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Metformin Alleviates Delayed Hydrocephalus after Intraventricular Hemorrhage by Inhibiting Inflammation and Fibrosis
Yi Cao1,2, Chang Liu1, Gaowei Li1
1Department of Neurosurgery and State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan, 610041, People's Republic of China.
Translational Stroke Research
|July 19, 2022
Summary
Metformin reduces brain damage and swelling after intraventricular hemorrhage (IVH). It also prevents delayed hydrocephalus by decreasing inflammation and fibrosis via the AMPK/SIRT1/NF-κB pathway.
Area of Science:
- Neuroscience
- Pharmacology
- Pathology
Background:
- Intraventricular hemorrhage (IVH) leads to significant morbidity and mortality.
- Posthemorrhagic hydrocephalus (PHH) is a common complication of IVH, driven by inflammation and fibrosis.
- The precise mechanisms underlying PHH development remain unclear.
Purpose of the Study:
- To investigate the neuroprotective effects of metformin in a mouse model of IVH.
- To elucidate the molecular mechanisms by which metformin influences IVH and subsequent PHH.
Main Methods:
- Adult male mice received varying doses of metformin following induced IVH.
- Neuroprotection, inflammation, fibrosis, neurocognitive function, and hydrocephalus were assessed.
- Molecular mechanisms involving AMPK, SIRT1, and NF-κB pathways were analyzed.
Main Results:
- Metformin demonstrated dose-dependent neuroprotection, reducing apoptosis, neuronal damage, and brain edema in the acute phase.
- High-dose metformin decreased inflammatory cell infiltration and pro-inflammatory factors.
- Metformin improved neurocognitive function, reduced hydrocephalus, inhibited fibrosis and glial scarring in the chronic phase.
Conclusions:
- Metformin attenuates neuroinflammation and fibrosis post-IVH by modulating the AMPK/SIRT1/NF-κB pathway.
- Metformin shows potential as a therapeutic agent to prevent delayed hydrocephalus following IVH.
