Aim To observe the change of NF-?B and expression of Bax and Bcl-2 related to apoptosis regulation in the cerebral infarction rat and study the protective effect of iridoid glycoside(IG) extracted from cornus officinalis on focal cerebral ischemia injury and its mechanism of action.Methods Rats were pretreated with drugs by mouth for 7 d and a focal cerebral infarction model of rat was induced by photochemical reaction.Immunohistochemistry and western blot were used to detect the change of expression of NF-?B,Bax and Bcl-2 in the cortex.Results Compared with control group,expression of NF-?B and Bax were increased while expression of Bcl-2 was decreased.Compared with model group,IG(IG 20、60、180 mg?kg~(-1)) markedly decreased the expression of NF-?B and Bax and increased expression of Bcl-2.Conclusion IG has therapeutical effect on cerebral infarction through regulating the expression of NF-?B and apoptosis related genes

Objective To investigate the effects of Morroniside on H2O2-induced oxidative injury in SH-SY5Y neuroblastoma cells.MethodsSH-SY5Y cells were pre-incubated with Morroniside(1,10,and 100 μmol/L)for 24 h prior to exposure to H2O2(500 μmol/L)for 18 h.The content of reactive oxygen species(ROS),nitric oxide(NO),glutathione(GSH)were determined.ResultsPretreatment the cells with Morroniside(10 and 100 μmol/L)lowered H2O2-induced ROS release by 37%(P<0.01)and 27%(P<0.05)versus H2O2,and NO release in a dose-dependent manner by 31%(P<0.05),53%(P<0.01)versus H2O2.Morroniside(1,10,and 100 μmol/L)increased GSH level in cells treated with H2O2 in comparison with cells exposed only to H2O2,respectively.ConclusionMorroniside shows neuroprotection effect against H2O2-induced oxidation injury in SH-SY5Y cell.

Objective To study the effects of morroniside on the expression of Wnt signaling-related transcription factors neurogenin 2 (Ngn2), Pax6 and Tbr2 in the ischemic ipsilateral cortex 7 days after cerebral ischemia-reperfusion in rats. Methods 15 male Sprague-Dawley rats were randomly divided into sham group (n=3), ischemia group (n=3), and morroniside groups (low, medium and high dosage groups, n=3). The middle cerebral artery were occluded for 30 min, and re-perfused. Morroniside was administered intragastrically once a day at dose of 30 mg/kg, 90 mg/kg and 270 mg/kg 3 hours after operation. The expression of Ngn2, Pax6 and Tbr2 in the ischemic ipsilateral cortex were detected with Western blotting analysis 7 days after operation. Results The expression of Ngn2 increased in the ischemia group compared with the sham group (P<0.05), and it further increased the morroniside groups of medium and high dosage compared with the ischemia group (P<0.01). There was no significant difference between the ischemia group and sham group in the expression of Pax6, while it increased the morroniside groups of medium and high dosage compared with the ischemia group (P<0.01). There was no significant difference among all the groups in the expression of Tbr2. Conclusion Morroniside could increase the expression of Ngn2 and Pax6 in the ischemic ipsilateral cortex 7 days after ischemia-reperfusion in rats, suggesting promoting the neurogenesis after ischemia.

Objective To study the effects of morroniside on the expression of matrix metalloproteinase (MMP) -2 and MMP-9 in the peri- infarct cortex 3 days after cerebral ischemia- reperfusion. Methods 15 male Sprague-Dawley rats were randomly divided into sham group (n=3), ischemia group (n=3), and morroniside groups (low, medium and high dosage groups, n=3). The middle cerebral artery were occluded for 30 min, and re-perfused. Morroniside was administered intragastrically once a day at dose of 30 mg/kg, 90 mg/kg and 270 mg/kg 3 hours after operation. The expression of MMP-2 and MMP-9 in peri-infarct cortex were detected with immunohistochemistry staining 3 days after operation. Results The expression of MMP-2 and MMP-9 increased in the ischemia group compared with the sham group (P<0.01), and it decreased in all the morroniside groups compared with the ischemia group (P<0.01). Conclusion Morroniside could decrease the expression of MMP-2 and MMP-9 in the peri-infarct cortex 3 days after ischemia, suggesting protecting the function of blood-brain barrier from ischemia.

