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Updated: Mar 14, 2026

A Model for Encephalomyosynangiosis Treatment after Middle Cerebral Artery Occlusion-Induced Stroke in Mice
Published on: June 22, 2022
Neuroprotective effect of mesenchymal stem cell through complement component 3 downregulation after transient focal
Hye-Seon Jung1, Si-Yeon Jeong1, Jiwon Yang1
1College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
Abstract:
Bone marrow-derived mesenchymal stem cells (MSCs) are used in stroke treatment despite the poor understanding of its mode of action. The immune suppressive and anti-inflammatory properties of MSCs possibly play important roles in regulating neuroinflammation after stroke. We investigated whether MSCs reduce the inflammatory complement component 3 (C3) levels, thus, providing neuroprotection during stroke. Mice were subjected to transient focal cerebral ischemia (tFCI), after which MSCs were intravenously injected. The infarct volume of the brain was reduced in MSC-injected tFCI mice, and C3 expression was significantly reduced in both the brain and the blood. Additionally, the profiles of other inflammatory mediators demonstrated neuroprotective changes in the MSCs-treated group. In order to analyze the effect of MSCs on neurons during cerebral ischemia, primary cortical neurons were co-cultured with MSCs under oxygen-glucose deprivation (OGD). Primary neurons co-cultured with MSCs exhibited reduced levels of C3 expression and increased protection against OGD, indicating that treatment with MSCs reduces excessive C3 expression and rescues ischemia-induced neuronal damage. Our finding suggests that reduction of C3 expression by MSCs can help to ameliorate ischemic brain damage, offering a new neuroprotective strategy in stroke therapy.
Insights
Mesenchymal stem cells (MSCs) reduce brain damage after stroke by lowering complement component 3 (C3) levels. This finding offers a novel neuroprotective strategy for stroke therapy.
Area of Science:
- Neuroscience
- Immunology
- Regenerative Medicine
Background:
- Mesenchymal stem cells (MSCs) show promise in stroke treatment, but their mechanism of action is unclear.
- MSCs possess immune-suppressive and anti-inflammatory properties that may modulate neuroinflammation post-stroke.
Purpose of the Study:
- To investigate if MSCs reduce complement component 3 (C3) levels, thereby providing neuroprotection in stroke.
- To elucidate the role of C3 reduction in MSC-mediated neuroprotection during ischemic stroke.
Main Methods:
- Mice underwent transient focal cerebral ischemia (tFCI) followed by MSC intravenous injection.
- Primary cortical neurons were co-cultured with MSCs under oxygen-glucose deprivation (OGD) to assess direct neuronal effects.
Main Results:
- MSC treatment significantly reduced infarct volume in tFCI mice.
- C3 expression was markedly decreased in both the brain and blood of MSC-treated mice.
- MSC co-culture protected primary neurons against OGD-induced damage, with reduced C3 expression.
Conclusions:
- MSC administration ameliorates ischemic brain damage by reducing C3 expression.
- Reduction of C3 by MSCs represents a potential neuroprotective strategy for stroke therapy.

