Objective To study the effect and mechanism of Suifukang （brain-marrow rehabilitation formula） on cerebral ischemic injury in rats.Methods Totally 144 rats were randomized into the normal group

model group

positive control group and Suifukang large-dose

middle-dose and small-dose groups

with 24 in each.The right middle cerebral artery occlusion （MCAO） and reperfusion rat models were established in each group except the normal group.The rats in Suifukang large-dose

middle-dose and small-dose groups were gavaged with 5 g

2.5 g and 1.25 g crude drug of Suifukang per 100 g once daily.The positive control group was given intraperitoneal injection of 30 mg/kg methylprednisolone every other day.The model group was gavaged with the same amount of normal saline and the normal group received no treatment.The brain tissues were removed in each group on the 15th and 30th day of administration.The expression of chondroitin sulfate proteoglycans （CSPGs）and growth associated protein 43 （GAP-43）CSPGs and GAP-43 in ischemic brain region of rats in each group was detected by immunohistochemistry method.Results In-group comparisons showed that there was no significant difference in the expression of GSPGs and GAP-43 on the 8th

15th and 30th day of administration （P>0.05）.Comparing with the normal group

the expression of GSPGs was significantly increased in the model group （P<0.01）.Comparing with the model group

the expression of GSPGs in the administration groups were significantly decreased （P<0.05 or P<0.01）.There was no significant difference in the expression of GAP-43 between the normal group and model group （P>0.05）.Comparing with the model group

the expression of GAP-43 in the Suifukang large-dose

middle-dose and small-dose groups was significantly increased （P<0.05 or P<0.01）.Conclusion Suifukang can inhibit the expression of GSPGs and promote the expression of GAP-43 in ischemic brain region of rats

which may be related to improving the microenvironment of axonal regeneration in ischemic brain region and promoting axonal regeneration after cerebral ischemia.