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AIM: To explore whether free radicals participate in cerebral ischemic tolerance and the up-regula-tion of p38 MAPK and ERK signaling pathways in rats induced by limb ischemic preconditioning (LIP). METHODS: A total of 128 Wistar rats with permanent occlusion of bilateral vertebral arteries were randomly divided into sham group (n=16), cerebral ischemia (CI) group (n=16), LIP+CI group (n=16), DMTU (a free radical scavenger)+LIP+CI group (n=64) and DMTU+sham group (n=16). Six rats in each group were used to observe the delayed neuronal death (DND) in hippocampal CA1 region by thionin staining at 7 d after the end of operation. Other 10 rats in each group were used to de-tect the expression of p38 MAPK and ERK in hippocampal CA1 region by immunohistochemistry and Western blot. RE-SULTS: Lethal CI resulted in obvious DND in hippocampal CA1 region. However, LIP reversed the above injurious changes, represented by the decrease in histological grade and the increase in neuronal density compared with CI group (P<0. 01). Moreover, LIP significantly up-regulated the expression of p38 MAPK and ERK in hippocampal CA1 region com-pared with CI group (P<0. 01). Administration of free radical scavenger DMTU via femoral vein before LIP partially re-versed the neuroprotective effect of LIP, and blocked the up-regulation of p38 MAPK and ERK expression in hippocampal CA1 region in rats compared with LIP+CI group (P<0. 01). CONCLUSION: Free radicals are involved in the neuropro-tection and up-regulation of p38 MAPK and ERK expression induced by LIP in rats.
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The mice models of blood stasis were established by injecting dexamethasone into the intramuscular of side the thigh for successive 15 days, and giving related drugs via an intragastric administration. Firstly, the method of blocking the bilateral common carotid artery (CCA) was used for 10 minutes, and then perfusion restore for 5 days. Secondly, the method of CCA was used for 30 minutes, and then reperfusion for 24 hours. The whole blood viscosity and plasma viscosity, the activity of NOS and ATPase and the level of NOS, and the content of Glu in the ischemic brain were measured. The morphological changes of brain tissue were observed by eosin (HE) staining technique. The results showed that compared with IPC model group the large doses of the flavonoids could reduce the viscosity of whole blood significantly (P<0.01). The small and medium doses of flavonoids could reduce the whole blood viscosity low-shear obviously (P<0.01). The medium doses of flavonoids could reduce the midst-shear obviously (P<0.05). The large and medium dose of flavonoids could significantly improve the ATP activity (P<0.01). The medium dose of flavonoids could improve the Na⁺-K⁺-ATPase activity significantly (P<0.01). The small dose of flavonoids could improve the Na⁺-K⁺-ATPase activity obviously (P<0.05). The large doses of flavonoids could reduce the content of gluin the ischemic brain significantly (P<0.01). And the others does of flavonoids could reduce the content of gluin the ischemic brain obviously (P<0.05). The large doses of flavonoids could reduce the activity of TNOS and iNOS significantly (P<0.01). The medium doses of flavonoids could reduce the activity of TNOS and iNOS obviously (P<0.05). The small doses of flavonoids could reduce the activity of iNOS obviously (P<0.05). Total flavonoids could obviously or significantly decrease the whole blood viscosity, the activity of NOS and the content of gluin the ischemic brain, increase the activity of ATPase significantly or obviously, could significantly relieve the degree of pathological injury of brain tissue of animal models.
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Hypoxia inducible factor 1 (HIF-1), a nuclear protein with transcription activity, can make the body produce adaptive response to hypoxia/ischemia by binding to target gene, transcription and post-transcriptional control. Ischemic tolerance refers to the adaptive response to transient ischemia and reperfusion, which can improve tissue tolerance during the following damage caused by more severe ischemic events. The recent studies have found that the expression of HIF-1 has an important significance in ischemic tolerance. HIF-1 may be a key factor of the oxygen signal transduction pathway in the development of cerebral ischemic tolerance.
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AIM: To investigate the relationship between astroglial activation state and ischemic tolerance induced by low dose of 3 nitropropionic acid (3 NPA) in gerbil hippocampus. METHODS: Transient forebrain ischemic model was induced by bilateral common carotid arteries occlution. HE staining and immunohistochemistry were used to identify neuronal and astrocyte response. RESULTS: Preconditioning with 3 NPA produced protective effects of CA 1neurons. The number of glial fibrillary acidic protein positive astrocyte in hippocampal CA 1 region increased slightly in control group, but increased significantly in preconditioning of the brain with 3 nitropropionic acid. CONCLUSION: The state of astroglial activation is related to neuronal survival in ischemic tolerance induced by low dose of 3 nitropropionic acid.
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0.05) ;TNF-? 0.5 ?g and TNF-? 1.0 ?g pretreatment groups showed reduced volume of lesion(all P