AI Article Synopsis
- The retina's aging leads to oxidative stress from reactive oxygen species (ROS), which can harm retinal pigment epithelium (RPE) cells and contribute to conditions like age-related macular degeneration (AMD).
- Researchers investigated how substance P (SP) helps recover RPE cells injured by oxidative stress.
- Findings showed that SP boosts cell survival, proliferation, and reduces apoptosis by activating the Akt/GSK-3β signaling pathway, presenting SP as a potential treatment for oxidative stress-related eye diseases.
Article Abstract
Purpose: Senescence of the retina causes an accumulation of reactive oxygen species (ROS). Oxidative stress associated with ROS can damage RPE cells, leading to neovascularization and severe ocular disorders, including age-related macular degeneration (AMD). Thus, the early treatment of the damage caused by oxidative stress is critical for preventing the development of ocular diseases such as AMD. In this study, we examined the role of substance P (SP) in the recovery of RPE cells damaged by oxidative stress.
Methods: To induce oxidative stress, RPE cells were treated with H2O2 at various doses. Recovery from oxidative stress was studied following treatment with SP by analyzing cell viability, cell proliferation, cell apoptosis, and Akt/glycogen synthase kinase (GSK)-3β activation in RPE cells in vitro.
Results: H2O2 treatment reduced cellular viability in a dose-dependent manner. SP inhibited the reduction of cell viability due to H2O2 and caused increased cell proliferation and decreased cell apoptosis. Cell survival under oxidative stress requires the activation of Akt signaling that enables cells to resist oxidative stress-induced damage. SP treatment activated Akt/GSK-3β signaling in RPE cells, which were damaged due to oxidative stress, and the inhibition of Akt signaling in SP-treated RPE cells prevented SP-induced recovery. Pretreatment with the neurokinin 1 receptor (NK1R) antagonist reduced the recovery effect of SP on damaged RPE cells.
Conclusions: SP can protect RPE cells from oxidant-induced cell death by activating Akt/GSK-3β signaling via NK1R. This study suggests the possibility of SP as a treatment for oxidative stress-related diseases.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4982481 | PMC |
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