ArticleIrish journal of medical science2026
Transient receptor potential channel 5 knockdown alleviates sevoflurane-induced neural injury by repressing oxidative stress.
Article in Irish journal of medical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveSevoflurane is a commonly applied inhalational general anesthetic, but its related neural injury is unavoidable. This study aimed to investigate the effects of transient receptor potential channel 5 (TRPC5) knockdown on sevoflurane-induced neural injury and its interaction with oxidative stress.
methodsHT-22 cells were transfected with siRNA to knockdown TRPC5 and then treated with sevoflurane. Afterward, H
resultsAfter sevoflurane treatment, apoptosis, ROS, MDA, and LDH increased, whereas cell viability and SOD activity decreased, suggesting that sevoflurane induced neural injury and oxidative stress; moreover, the expressions of TRPC5 and p-ERK increased after sevoflurane treatment. TRPC5 knockdown increased cell viability and the levels of ROS, MDA, and LDH, suggesting that it relieved sevoflurane-induced neural injury and oxidative stress. Afterward, H
conclusionTRPC5 knockdown may relieve sevoflurane-induced neural injury by suppressing oxidative stress, supporting its potential as a target for sevoflurane-induced neural injury, but further validation is still needed.
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