[Protective effect of ferulic acid on neuronal apoptosis of spinal cord subsequent to aortic blood cross-clamping in rabbits].

OBJECTIVE: To investigate the protective effect of ferulic acid on neuronal apoptosis of the spinal cord after aortic blood cross-clamping and its mechanism in rabbits. METHODS: Twenty-four rabbits were randomly divided into sham operation group, ischemia/reperfusion (I/R) injury group and ferulic acid group. Spinal cord I/R injury model was replicated by clamping blood of the infrarenal aorta for 40 minutes followed reperfusion for 7 days. Ferulic acid 50 mg/kg was injected 15 minutes before aortic clamping in ferulic acid group. The aorta was not clamped in sham operation group. Contents of malondialdehyde (MDA) and superoxide dismutase (SOD) in plasma were assayed at 10 minutes before clamping (C-10), before removal of occlusion (C40), at 60 minutes (R60) and on the 7 th day (R7d) after reperfusion. Apoptosis of neurones of spinal cord and the expressions of Bax and Bcl-2 protein were assayed by immunohistochemical technique. Neurologic function score of hind limb was observed after operation. RESULTS: (1)The activity of MDA after I/R in I/R injury group was increased significantly compared with those before clamping and those in sham operation group (P<0.05 or P<0.01). The activity of MDA in ferulic acid group was significantly higher than that at C-10 (P<0.05), while significantly lower than those in I/R injury group at any time point (P<0.05 or P<0.01), but showed no significant difference compared with sham operation group. Changes in SOD activities were opposite to that of MDA. (2)The expression of Bax protein in I/R injury group was increased significantly (P<0.05), but the expression of Bcl-2 protein was decreased significantly compared with that in sham operation group (P<0.01). In ferulic acid group, the expression of Bax protein was significantly lower than that in I/R injury group and higher than that in sham operation group (P<0.01 and P<0.05), and the expression of Bcl-2 protein was higher than those in I/R injury group and sham operation group (both P<0.01). (3)The index of neuronal apoptosis in I/R injury group was significantly higher than that in sham operation group (P<0.01), and that in ferulic acid group was much lower than that in I/R injury group, but higher than sham operation group (P<0.01 and P<0.05). (4)The degree of paralysis in ferulic acid group was significantly lower than that in I/R injury group, and a higher neurologic score was observed (both P<0.01). CONCLUSION: Ferulic acid can reduce the spinal cord neuronal apoptosis as a result of aortic occlusion in rabbits. The possible mechanism is that it decreases protein expression of Bax, increases that of Bcl-2 and enhances antioxidation.

Targeting brain microvascular endothelial cells: a therapeutic approach to neuroprotection against stroke.

Brain microvascular endothelial cells form the interface between nervous tissue and circulating blood, and regulate central nervous system homeostasis. Brain microvascular endothelial cells differ from peripheral endothelial cells with regards expression of specific ion transporters and receptors, and contain fewer fenestrations and pinocytotic vesicles. Brain microvascular endothelial cells also synthesize several factors that influence blood vessel function. This review describes the morphological characteristics and functions of brain microvascular endothelial cells, and summarizes current knowledge regarding changes in brain microvascular endothelial cells during stroke progression and therapies. Future studies should focus on identifying mechanisms underlying such changes and developing possible neuroprotective therapeutic interventions.