Curcumin attenuates the middle cerebral artery occlusion-induced reduction in gamma-enolase expression in an animal model / 한국실험동물학회지

Curcumin exerts a protective effect in cerebral ischemia through its anti-oxidant and anti-inflammatory activities. gamma-enolase is a glycolytic enzyme expressed in neurons that is known to exerts a neuroprotective effect. We investigated whether curcumin regulates gamma-enolase expression in focal cerebral ischemic injury in rats. Middle cerebral artery occlusion (MCAO) was performed to induce focal cerebral ischemia. Adult male rats were injected intraperitoneally with either vehicle or curcumin (50 mg/kg) 1 h after MCAO and cerebral cortex tissues were isolated 24 h after MCAO. We found that MCAO-induced injury resulted in a reduction in gamma-enolase expression in vehicle-treated animals using a proteomics approach. However, this reduction was attenuated in animals with MCAO treated with curcumin. Reverse-transcription PCR and Western blot analyses also showed that curcumin treatment prevented the MCAO injury-induced reduction in gamma-enolase expression. The results of this study suggest that curcumin exerts its neuroprotective function in focal cerebral ischemia by regulating the expression of gamma-enolase.

Ferulic acid prevents the injury-induced decrease of gamma-enolase expression in brain tissue and HT22 cells / 한국실험동물학회지

Ferulic acid is known to act as a protective agent in cerebral ischemia through its anti-oxidant activity. gamma-Enolase is a neuron-specific enolase that also exerts a neuroprotective effect. Here, we investigated whether ferulic acid regulates the expression level of gamma-enolase in middle cerebral artery occlusion (MCAO)-induced brain injury and glutamate exposure-induced neuronal cell death. Adult male rats were treated with either vehicle or ferulic acid (100 mg/kg, i.v.) after MCAO and cerebral cortex tissues were collected 24 h after MCAO. Using a proteomics approach, we found that gamma-enolase expression was decreased in MCAO-injured animals treated with vehicle alone, whereas ferulic acid treatment attenuated this decrease. Reverse-transcription PCR and Western blot analyses confirmed that ferulic acid treatment prevented MCAO injury-induced decrease in gamma-enolase. Furthermore, in hippocampal-derived cell lines, glutamate exposure also decreased gamma-enolase expression and ferulic acid treatment attenuated this glutamate-induced decrease in gamma-enolase. These findings suggest that ferulic acid mediates a neuroprotective effect by attenuating injury-induced decreases of gamma-enolase expression in neuronal cells.