Objective To explore the possible mechanism of Naomaitai Capsule（脑脉泰胶囊） for treatment of cerebral infarction. Methods Ultrapure water was used to dissolve Naomaitai Capsules; the solutions of Naomaitai Capsules at different concentrations of 50

100

250

500

1000

and 1500μg/ml were used to keep 30 wild-type AB zebrafish for 24 hours

respectively. The number of zebrafish deaths in each group was counted; the concentration-effect curve was drawn; the maximum non-lethal concentration was calculated; and the suitable concentration used for the experiment was screened. The transgenic zebrafish with fluorescent motor neurons one day after fertilization were grouped into blank control group

model group

positive control group

Naomaitai Capsule high

medium and low dose group

with 30 zebrafish in each group. Ethanol（1.5%） was used on zebrafish for 48 hours to establish the model of peripheral neuronal injury in all groups except for blank control group. After modelling

L-thyroxine sodium at concentration of 0.08μmol/L was given to positive control group

and fish-farming water was used in blank control group and model group; Naomaitai Capsules at the screened concentrations were given to zebrafish for 24 hours in Naomaitai Capsule low

medium and high dose groups

respectively. After the interventions

the image processing software was used to measure the neuronal length of peripheral motor neurons

and the nerve regeneration rate was calculated. Results There was no deaths of zebrafish when the concentration of Naomaitai Capsule solution was 50 or 100μg/ml

and zebrafish began to die when the concentration was 250μg/ml. According to the concentration-effect curve

the maximum non-lethal concentration was 170μg/ml

and therefore the concentrations used in the Naomaitai Capsule low

medium and high dose group were set as 17

57 and 170μg/ml

respectively. The length of peripheral motor neurons of zebrafish in model group was significantly shorter than that of blank control group（P<0.01）

and that in positive control group

Naomaitai Capsule low

medium and high dose groups was longer than that in the model group（P<0.01）; There was no significant difference in length of peripheral motor neurons in comparison with positive control group

Naomaitai Capsule medium and high dose groups（P>0.05）

while there was significantly decreased length of peripheral motor neurons in Naomaitai Capsule low dose group（P<0.01）. The nerve regeneration rate of positive control group

Naomaitai Capsule low

medium and high dose groups were 31%

17%

29%

and 30% respectively. Conclusion The effect of Naomaitai Capsule on promoting nerve regeneration of peripheral neurons may be related to its mechanisms of treating cerebral infarction.