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Corin inhibits microglial inflammatory activation by suppressing mitochondrial dysfunction in intracerebral
Rui Yin1, Caixia Qiu2, Qikai Shen3
1Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou 215006, Korea; Department of Neurosurgery, Huzhou Central Hospital, Huzhou 313000, China.
Abstract:
Microglial activation driving neuroinflammation is a key factor in secondary brain injury after intracerebral hemorrhage (ICH); however, the regulatory mechanisms remain unknown. This study investigates how corin influences microglial inflammatory activation and its underlying mechanisms. Corin expression in rat ICH brain tissue was assessed at multiple time points. To assess corin's effect on neurological function and microglial inflammation, ICH rats and oxygen-glucose deprivation plus hemin (OGD/H)-stimulated HAPI microglia were treated with corin-encoding lentivirus. Neurobehavioral performance was evaluated using the Morris water maze (MWM). Microglial activation was assessed via Iba-1, iNOS, and Arg-1 expression, cytokine secretion, and migration assays. To determine whether AMPK mediates corin's effects, cells were co-treated with Compound C (an AMPK inhibitor) and corin lentivirus. Corin expression decreased in ICH rat brain tissue, reaching its lowest level on day 3 post-ICH. Corin overexpression protected against ICH-induced neuronal apoptosis and improved neurological deficits as confirmed by MWM. Moreover, corin overexpression reduced microglial activation and inflammation in both ICH rats and OGD/H-stimulated microglial cells, ameliorated mitochondrial dysfunction, and increased the p-AMPK/AMPK ratio. The protective effects of corin on cell migration, inflammation, and mitochondrial function were reversed by Compound C, indicating AMPK is a downstream mediator of corin. Targeting corin offers a promising therapeutic strategy for ICH by reducing neuroinflammation and mitochondrial damage through AMPK activation and modulation of microglial inflammatory phenotype polarization. [BMB Reports 2026; 59(2): 143-150].
Insights
Corin protects against brain injury after intracerebral hemorrhage (ICH) by reducing neuroinflammation and mitochondrial damage. This occurs through activating AMPK, offering a potential therapeutic target for ICH treatment.
Area of Science:
- Neuroscience
- Cellular Biology
- Biochemistry
Background:
- Microglial activation drives neuroinflammation, a key factor in secondary brain injury post-intracerebral hemorrhage (ICH).
- Regulatory mechanisms of microglial activation in ICH remain largely unknown.
- Corin's role in microglial inflammatory activation requires elucidation.
Purpose of the Study:
- To investigate the influence of corin on microglial inflammatory activation and its underlying mechanisms in ICH.
- To assess corin's therapeutic potential for mitigating secondary brain injury.
Main Methods:
- Corin expression was assessed in rat ICH brain tissue.
- ICH rats and oxygen-glucose deprivation/hemin-stimulated microglia were treated with corin-encoding lentivirus.
- Neurobehavioral performance (Morris water maze), microglial activation markers (Iba-1, iNOS, Arg-1), cytokine secretion, mitochondrial function, and AMPK signaling were evaluated.
Main Results:
- Corin expression decreased post-ICH, with lowest levels on day 3.
- Corin overexpression improved neurological deficits and reduced neuronal apoptosis in ICH rats.
- Corin reduced microglial activation, inflammation, and mitochondrial dysfunction, increasing the p-AMPK/AMPK ratio.
- AMPK inhibition reversed corin's protective effects, confirming AMPK as a downstream mediator.
Conclusions:
- Corin plays a protective role in ICH by suppressing neuroinflammation and mitochondrial damage.
- Corin exerts its effects through AMPK activation, modulating microglial inflammatory phenotype polarization.
- Targeting corin presents a promising therapeutic strategy for ICH.
