Effects of ALDH2 gene expression on the oxidative stress mediated NF B/mTOR pathway in ketamine induced cystitis.

Aldehyde dehydrogenase 2 (ALDH2) serves an important role in regulating the development of organ injury. The present study aimed to investigate the effects of ALDH2 gene expression on the oxidative stress mediated NF B/mTOR pathway in ketamine (Ket) induced cystitis (KIC). Primarily, human bladder epithelial cells of the SV HUC 1 cell line were divided into groups for incubation with different concentrations of Ket: 0, 0.5, 1, 1.5 and 2 mM. ALDH2 protein expression was then detected after 48 h of incubation with Ket. Subsequently, SV HUC 1 cells were separated into a number of treatment groups, including: i) Control groups, comprising negative control (NC), NC + mTOR activator MHY1485 (Act), NC + Ket and NC + Ket + Act groups; ii) ALDH2 knockdown groups that were transfected with siRNA sequences targeting ALDH2 (si ALDH2), including si ALDH2, si ALDH2 + Act, si ALDH2 + Ket and si ALDH2 + Ket + Act groups; and iii) ALDH2 overexpression (OE ALDH2) transfection groups, comprising OE ALDH2, OE ALDH2 + Act, OE ALDH2 + Ket and OE ALDH2 + Ket + Act groups. The levels of apoptosis, oxidative stress and inflammatory protein expression were assessed in each group. The results of the present study demonstrated that ALDH2 protein expression was significantly higher after treatment with Ket compared with the control group. Further analysis revealed that the si ALDH2 + Ket group demonstrated the highest levels of apoptosis, oxidative stress and inflammatory protein expression amongst all treatment groups. The levels of these indicators notably improved in the OE ALDH2 + Ket group compared with the NC + Ket group. Therefore, the results of the present study revealed that ALDH2 overexpression reduced Ket induced apoptosis, oxidative stress and in ammatory protein expression. Furthermore, co treatment with Act was shown to mitigate these factors. Additionally, ALDH2 may have modulated the inflammatory response by promoting mTOR activation and inhibiting NF B phosphorylation. The present study concluded that ALDH2 may represent a novel target for KIC treatment.