Objective: To observe the effect of Shida Lazhi Wan (SDLZW) on Fas and FasL protein and mRNA expressions in the hippocampus of brain tissues of ischemia-reperfusion injury rats. Method: One week after the adaptive feeding

108 SPF SD rats were divided into 6 groups according to random number table method:control group

ischemia-reperfusion model group (hereinafter referred to as model group)

Jinnaduo group

SDLZW low dose group

SDLZW middle dose group

SDLZW high dose group. Based on different reperfusion time

these groups were further divided into 12

24

72 h subgroups

with 6 SD rats in each subgroup. Cerebral ischemia-reperfusion model was established by using the modified rat middle cerebral artery (MCA) occlusion method

and reperfusion was performed 2 h after the operation. Jinnaduo group

SDLZW low dose group

SDLZW middle dose group

SDLZW high dose group were given with the corresponding drugs by gavage for the first time 30 min before making cerebral ischemia-reperfusion model

and later administered for 2 times a day with the SDLZW (low dose 11.92 g·kg-1

SDLZW middle dose 23.83 g·kg-1

SDLZW high dose 47.66 g·kg-1) and Jinnaduo (Ginkgo biloba extract

dose 14.44 g·kg-1)

with the gavage volume of 10 mL·kg-1

control group and model group were given by gavage with distilled water according to the same method. Brains were collected from each of the three subgroups after 12

24

72 h. Western blot and Real-time PCR method were adopted to observe the effects of SDLZW on Fas and FasL protein and mRNA expressions in rat brains after cerebral ischemia-reperfusion. Result: Compared with the control group

the expression of Fas and FasL in the model group and all of treatment groups were increased at each time point (P < 0.01)

compared with the model group

Fas and FasL expressions at each time point in observed group were reduced (P < 0.01)

compared with the Jinnaduo group

the SDLZW middle dose group showed no significant difference in Fas and FasL expressions

and the SDLZW high dose group showed decreases in Fas and FasL expressions (P < 0.05

P < 0.01)

especially obviously reduced in the 72 h group (P < 0.01). Conclusion: SDLZW has a good protection on cerebral ischemia-reperfusion injury

and its mechanism may be related to inhibition of apoptosis of hippocampus.