The rh-CSF1 improves mitochondrial function and cell apoptosis in neurons under oxygen-glucose deprivation
Journal Title: Chinese Journal of Nervous and Mental Diseases - Year 2024, Vol 50, Issue 8
Abstract
[Objective] To investigate the mechanism by which Colony Stimulating Factor-1 (CSF1) inhibits apoptosis in neurons subjected to oxygen-glucose deprivation (OGD). [Methods] Primary rat cortical neurons were divided into the OGD damaged neuron model group (OGD group), the rh-CSF1 intervention group (rh-CSF1 group),and control group. The sample size for each group was 3. After intervention with recombinant human CSF1 (rh-CSF1), neuronal apoptosis rate and intracellular ATP content, reactive oxygen species levels, mitochondrial membrane potential, and mitochondrial DNA copy number were measured. The content of malondialdehyde within mitochondria and the activity of superoxide dismutase were also assessed. [Results] Intervention with rh-CSF1 increased mitochondrial membrane potential (0.55±0.03 vs. 0.43±0.06, P<0.01), mitochondrial DNA copy number(0.88±0.05 vs. 0.72±0.06,P<0.05), ATP content [(15.70±0.99) mmol/mg vs. (11.70±1.00) mmol/mg, P<0.01)], and superoxide dismutase [(18.47±1.38) U/mg vs. (14.78±1.81) U/mg, P<0.05)] activity in neurons injured by OGD. It also reduced levels of rectivereactive oxygen species(3.64±0.21 vs. 4.45±0.33, P<0.05) and malondialdehyde within mitochondria [(2.13±0.19) mmol/mg vs. (2.78±0.20) mmol/mg, P<0.05)], and inhibited neuronal apoptosis(10.12±0.78 vs. 17.04±1.23, P<0.01) [Conclusion] rh-CSF1 may alleviate the damage in neurons induced by OGD by improving mitochondrial function, reducing oxidative stress, and inhibiting cell apoptosis.
Authors and Affiliations
Rui LIU, Kuan FAN, Pengju ZHANG, Yu TIAN, Wei SI, Shirong LI, Lu WANG, Ran GU, Xiao HU
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