Neural stem cells are a category of cells with self-renewal and differentiation potential. Proliferation and differentiation of neural stem cells have closely relation with growth factor, cell factor, environmental signal, and so on. In recent years, evidence indicates that neural stem cells possessing multipotency naturally occur in adult brain. The found of adult neural stem cells have changed the theory that central nervous system cannot regenerative. Chinese Traditional Medicine can effectively induce adult neural stem cells to proliferate and differentiate, opening up unprecedented direction in the research for the treatment of nerve regeneration, and showing great potency for curing cerebral ischemic injury.

ObjectiveTo explore the mechanism of protection of 2,3,5,4'-tetrahydroxy stilbene-2-O-β-D-glucoside(TSG) on brain.MethodsThe bilateral carotid arteries of mice were occluded and then reperfused. The mice were sacrificed to get the brain tissue. Brain water content(BWC) was assayed by dry-wet method; malondialdehyde (MDA) content was determined by thiobarbiturate method and the activity of superoxide dismutase(SOD) was estimated by nitrite salt assay.ResultsBWC of model group was significantly higher than that of sham-operation group, while the TSG treatment reduced the BWC remarkably in mice with ischemia-reperfusion. SOD activity of model group was significantly lower than that of sham-operation group, while MDA content increased remarkably. Comparing with the model group, the SOD activity of mice treated with TSG was higher and the MDA content was lower.ConclusionTSG may reduce brain edema, improve the anti-oxidative ability of the brain tissue, and therefore, have protective effects on the brain.

ObjectiveTo investigate effects of 2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glucoside (TSG), on learning and memory function and excitability in Alzheimer's disease rat model induced by cholinergic damage.MethodsBasal forebrain of rats were injured by ibotenic acid injection of 10μg each side. Rats were divided into six groups as the operation, model, positive control drug donepezil hydrochloride, TSG low (0.03g/kg), middle (0.06g/kg) and high (0.12g/kg) dose groups. These drugs were intragastrically administrated for 1 month. The learning and memory function were determined with Morris water maze, channel water maze and step through tests, and the excitability was evaluated by open field analysis. Results TSG (low, middle and high dose)significantly decreased the swimming time and error times (P<0.05) in water maze test and TSG high dose improved the ability of passive avoidance response at step through test.Open field test showed that there was no significant difference on excitability between each group ConclusionTSG can improve learning and memory abilities of Alzheimer's disease rat induced by cholinergic damage, TSG(low and middle dose)improve excitability of central nervous system in Alzheimer's disease rat model,but TSG dose maybe inhibite excitability of central nervous system.

OBJECTIVE:To study the effects of taurine on oxidative stress and calcium overload induced by cerebral cortex contusion.METHODS:SD rats were randomly divided into normal control group,brain contusion model group,taurine groups(high dose,middle dose and low dose respectively),and nimodipine group.After being fed with corresponding drugs for7days,all rats were subjected to modeling by brain contusion.For intracellular calcium detection,rats were sacrificed2h after modeling,and the brain slices were prepared to fluorescence labeling and confocal microscopy detection.For the detection of oxidative stress,rats were sacrificed24h after modeling,the cortex of contusion side was homogenated and then the activity of superoxide dis?mutase(SOD)and content of malondialdehyde(MDA)were detected through biochemical method.RESULTS:Compared with model group,all taurine groups were shown to have markedly less MDA and intracellular calcium content,and the high dose group had markedly stronger SOD activity.CONCLUSION:Taurine is effective in counteracting the oxidative stress and calcium overload caused by brain contusion.

Objective To investigate the effects of morroniside on total antioxidative capacity (T-AOC) in rat cortex with focal cerebral ischemia/reperfusion. Methods The animal model was induced with occlusion of middle cerebral artery. The T-AOC was detected with spectrophotometer. Results Compared with model group, morroniside （270 mg/kg） increased the T-AOC significantly. Conclusion Morroniside may take the neuroprotection through increased T-AOC of rat cortex.

ObjectiveTo investigate the effects of morroniside on super oxide dismutase (SOD) and neurons in rats cortex with focal cerebral ischemia/reperfusion. MethodsThe animal model was induced by middle cerebral artery occlusion with suture embolus, cerebral ischemia 30 min and reperfusion 3 d or 7 d. Vitamin E for the positive control. The content of SOD was detected with spectrophotometry and the nerve cells was observed with immunohistochemistry. ResultsCompared with model group, morroniside （270 mg/kg）increased the activity of SOD and the number of neurons （30 mg/kg, 90 mg/kg, 270 mg/kg） significantly. ConclusionMorroniside may have neuroprotective effect and increasing the activity of SOD in rats cortex.