Open Access

Aldh2 gene reduces oxidative stress in the bladder by regulating the NF‑κB pathway in a mouse model of ketamine‑induced cystitis

  • Authors:
    • Xiao Jian Xi
    • Shao Hua Chen
    • Hua Mi
  • View Affiliations

  • Published online on: September 18, 2020     https://doi.org/10.3892/etm.2020.9239
  • Article Number: 111
  • Copyright: © Xi et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Aldehyde dehydrogenase 2 (aldh2) serves an important role in the development of organ injury. Therefore, the present study investigated the effects of aldh2 on the oxidative stress response in a mouse model of ketamine‑induced cystitis (KIC). A total of 60 8‑week‑old male Institute of Cancer Research wild‑type (WT) mice and 45 aldh2 knock‑out (KO) mice were randomized to receive low‑dose ketamine (30 mg/kg), high‑dose ketamine (60 mg/kg) or normal saline (controls). At 4, 8 and 12 weeks post‑injection, bladder tissues were harvested and used to investigate the protective mechanisms of aldh2 on bladder function. The results demonstrated that aldh2 KO mice exhibited significant weight loss following chronic ketamine injection compared with that in WT mice. Furthermore, ketamine treatment increased the urination rate (P<0.05), pathological score (P<0.05), levels of the oxidative stress product malondialdehyde (P<0.05) in addition to reducing the expression of the anti‑oxidative stress enzyme superoxide dismutase (P<0.05) and glutathione‑SH (P<0.05). Oxidative stress in aldh2 KO mice was also found to significantly enhance the expression of proteins associated with the NF‑κB signaling pathway, which promoted the expression of inducible nitric oxide synthase (P<0.05) and cyclooxygenase‑2 (P<0.05) further. Finally, aldh2 KO mice demonstrated higher severity of fibrosis in the submucosal and muscular layers of the bladder. In conclusion, the present study suggests that aldh2 serves a protective role in preventing inflammation and fibrosis in KIC.
View Figures
View References

Related Articles

Journal Cover

November-2020
Volume 20 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Xi X, Chen S and Mi H: <em>Aldh2</em> gene reduces oxidative stress in the bladder by regulating the NF‑&kappa;B pathway in a mouse model of ketamine‑induced cystitis. Exp Ther Med 20: 111, 2020.
APA
Xi, X., Chen, S., & Mi, H. (2020). <em>Aldh2</em> gene reduces oxidative stress in the bladder by regulating the NF‑&kappa;B pathway in a mouse model of ketamine‑induced cystitis. Experimental and Therapeutic Medicine, 20, 111. https://doi.org/10.3892/etm.2020.9239
MLA
Xi, X., Chen, S., Mi, H."<em>Aldh2</em> gene reduces oxidative stress in the bladder by regulating the NF‑&kappa;B pathway in a mouse model of ketamine‑induced cystitis". Experimental and Therapeutic Medicine 20.5 (2020): 111.
Chicago
Xi, X., Chen, S., Mi, H."<em>Aldh2</em> gene reduces oxidative stress in the bladder by regulating the NF‑&kappa;B pathway in a mouse model of ketamine‑induced cystitis". Experimental and Therapeutic Medicine 20, no. 5 (2020): 111. https://doi.org/10.3892/etm.2020.9239