Objective To explore the effect of Wuzi Yanzong Pills（WYP

五子衍宗丸） on the myelin sheath of demyelination model mice as well as the underlying molecular mechanism. Methods Twenty-four C57 BL/6 male mice were randomly divided into a blank group

model group and WYP group

with eight mice in each group. Mice in the model group and WYP group were fed with 0.2% dicyclohexanone oxalyl dihydrazone for six weeks

while those in the blank group were fed normally. On the second weekend of feeding

16 g/（kg·d） WYP solution was administered by gavage in the WYP group

while 0.5 ml normal saline was given by gavage in the blank group and model group

for four weeks. Lucas fast blue staining was used to observe the demyelination of the brain tissue and to calculate the average optical density value in the corpus callosum region; Western blot method was used to detect myelin basic protein（MBP）

glial fibrillary acidic protein（GFAP）

glial cell line-derived neurotrophic factor（GDNF）

brain-derived neurotrophic factor（BDNF）

neuron-glial antigen 2（NG2）

ciliary neurotrophic factor（CNTF） protein expression levels. Results The blue staining color of the corpus callosum region of the model group was lighter than that of the normal group

and the tissue structure was more loose and sparse

showing a shrinking state; while there were darker blue staining color

denser tissue structure and fuller thickness of the corpus callosum in the WYP group. Compared to the blank group

the model group significantly decreased the average optical density value in the corpus callosum region

as well as reduced the expression levels of MBP

BDNF

GDNF

CNTF

and NG2 proteins in the brain tissue（P<0.01）. Compared to the model group

the WYP group significantly increased the average optical density value in the corpus callosum region

as well as increased the MBP

GFAP

BDNF

GDNF

CNTF

and NG2 protein expression levels（P<0.05 or P<0.01）. Conclusion WYP can protect the myelin in the demyelination model mice

which may be related to the promotion of the proliferation and differentiation of oligodendrocytes by accelerating astrocytes to secrete neurotrophic factors.