Objective: To explore the pathology and relevant mechanisms of cantharidin (CTD) in inducing acute cystitis in mice through intragastric administration under the condition of 1/2 median lethal dose (LD50). Method: Balb/c mice were divided into control group and 1-14 day cantharidin administration groups. The administration groups were intragastrically given cantharidin at 1/2 LD50 for different days

while the control group was given the same amount of 0.5% carboxymethyl cellulose sodium (CMCNa). 3 h later after the last administration

bladders of 1-14 day cantharidin administration groups were collected for pathological detection by hematoxylin-eosin (HE) staining

and the bladder protein expressions of the 1 day cantharidin administration group was detected by Western blot (WB). Result: Compared with the control group

1

3

8-12 day cantharidin administration groups showed mucosal epithelial exfoliation

mucosal epithelial hyperplasia

edema of the lamina propria with bleeding

and mucosal inflammatory cell infiltration in bladder. Western blot results showed that on the 1st day after cantharidin administration

levels of phosphorylatedprotein kinase B (p-Akt)

protein kinase B (Akt)

p-nuclear transcription factor-kappa B (NF-κB)p65

p-NF-κB inhibitor α(p-IκBα)and IκBα increased significantly (P<0.01). Conclusion: Acute cystitis in mice can be induced by the 3 h administration with cantharidin. After 1-7 day administration with the drug

the bladder injury caused by CTD could be repaired

but the bladder showed an irreversible and gradually aggravated inflammatory lesion on the 8-14 day. The activation of Aktsignaling pathway and NF-κB signal pathway is related to CTD-induced acute cystitis.