示补
阳还五汤及其有效部位组方可能通过抗脑缺血作用而抑制了缺血后
HSP70mRNA的表达，但两者并不影响HSP70蛋白的表达，这对于缺
血后神经元的修复是有益的。
3、对沙土鼠脑缺血再灌注后海马CA_1区神经元凋亡的影响：脑
缺血 15分钟再灌注 48小时后，神经元凋亡指数明显升高，补阳还五
汤原方和有效部位组方均能明显降低海马CAI 区神经元凋亡指数。
提示补阳还五汤原方和有效部位组方可能通过抑制神经元凋亡而对抗
脑缺血的迟发性神经元损伤。
4、对沙土鼠脑缺血再灌注后海马CA；区反应性星形胶质细胞活
化的影响：缺血 15分钟后各组脑组织无 GFAP表达；再灌注 24小时
后，脑组织GFAP表达达高峰（主要在海马区），补阳还五汤及其有
效部位组方可使GFAP表达减弱，二者作用相近；再灌注48小时后，
GFAP表达有所下降，而补阳还五汤和有效部位组方 Go表这较模
型组有所增强，二者作用相近。提示星形雕细胞活化主要在脑缺血
后再灌注期，在再灌注早期，补阳还五汤及其有效部位组方通过对抗
缺血性脑损伤而改善星形胶质细胞功能的紊乱，在再灌注后期，则通
过促进星形细胞的活化，有利于缺血损伤的修复。
With the living gerbils model of cerebral ischemia reperfusion injury, this
research studied the effects of Bu Yang Huan Wu Decoction(BYHWD)and
its available compostion combination on pathologic change of neuronal
structure in hippocampal gyrus CA1 area, neuronal apoptosis, the
expression of heat shock protein70 (HSP7O) and the reactive Astrocyte
activation after cerebral ischemia and reperfusion. The results showed:
1. Effect on pathologic change of neuronal structure in hippoccampal gyrus
CA1 area: After cerebral ischemia for 15 mm followed. reperfiision for Sd
in cerebral tissue, BYI-IWD and its available composition combination
have similar effects on increasing the neuronal density and improving the
pathological changes in hippocampal CA1 area. The results suggested that
BYHWD and its available composition combination could contagonize the
loss of the neuron in hippocampal gyms CA1 area and the delayed injury of
cerebral tissue after cerebral ischemia.
2. Effect on the expression of HSP7O: After cerebral ischemia for 15 mm
lg-
followed reperfusion for 48h in cerebral tissue, the level of HSP7O mRNA
and protein increased significantly. Both the BYI-IWD and its available
composition combination decreased the level of HSP7O mRNA remarkably,
the prior is superior to the latter. Neither the BYHWD nor its available
composition combination showed any effects on the expression of HSP7O
protein. The results suggested that downregulating the expression level of
HSP7O mRNA might result in the anti-ischemia effect of BYHWD and its
available composition combination, and this is benefit for the repair of the
neurons after ischemia.
3. Effect on neuronal apoptosis in hippocanipal gyrus CA1 area: After
cerebral ischemia for 15 mm followed reperfusion for 48h, the percentages
of neuronal apoptosis increased obviously, both BYHWD and its available
composition combination could antagonize neuronal apoptosis. The results
suggested that BYHWD and its available composition combination could
antagonize the delayed injury of cerebral tissue maybe by antagonizing
neuronal apoptosis.
4. Effect on. reactive astrocyte activation after cerebral ischemia: There
were no expression of GFAP in cerebral tissue at 15 mm following cerebral
ischemia, but the expression of GFAP reached peak after cerebral ischemia
for 15 mm followed by reprefusion for 24h, it occurred mainly in
hippocampal CA1 area. BYHWD could weaken the expression of GFAP,
the effect of its available composition combination was similar to it.
Expression if GFAP weakened after cerebral ischerria for 15 mm followed
by reperfusion for 48h. Compared with model group, the expression of
GFAP strengthened in BYHWD and its available composition combination
group, comparable expression of GFAP were observed in both groups. The
results suggested that Astrocyte activation occurred mainly during
reperfusion after cerebral ischemia. BYHWD and its available composition
combination could inhibit activation of astrocyte by antagonizing ischemic
injury during early stage of reperfusion, both helped improve the repair of
lesion by facilitating astrocyte activation during late stage of reperfusion~
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