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Neuroprotective effects of Aucubin against cerebral ischemia-reperfusion injury
Ying Liang1, Liqiu Chen1, Jing Huang1
1Department of Neurology, Nanjing Drum Tower Hospital, Clinical College of Nanjing University of Chinese Medicine, Nanjing 210008, China; Department of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210008, China.
Aims:
To study the role of Aucubin (AU) in cerebral ischemia-reperfusion injury and investigate the potential mechanisms.
Methods:
For the in vitro experiment, primary microglia were cultured and stimulated by Lipopolysaccharides (LPS) and treated with AU. Male C57/BL6J mice were used and middle cerebral artery occlusion (MCAO) model was performed to induce cerebral ischemia-reperfusion injury. For the short-term effects, mice administrated with AU (40 mg/kg) for 3 days after MCAO were evaluated for the infarct volume and neurological deficits. The neuroinflammatory factors and microglia activation were determined by Real-time PCR, western blot and immunofluorescence staining. For the long-term effects, MCAO mice were injected daily with AU (5 mg/kg or 10 mg/kg) for 28 days. Behavior tests were used to assess the neurological deficits of MCAO mice, and white matter integrity was determined by myelin basic protein (MBP) staining and black-gold staining.
Results:
AU suppressed LPS-induced activation of microglia and pro-inflammatory cytokines release, and downregulated the NF-κB and MAPK pathways in primary microglia. In addition, AU attenuated ischemic injury and inhibited the neuro-inflammatory response in MCAO mice. Moreover, AU induced prolonged improvements in sensorimotor function and memory function following MCAO, and preserved white matter integrity in the long-term experiments.
Conclusions:
AU protected against ischemic injury, which might be correlated with the downregulation of NF-κB and MAPK signaling pathways. Furthermore, AU alleviated cognitive impairment after stroke and restored white matter integrity. Our data indicated that AU might be a potential compound for the treatment of stroke and post-stroke cognitive impairment.
Insights
Aucubin (AU) protects the brain from stroke-related injury by reducing inflammation and improving cognitive function. This natural compound may offer a new treatment for stroke and its cognitive consequences.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Cerebral ischemia-reperfusion injury (I/R) is a major cause of stroke, leading to significant neurological deficits and cognitive impairment.
- Neuroinflammation and white matter damage are key pathological features following ischemic stroke.
- Aucubin (AU), a natural compound, has demonstrated anti-inflammatory and antioxidant properties, suggesting potential therapeutic benefits.
Purpose of the Study:
- To investigate the protective effects of Aucubin (AU) against cerebral ischemia-reperfusion (I/R) injury.
- To elucidate the underlying mechanisms of AU's action, focusing on neuroinflammation and white matter integrity.
Main Methods:
- In vitro studies involved stimulating primary microglia with lipopolysaccharides (LPS) and treating with AU, analyzing inflammatory markers and signaling pathways (NF-κB, MAPK).
- In vivo studies utilized a middle cerebral artery occlusion (MCAO) model in mice to induce cerebral I/R injury.
- Short-term effects were assessed by infarct volume and neurological deficits after AU administration (40 mg/kg).
- Long-term effects were evaluated through behavioral tests and white matter integrity assessments (MBP, black-gold staining) after daily AU treatment (5 or 10 mg/kg) for 28 days.
Main Results:
- Aucubin (AU) suppressed LPS-induced microglial activation and pro-inflammatory cytokine release in vitro, downregulating NF-κB and MAPK pathways.
- In vivo, AU attenuated ischemic injury and neuroinflammation in MCAO mice.
- Long-term administration of AU improved sensorimotor and memory functions and preserved white matter integrity in MCAO mice.
Conclusions:
- Aucubin (AU) demonstrates significant neuroprotective effects against cerebral ischemia-reperfusion injury.
- The protective mechanisms involve the downregulation of NF-κB and MAPK signaling pathways, reducing neuroinflammation.
- AU alleviates post-stroke cognitive impairment and restores white matter integrity, indicating its potential as a therapeutic agent for stroke and related cognitive deficits.
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