Ferulic Acid Modulates Calbindin-D28K Expression in Focal Cerebral Ischemia and Glutamate-Exposed HT22 Cells
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Calbindin-D28k is a calcium-binding protein that mediates intracellular calcium concentrationsand exerts a neuroprotective effect against ischemic injury. Ferulic acid provides aneuroprotective effect against focal cerebral ischemia through its anti-oxidative andanti-inflammatory mechanisms. In this study, we investigated whether ferulic acid regulatescalbindin-D28k expression during focal cerebral ischemia and glutamate treatment-inducedneuronal cell death. Middle cerebral artery occlusion (MCAO) was performed to induce focalcerebral ischemia. Ferulic acid (100 mg/kg, i.v.) or vehicle was immediately administered afterMCAO, and brain tissues were isolated 24 h after MCAO. RT-PCR and Western blot analysesshowed a decrease in calbindin-D28k in MCAO-operated animals. We found that ferulic acidtreatment prevented the MCAO-induced decrease in calbindin-D28k expression. Glutamateexposure elevated the intracellular calcium levels in cultured hippocampal cells, and ferulic acidprevented the glutamate exposure-induced increase in calcium levels. Moreover, ferulic acid alsoattenuated the glutamate toxicity-induced decrease in calbindin-D28k. Taken together, these invivo and in vitro results demonstrate that ferulic acid regulates calbindin-D28k expression inneuronal cell injury. Therefore, these findings suggest that ferulic acid exerts a neuroprotectiveeffect by modulating calbindin-D28k expression.
Abstract
Calbindin-D28k is a calcium-binding protein that mediates intracellular calcium concentrationsand exerts a neuroprotective effect against ischemic injury. Ferulic acid provides aneuroprotective effect against focal cerebral ischemia through its anti-oxidative andanti-inflammatory mechanisms. In this study, we investigated whether ferulic acid regulatescalbindin-D28k expression during focal cerebral ischemia and glutamate treatment-inducedneuronal cell death. Middle cerebral artery occlusion (MCAO) was performed to induce focalcerebral ischemia. Ferulic acid (100 mg/kg, i.v.) or vehicle was immediately administered afterMCAO, and brain tissues were isolated 24 h after MCAO. RT-PCR and Western blot analysesshowed a decrease in calbindin-D28k in MCAO-operated animals. We found that ferulic acidtreatment prevented the MCAO-induced decrease in calbindin-D28k expression. Glutamateexposure elevated the intracellular calcium levels in cultured hippocampal cells, and ferulic acidprevented the glutamate exposure-induced increase in calcium levels. Moreover, ferulic acid alsoattenuated the glutamate toxicity-induced decrease in calbindin-D28k. Taken together, these invivo and in vitro results demonstrate that ferulic acid regulates calbindin-D28k expression inneuronal cell injury. Therefore, these findings suggest that ferulic acid exerts a neuroprotectiveeffect by modulating calbindin-D28k expression.
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