Objective  To investigate the effect of down-regulation the expression of transient receptor potential channel M2 (TRPM2) on ketamine induced bladder epithelial cell injury.Methods  TRPM2 small interfering RNA (siRNA-TRPM2) and its negative control (siRNA-NC) were transfected into human normal bladder epithelial cells (SV-HUC-1) cultured in vitro and treated with ketamine, which were recorded as si-TRPM2+ketamine group (si-TRPM2+ketamine group) and si-NC+ketamine group (si-NC+ketamine group), and ketamine group  and control group were set up. The expression of TRPM2 in SV-HUC-1 cells was detected by qRT-PCR, the proliferation activity was detected by CCK-8, the apoptosis rate was detected by flow cytometry, and the levels of interleukin-6 (IL-6), interleukin-1β (IL-1 β), Tumor necrosis factor-α (TNF-α), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) were detected by ELISA, and the expression level of related proteins was detected by Western blot.Results  Compared with the control group, the proliferation activity, SOD, GSH-Px activity and Bcl-2 protein expression of SV-HUC-1 cells in ketamine group were significantly decreased(all P<0.05), and the expression of TRPM2 mRNA and TNF-α, IL-1 β, IL-6 level, MDA content and apoptosis rate, Bax, Cleared Caspase-3 protein expression, NLRP3, ASC and Caspase-1 protein expression were significantly increased (all P<0.05). Compared with ketamine group, there was no significant difference in the above indexes in si-NC+ketamine group (all P>0.05). Compared with si-NC + ketamine group, the proliferation activity, SOD, GSH-Px activity and Bcl-2 protein expression of SV-HUC-1 cells in si-TRPM2+ketamine group were significantly increased(all P<0.05), and the expression of TRPM2 mRNA and TNF-α, IL-1 β, IL-6 level, MDA content and apoptosis rate, Bax, Cleared Caspase-3 protein expression, NLRP3, ASC and Caspase-1 protein expression were significantly decreased (all P<0.05).Conclusions  Down-regulation of TRPM2 expression can inhibit ketamine induced apoptosis, inflammatory response and oxidative stress of bladder epithelial cells, and then reduce the damage of bladder epithelial cells, it may play a role by inhibiting the activation of NLRP3 inflammasome.