Objective To investigate the characteristics and possible material basis of drug-induced syndromes in mice induced by prednisolone. Methods A total of 80 Institute of Cancer Research（ICR） mice were randomly divided into a normal control group

a very low dose group

a low dose group

a middle dose group and a high dose group

with 16 mice in each group. The very low dose group

low dose group

middle dose group and high dose group were given 0. 25

0. 5

2. 5

12. 5 mg/（kg·d） of prednisolone acetate tablets

while the normal control group was given equlivalent distilled water 8 mice of each group were intervened for 7 days

and another 8 mice were intervened for 14 days. The body weight of the mice was dynamically observed every other day. After 7 and 14 days of intervention

the characterization information of body mass

grip strength

axillary temperature

open field activity

and infrared temperature of different parts of the body were compared respectively. The spleen

thymus and testis were weighed and the organ index was calculated. The serum corticosterone and adrenocorticotropic hormone（ACTH） levels were measured; The adrenal function-related gene expression and adrenal low-density lipoprotein receptor（LDLR）

scavenger receptor class B type I（SRBI）

steroidogenic acute regulatory protein（St AR） protein expression were detected.Results After 7 and 14 days of intervention

the middle dose and high dose groups

the body weight

spleen mass

thymus mass

spleen index and thymus index of the mice decreased than those of the normal control group and the very low dose group at same time

while serum corticosterone and ACTH content

the expression of adrenal gland function-related genes and adrenal LDLR

SRBI and StAR proteins were decreased to different degrees（P < 0. 05）

but there was no statistical difference in the grip force

axillary temperature

open field activity and infrared temperature of different parts of the mice（P > 0. 05）. Conclusion The drug-induced deficiency syndrome caused by prednisolone is yin deficiency syndrome. The material basis of the drug-deficiency syndrome may be inhibited expression of adrenal corticosteroid synthase and inhibited function of the cortical axis of the pituitary adrenal gland.