[Protective effect of Na2SeO3 against cerebral ischemia-reperfusion injury to the hippocampal neurons in rats].

OBJECTIVE: To investigate the protective effects of selenium on rat hippocampal neurons against ischemia-reperfusion (IR) injury. METHODS: Thirty-two rats were randomly divided into sham-operated group, IR group and selenium-treated group, and in the latter two groups, cerebral IR injury was induced by middle cerebral artery occlusion; Na2SeO3 treatment was administer in selenium-treated group. At 14 days after reperfusion, the brain tissues were harvested from the rats and hippocampal neuron injuries were observed by TUNEL and Methylene Blue staining. The levels of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and nerve growth factor (NGF) in the hippocampal tissues were measured by ELISA. RESULTS: Compared with IR group, the rats in selenium-treated group showed no significant increase in the expression of m-NGF (P>0.05), but pro-NGF expression was significantly increased (P<0.05) in the hippocampal tissue. Na2SeO3 treatment significantly inhibited the expressions of TNF-α and IL-1ß and decreased the apoptosis of hippocampal neurons following cerebral IR injury (P<0.05). CONCLUSION: Selenium produces antiapoptotic effect to protect the hippocampal neurons following cerebral IR injury possibly not by increasing the level of m-NGF but by decreasing the expressions of the inflammatory factors.

Hemorrhagic pure sensory strokes in the thalamus and striatocapsular area: causes, clinical features and long-term outcome.

BACKGROUND: Although there have been sporadic reports of patients with hemorrhagic pure sensory strokes (HPSS) in the thalamus and striatocapsular areas, the causes, clinical featuring and long-term outcome have not been adequately investigated. METHODS: We recruited 7 consecutive patients without hemiparetic stroke who had HPSS in the thalamic and striatocapsular areas. A CT scan was performed to verify brain imaging patterns, and their causes, clinical featuring and long-term outcome were observed. RESULTS: We studied 7 patients who had HPSS in the thalamic and striatocapsular areas as seen in CT scans. The 7 patients had hypertension, and small hemorrhages were found in the thalamus of 2 patients and in the posterior quarter of the posterior limb of the internal capsule in 4 patients; only 1 patient had a microhemorrhage in the thalamus. The volume of the hemorrhages ranged from 0.3 to 6.3 ml, with a mean of 2.3 ± 1.9 ml. Three patients showed a decreased sense of spinothalamic modality, and position and vibration senses were spared. Four patients showed a sensory deficit of both spinothalamic and medial lemniscal type. The outcomes were excellent and without post-stroke pain in all patients. CONCLUSION: HPSS in the thalamus and striatocapsular area are usually small hemorrhages or microhemorrhages from rupturing of the microvessels or the branches of small vessels. HPSS only have an impact on the adjacent sensory nucleus or pathway, and have a good outcome without post-stroke pain.