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Updated: Jun 13, 2026
Isolating Nasal Olfactory Stem Cells from Rodents or Humans
Published on: August 22, 2011
Olfactory Mucosa MSCs-Derived Exosomal RPL6 Attenuates Seizure-Induced Neuronal Damage via FGF2-Mediated Oxidative
Zijie Wang1, Xiqi Hu2, Yuchang Liang1
1Department of Neurosurgery, Haikou Affiliated Hospital of Central South University Xiangya School of Medicine, Haikou, 570208, China.
Abstract:
Evidence suggests that olfactory mucosa-derived mesenchymal stem cells (OM-MSCs) can benefit epilepsy treatment in both clinical patients and mouse models, although their precise mechanism remains unclear. Given the advantages of exosomes in precise cellular regulation, ease of storage, and long-term stability, this study investigated the role of OM-MSCs-derived exosomes (OM-MSCs-exos) in status epilepticus (SE) models. Here, SE mouse models were induced by intraperitoneal injection of pilocarpine. OM-MSCs, differentially treated OM-MSCs-exos, and recombinant FGF2 protein were injected into SE model mice to investigate the effects of OM-MSCs-exos on SE models and their potential mechanisms. Functionally, treatment with OM-MSCs and OM-MSCs-exos significantly improved cognitive function, as evidenced by increased target quadrant duration, decreased escape latency, increased average speed, and more platform crossings in behavioral tests. Furthermore, this treatment further alleviated hippocampal tissue damage by reversing pilocarpine-induced oxidative damage, neuronal injury, and excessive mitophagy. Consistent outcomes were confirmed in vitro. Mechanistically, RPL6 was screened and confirmed as a key protein in OM-MSCs-exos, which interacts with FGF2 to promote FGF2 expression, thereby alleviating oxidative stress and mitochondrial dysfunction induced by H2O2. In conclusion, the RPL6 protein derived from OM-MSCs-exos improves neuronal damage post-SE by activating FGF2 to suppress oxidative stress and mitophagy, laying a theoretical foundation for the development of exosome-related drugs for treating epilepsy clinically.
Insights
Olfactory mucosa-derived mesenchymal stem cell exosomes (OM-MSCs-exos) show promise for epilepsy treatment. These exosomes, containing RPL6 protein, activate FGF2 to reduce neuronal damage and improve cognitive function in status epilepticus models.
Area of Science:
- Neuroscience
- Cell Biology
- Regenerative Medicine
Background:
- Olfactory mucosa-derived mesenchymal stem cells (OM-MSCs) show therapeutic potential for epilepsy.
- The precise mechanisms of OM-MSCs in epilepsy treatment are not fully understood.
- Exosomes offer advantages for cellular regulation, storage, and stability in therapeutic applications.
Purpose of the Study:
- To investigate the role and mechanism of OM-MSCs-derived exosomes (OM-MSCs-exos) in status epilepticus (SE) mouse models.
- To explore the therapeutic effects of OM-MSCs-exos on cognitive function and hippocampal damage in SE.
- To elucidate the molecular mechanism involving RPL6 and FGF2 in OM-MSCs-exos-mediated neuroprotection.
Main Methods:
- Status epilepticus (SE) mouse models were induced using pilocarpine.
- OM-MSCs and OM-MSCs-exos were administered to SE model mice.
- Behavioral tests assessed cognitive function, including target quadrant duration and escape latency.
- Histological and biochemical analyses evaluated hippocampal tissue damage, oxidative stress, and mitophagy.
- In vitro experiments confirmed findings, and RPL6 protein's interaction with FGF2 was investigated.
Main Results:
- OM-MSCs and OM-MSCs-exos significantly improved cognitive function in SE mice.
- Treatment reversed pilocarpine-induced hippocampal damage, including oxidative stress, neuronal injury, and excessive mitophagy.
- RPL6 protein within OM-MSCs-exos was identified as crucial for interacting with FGF2.
- This interaction promoted FGF2 expression, alleviating oxidative stress and mitochondrial dysfunction.
Conclusions:
- OM-MSCs-exos demonstrate significant therapeutic potential for epilepsy by improving cognitive function and reducing neuronal damage.
- The RPL6 protein in OM-MSCs-exos plays a key role in neuroprotection by activating FGF2, suppressing oxidative stress, and mitigating mitophagy.
- These findings provide a theoretical basis for developing exosome-based therapies for clinical epilepsy treatment.
