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Curcumin inhibits mitochondrial injury and apoptosis from the early stage in EAE mice
Jinzhou Feng1, Tao Tao2, Weiping Yan1
1Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Abstract:
The exact pathophysiological change concerning mitochondrial injury and oligodendrocyte apoptosis in MS and EAE model is still unknown. Whether curcumin is able to inhibit mitochondrial injury and suppress the apoptosis in the early stages of MS/EAE is still unclear. We first explored mitochondrial injury and apoptosis at different time points p.i. in C57 BL/6 EAE mice. We then explored the effects of curcumin on mitochondria and apoptosis. Results showed that mitochondrial injury can be observed 3 days p.i. Apoptosis in the spinal cord occurred 3 days p.i. and the apoptotic cells were shown to be oligodendrocytes and neuronal cells. Curcumin significantly reduced the number of apoptotic cells and inhibited the upregulation of cyt-c, caspase-9, and caspase-3 at 7 days p.i. in the EAE mice. These observations demonstrate that mitochondrial injury and oligodendrocyte/neuronal apoptosis occur in the early stages of EAE. Curcumin can inhibit apoptosis in EAE mice which maybe act through protection of mitochondrial injury and inhibition of the intrinsic apoptotic pathway.
Insights
Mitochondrial injury and oligodendrocyte apoptosis occur early in experimental autoimmune encephalomyelitis (EAE). Curcumin treatment protects against this damage, suggesting a therapeutic role in early-stage multiple sclerosis (MS) models.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- The precise mechanisms of mitochondrial damage and oligodendrocyte apoptosis in multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), remain unclear.
- The potential of curcumin to mitigate mitochondrial injury and apoptosis during the early phases of MS/EAE requires further investigation.
Purpose of the Study:
- To investigate mitochondrial injury and apoptosis dynamics at various time points post-infection (p.i.) in C57 BL/6 EAE mice.
- To evaluate the therapeutic effects of curcumin on mitochondrial function and apoptosis in the EAE model.
Main Methods:
- Induction of EAE in C57 BL/6 mice.
- Assessment of mitochondrial injury and apoptosis markers at different time points p.i.
- Administration of curcumin and analysis of its impact on apoptotic cells and key proteins in the intrinsic apoptotic pathway (cytochrome c, caspase-9, caspase-3).
Main Results:
- Mitochondrial injury and spinal cord apoptosis, affecting oligodendrocytes and neuronal cells, were evident as early as 3 days p.i. in EAE mice.
- Curcumin treatment significantly decreased the number of apoptotic cells by 7 days p.i.
- Curcumin inhibited the upregulation of cytochrome c, caspase-9, and caspase-3 in EAE mice.
Conclusions:
- Mitochondrial injury and oligodendrocyte/neuronal apoptosis are early pathological events in EAE.
- Curcumin demonstrates a protective effect against apoptosis in EAE, potentially by safeguarding mitochondrial integrity and inhibiting the intrinsic apoptotic pathway.
