Effect of ALDH2 gene expression on ketamine-induced cystitis based on oxidative stress-mediated NF-κB pathway
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Abstract
Objective: To investigate the effect of acetaldehyde dehydrogenase 2 (ALDH2) gene expression on oxidative stress-mediated NF-κB pathway in ketamine-induced cystitis (KIC). Methods: SV-HUC-1 cells were divided into different concentrations of ketamine groups (0 mmol/L, 0.5 mmol/L, 1 mmol/L, 2 mmol/L), and the expression of ALDH2 protein was detected after induction for 48 hours. The SV-HUC-1 cell constructs were divided into control group (si-NC group, OE-NC group), ALDH2 silencing group (Si-ALDH2 group), and ALDH2 overexpression group (OE-ALDH2 group). The cells were induced with complete medium and ketamine (1 mmol/ L) for 48 hours respectively, and the levels of inflammatory factors and inflammatory proteins were detected in each group. Results: Western blotting showed that the relative expression of ALDH2 protein after treatment with ketamine (0.5 mmol/L, 1 mmol/L) was significantly higher than that in the 0 mmol/L group (P<0.05). In the further comparison of ketamine-induced group (1 mmol/L), it was found that the expression of inflammatory cytokines interleukin-1β (IL-1β) and interleukin-6 (IL-6) in the si-ALDH2 group was significantly higher than that in the si-ALDH2 group (P<0.05); the expression of IL-1β and IL-6 in the OE-ALDH2 group was significantly lower than that in the OE-NC group (P<0.05). The expression levels of inflammatory protein nuclear factor-κB (NF- κB), cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in the si-ALDH2 group were higher than those in the si-NC group (P<0.05). The expression levels of inflammatory proteins NF-κB, COX-2 and iNOS in the OE-ALDH2 group were lower than those in the OE-NC group (P<0.05). In the control group (0 mmol/L), there were no significant differences in the levels of inflammatory factors and inflammatory proteins between si-ALDH2 group and si-NC group, as well as OE-ALDH2 group and OE-NC group (P>0.05). Conclusion: ALDH2 gene may play a certain anti-inflammatory protective role in the occurrence of KIC.
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