Nicorandil Ameliorates Depression‐Like Behaviors After Traumatic Brain Injury by Suppressing Ferroptosis Through the SLC7A11/GPX4 Axis in the Hippocampus DOI Creative Commons
Ya Tu, Ming Tan, Yao Li

и другие.

Brain and Behavior, Год журнала: 2024, Номер 15(1)

Опубликована: Дек. 31, 2024

ABSTRACT Introduction Depression is a prevalent and significant psychological consequence of traumatic brain injury (TBI). Ferroptosis, an iron‐dependent form regulated cell death, exacerbates the neurological damage associated with TBI. This study investigates whether nicorandil, potassium channel opener nitrate‐like properties known for its antioxidative neuroprotective effects, can mitigate depression‐like behaviors following TBI by modulating ferroptosis. Methods A controlled cortical impact (CCI) device was used to establish model. Depression‐like in rats were assessed using sucrose preference test (SPT), tail suspension (TST), forced swimming (FST). The antioxidant system, lipid peroxidation, ferroptosis levels evaluated. SLC7A11/GPX4 axis analyzed quantitative real‐time PCR (qRT‐PCR) Western blot analysis. Results Nicorandil administration significantly ameliorated also effectively restored substantially reduced attenuated hippocampus Mechanistically, nicorandil promoted Crucially, knockdown hippocampal SLC7A11 abrogated protective effects on behaviors, Conclusion These findings indicate that ameliorates inhibiting through activation axis.

Язык: Английский

AGEING RESEARCH REVIEWS (ARR-D-24-01334R1) Metabolic dysfunction contributes to mood disorders after traumatic brain injury DOI
Lang Liu,

Peijun Jia,

Tongzhou Liu

и другие.

Ageing Research Reviews, Год журнала: 2024, Номер 104, С. 102652 - 102652

Опубликована: Дек. 31, 2024

Язык: Английский

Процитировано

0
Nicorandil Ameliorates Depression‐Like Behaviors After Traumatic Brain Injury by Suppressing Ferroptosis Through the SLC7A11/GPX4 Axis in the Hippocampus DOI Creative Commons
Ya Tu, Ming Tan, Yao Li

и другие.

Brain and Behavior, Год журнала: 2024, Номер 15(1)

Опубликована: Дек. 31, 2024

ABSTRACT Introduction Depression is a prevalent and significant psychological consequence of traumatic brain injury (TBI). Ferroptosis, an iron‐dependent form regulated cell death, exacerbates the neurological damage associated with TBI. This study investigates whether nicorandil, potassium channel opener nitrate‐like properties known for its antioxidative neuroprotective effects, can mitigate depression‐like behaviors following TBI by modulating ferroptosis. Methods A controlled cortical impact (CCI) device was used to establish model. Depression‐like in rats were assessed using sucrose preference test (SPT), tail suspension (TST), forced swimming (FST). The antioxidant system, lipid peroxidation, ferroptosis levels evaluated. SLC7A11/GPX4 axis analyzed quantitative real‐time PCR (qRT‐PCR) Western blot analysis. Results Nicorandil administration significantly ameliorated also effectively restored substantially reduced attenuated hippocampus Mechanistically, nicorandil promoted Crucially, knockdown hippocampal SLC7A11 abrogated protective effects on behaviors, Conclusion These findings indicate that ameliorates inhibiting through activation axis.

Язык: Английский

Процитировано

0