It remains unclear whether spinal cord ischemia-reperfusion injury caused by ischemia and other non-mechanical factors can be monitored by somatosensory evoked potentials. Therefore, we monitored spinal cord ischemia-reperfusion injury in rabbits using somatosensory evoked potential detection technology. The results showed that the somatosensory evoked potential latency was significantly prolonged and the amplitude significantly reduced until it disappeared during the period of spinal cord ischemia. After reperfusion for 30-180 minutes, the amplitude and latency began to gradual y recover; at 360 minutes of reperfusion, the latency showed no significant difference compared with the pre-ischemic value, while the somatosensory evoked potential amplitude in-creased, and severe hindlimb motor dysfunctions were detected. Experimental findings suggest that changes in somatosensory evoked potential latency can reflect the degree of spinal cord ischemic injury, while the amplitude variations are indicators of the late spinal cord reperfusion injury, which provide evidence for the assessment of limb motor function and avoid iatrogenic spinal cord injury.

Transient brain ischemia has been shown to induce hyperphosphorylation of the microtu-bule-associated protein tau. To further determine the mechanisms underlying these processes, we investigated the interaction between tau, glycogen synthase kinase (GSK)-3β and protein phos-phatase 2A. The results confirmed that tau protein was dephosphorylated during brain ischemia;in addition, the activity of GSK-3βwas increased and the activity of protein phosphatase 2A was de-creased. After reperfusion, tau protein was hyperphosphorylated, the activity of GSK-3β was de-creased and the activity of protein phosphatase 2A remained low. Importantly, the interaction of tau with GSK-3β and protein phosphatase 2A was altered during ischemia and reperfusion. Lithium chloride could affect tau phosphorylation by regulating the interaction of tau with GSK-3βand pro-tein phosphatase 2A, and improve learning and memory ability of rats after transient brain ischemia. The present study demonstrated that it was the interaction of tau with GSK-3β and protein phos-phatase 2A, rather than their individual activities, that dominates the phosphorylation of tau in tran-sient brain ischemia. Hyperphosphorylated tau protein may play an important role in the evolution of brain injury in ischemic stroke. The neuroprotective effects of lithium chloride partly depend on the inhibition of tau phosphorylation during transient brain ischemia.

丹参、黄芪合用对脑缺血再灌注后脑组织Fos,Jun蛋白表达的影响

AIM: To investigate the expression of Fos and Jun proteins in rat brainsafter focal cerebral ischemia followed by reperfusion and effects of RSMand astragus. METHODS: 30 SD adult male rats were divided into 5groups at random . Group A: sham-operated group; Group B: model group;Group C: treated with RSM; Group D: treated with astragus; Group E:treated with RSM and astragus. The immunohistochemistry and medicalimage processing system(MIPS) were used to measure the numbers andmean grey levels of Fos and Jun protein positive cells in rat cerebralcortex of 5 groups. RESULTS: ( 1 ) In cerebral cortex of group B , C , D, E, the numbers of Fos and Jun positive cells were more than those ingroup A and mean grey levels of Fos and Jun positive cells were lower thanthose in group A(P ＜ 0.01); (2) In cerebral cortex of ischemic sidesin group C, D, E,the numbers of Fos and Jun positive cells were less thanthose in group B and mean grey levels of Fos and Jun positive cells werehigher than those in group B(P ＜ 0.01) ; (3) Group E had more sig-nificant effects than group C or group D ( P ＜ 0. 01 ). CONCLUSION:The expression of Fos protein and Jun protein in model group increasedsignificantly, compared with sham-operated group; RSM , astragus , RSMand astragus all could inhibit partly the expression of Fos protein and Junprotein after cerebral ischemia and reperfusion; Prescription of RSM andastragus had stronger inhibiting effects than RSM or astragus. It may be oneof mechanisms that ischemic stoke is treated by reinforcing Qi and acti-vating blood circulation therapy in TCM clinic.