Objective: To explore whether norcantharidin (NCTD) could reduce camptothecin (CPT)-caused myelosuppression. Method: Balb/c mice were collected. Probit analysis was made to calculate CPT median lethal dose (LD50). With 1 mg·kg-1 dose as CPT

whole blood analyzer was used to detect white blood cell(WBC) concentration at different time points within 24 h

so as to provide a reference for the subsequent detection time point in the subsequent combined administration. Subsequently

Balb/c mice were randomly divided into six groups:control group

CPT (1 mg·kg-1) group

low-dose NCTD (10 mg·kg-1) group

high-dose NCTD (20 mg·kg-1) group

CPT (1 mg·kg-1) + low-dose NCTD (10 mg·kg-1) group and CPT (1 mg·kg-1) + high-dose NCTD (20 mg·kg-1) group. After continuous gavage for 2 weeks

eyeball sampling method and whole blood analyzer were used to measure relevant indicators. Flow cytometry was used to detect the differences of bone marrow neutrophils in each group. Histopathological sections evaluated the intestinal toxicity. Result: The CPT LD50 is 1 mg·kg-1.The number of white blood cells in mice was reduced to a minimum at 6 h after the single administration with CPT. Within 24 hours after the single treatment with CPT

the numbers of leukocytes and neutrophils in CPT and NCTD combined groups increased significantly (P<0.05)

with no significant change in the number of eosinophils and basophils. After continuous gavage for 2 weeks

compared with the single treatment with CPT

the number of white blood cells in CPT and NCTD combined groups also increased significantly (P<0.05)

and lymphocyte was significantly increased (P<0.01). No significant changes were observed in other cells. No significant difference in the mouse bone marrow neutrophil was detected by flow cytometry

hematoxylin-eosin (HE) staining showed no significant short-term or long-term pathological changes in intestine

the main target organ of toxicity of camptothecin. Conclusion: Norcantharidin can reduce the incidence of leucopenia caused by camptothecin

without increasing the intestinal toxicity. It provides a theoretical reference for the clinical application of camptothecin and its toxicity reduction.