ஜர்னல் ஆஃப் ஸ்பைன்

Protective Effect of Curcumin on Neural Myelin Sheaths by Attenuating Interactions between the Endoplasmic Reticulum and Mitochondria after Compressed Spinal Cord

Abstract

Hai jun Yu, Lan Ma, Jin Jiang and Shan Quan Sun

Oligodendrocyte apoptosis is the leading cause of demyelination in the central nervous system after compressed spinal cord injury (CSCI). Curcumin, which belongs to the curcuminoid family, is a phenolic yellow pigment derived from the powdered rhizome of Curcuma longa. It has been proved that curcumin exhibits neuroprotective effects against traumatic spinal cord injury by inhibiting neuronal apoptosis. However, whether curcumin has a protective effect on demyelination after CSCI by inhibiting the apoptosis of oligodendrocytes has not been reported. Therefore this study was designed to investigate whether curcumin has a reparative effect on CSCI-induced demyelination and, if so, how it does so. First, we found that the administration of 100 mg/kg curcumin intraperitoneally (IP) 60 minutes after CSCI at days 1, 3, and 7 could significantly relieve neurological deficits. After staining with osmic acid, we found that the swelling of myelin sheaths in the treated group was milder than that in the vehicle group. The results of luxol fast blue staining also indicated that the number of remaining myelin sheaths was significantly higher in the treated group. Next we detected the expressions of active caspase-3, caspase-12, cytochrome C, and myelin basic protein (MBP) by Western blot. This revealed that the expression of MBP was significantly enhanced in the curcumin-treated group, consistent with the number of remaining myelin sheaths found on luxol fast blue staining. But the expression of caspase-12, cytochrome C, and active caspase-3 was reduced; in addition, double immunofluorescence showed that active caspase-3–positive oligodendrocytes in the treatment group were fewer in number as compared with the vehicle group. These results suggested that curcumin did have a protective effect on demyelination—mainly through its mediating effects on the endoplasmic reticulum–mitochondrial pathway—to significantly reduce the expression of active caspase-3. In this way cucurmin reduced both the apoptosis of oligodendrocytes and demyelination, thus ameliorating the consequences of CSCI.