Journal
METABOLIC BRAIN DISEASE
Volume 37, Issue 4, Pages 1221-1230Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11011-022-00948-z
Keywords
Captopril; Inflammation; Hydrogen Peroxide; Oxidative Stress; Apoptosis; C6 cells
Categories
Ask authors/readers for more resources
Captopril has a protective effect on glial cell damage after H2O2-induced oxidative stress by inhibiting oxidative stress, reducing inflammation, and suppressing apoptosis.
Recent studies have shown that angiotensin-converting enzyme (ACE) inhibitors have reduced oxidative damage in the central nervous system (CNS). Accumulating evidence have also demonstrated that captopril, an ACE inhibitor, has protective effects on the CNS. However, its effects on hydrogen peroxide (H2O2)-induced oxidative damage in glial cells and interaction with the inflammatory system are still uncertain. Therefore, this study was aimed to investigate the protective effect of captopril on glial cell damage after H2O2-induced oxidative stress involved in the inflammatory and apoptotic pathways. The control group was without any treatment, and the H2O2 group was treated with 0.5 mM H2O2 for 24 h. The captopril group was treated with various concentrations of captopril for 24 h. The captopril +H2O2 group was pre-treated with captopril for 1 h and then exposed to 0.5 mM H2O2 for 24 h. In the captopril +H2O2 group, captopril at all concentrations significantly increased the cell viability in C6 cells. It also significantly increased the TAS and decreased the TOS levels which are an indicator of oxidative stress. Moreover, captopril significantly reduced the inflammation markers including NF-kB, IL-1 beta, COX-1, and COX-2 levels. Flow cytometry results also exhibited that captopril pretreatment significantly decreased the apoptosis rate. Besides, captopril significantly reduced apoptotic Bax and raised anti-apoptotic Bcl-2 protein levels. In conclusion, captopril has protective effects on C6 cells after H2O2-induced oxidative damage by inhibiting oxidative stress, inflammation, and apoptosis. However, further studies need to be conducted to evaluate the potential of captopril as a neuroprotective agent.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available