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Objective@#To investigate the effects of astaxanthin on neuronal injury in hippocampus of rats after acute carbon monoxide poisoning(ACMP) and the relationship with NF-κB inflammatory signaling pathway.@*Methods@#Male SD rats screened by water maze were randomly divided into three group(n=50): control group (NC group), CO poisoning group (COP group), CO poisoning+ astaxanthin group (AST group) . ACMP rat model was established by static inhaled exposure method. Meanwhile, rats in AST group were further given astaxanthin twice a day by gavage.At 1 day, 7 days, 14 days, 21 days and 28 days after CO poisoning (10 rats in each group were selected), the learning and memory abilities were evaluated by Morris water maze test. The pathological changes of the neurons in hippocampal CA1 region were observed by hematoxylin-eosin(HE) staining.The expression and activation of NF-κB in hippocampus were detected by immunoblotting and immunofluorescence, and the expression of TNF-α and IL-6 protein in hippocampus were examined by ELISA.@*Results@#Morris water maze test showed that there were no significant difference in escape latency and crossing platform times between the three groups (P>0.05). Compared with NC group, the escape latency of COP group was prolonged at 14, 21 and 28 days after CO poisoning (t=-6.04, -6.28, -8.18, all P<0.05), and the number of crossing platform was decreased (t= 5.96, 7.85, 6.51, all P<0.05). Compared with the COP group, the escape latency of the rats in AST group at the 14, 21 and 28 days was shortened (t=4.74, 4.82, 5.98, all P<0.05), and the number of crossing platform was increased (t=-3.72, -4.45, -6.53, all P<0.05). Compared with NC group, the number of NF-κ B positive cells in CA1 area of hippocampus in COP group increased at every time point (t=-8.62, -18.00, -16.67, -11.15, -6.22, all P<0.05); the number of NF-κ B positive cells in CA1 area in AST group decreased at 7 d, 14 d, 21 d and 28 d after CO poisoning, the difference was statistically significant (t= 6.55, 6.96, 4.40, 4.17; all P<0.05). Western blot showed that the changes of NF-κB protein was similar to that of immunofluorescence. After 7 days of CO poisoning, the level of NF-κB protein in hippocampus of COP group was (1.44±0.08), it was higher than that of NC group (t=-20.07, P<0.05), while that of AST group was (0.68±0.10), it was lower than that of COP group (t=10.23, P<0.05). The results of Elisa showed that TNF-α and IL-6 in the hippocampus of COP group were higher than those of NC group at every time point(all P<0.05), while compared with COP group, TNF-α and IL-6 in AST group were lower (all P<0.05). After 7 days of CO poisoning, TNF -α in COP group ((39.04±5.29) pg/ml)was higher than that in NC group ((14.13±2.12) pg/ml) (t=-7.58, P<0.05); TNF -α in AST group ((25.77±3.31) pg/ml) was lower than that in COP group (t=3.69, P<0.05). After 7 days of CO poisoning, the level of IL-6 in COP group ((181.79±9.12) pg/ml)was higher than that in NC group ((73.12±11.04) pg/ml) (t=-8.24, P<0.05), and the level of IL-6 in AST group ((121.47±9.80) pg/ml) was lower than that in COP group (t=7.80, P<0.05).@*Conclusion@#The excessive inflammatory response which mediated by NF-κB signaling pathway is involved in ACMP-induced neuronal damage in hippocampus.Astaxanthin can down-regulate the expression of NF-κB inflammatory signaling pathway related proteins, and pave a way for the treatment of ACMP brain damage and cognitive dysfunction.
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Objective To investigate the role of nuclear transcription factor kappa B (NF-κB) -matrix metalloproteinase-9 (MMP-9) signaling pathway in delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Methods 150 male SD rats were randomly assigned to air control group (AC group) , CO poisoning group (CO group) , pyrrolidine thiocarbamate (PDTC) + CO poisoning group (PC group). DEACMP model was reconstructed by modified intraperitoneal injections. The 1, 3, 7, 14, and 21 d after intraperitoneal injection were observed here by different approaches. Morris water maze test was used to test the learning and memory ability of rats.HE staining was used to observe the morphology of hippocampal CA3 cells. Immunofluorescence and Western Blot methods were used to detect the expression of NF-κB and MMP-9. RT-PCR was used to measure the expression of MMP-9 mRN A. Transmission electron microscopy was used to observe the ultrastructure of synapses. Results After14 days, the average intubation period of CO group was longer than that of AC group (P < 0.05) , and that of PC group was shorter than that of CO group (P < 0.05). However, average intubation period of PC group was longer than that of AC group (P< 0.05). In CO group, the expression of NF-κB in hippocampus increased (day 1). At day 3, the expression of NF-κB rapidly increased. The expression of MMP-9 gene and protein increased in the first three days and then decreased thereafter. The expression of NF-κB and MMP-9 in PC group was lower than that in CO group (P < 0.05) , while it was higher than AC group (P < 0.05). The peak value of apoptosis in CO group was delayed to 7-14 d after exposure, the apoptotic cells in PC group decreased significantly, and it was obvious on the 14 th day.Electron microscopy showed that the damage of synapses ultrastructure in CO group was significantly heavier than that in PC group on the 14 th day. Conclusions NF-κB-MMP-9 signal pathway leads to DEACMP, and PDTC could alleviate the impairment of learning and memory ability in rats with acute CO poisoning.
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Objective:To investigate the levels of AP-1 in hippocampus of rats at different time points after carbon monoxide poisoning.Methods: Carbon monoxide poisoning delayed encephalopathy model by using intraperitoneal injection of carbon monoxide.Uesd HE observed the pathological changes in hippocampus of rats.The levels of AP-1 was observed by immunohistochemistry and Western blot analysis.TUNEL was used to detect apoptotic neurons in hippocampal CA1 area.Results: HE dyeing conditions,the hippocampus cell of air group (AC) and blank group (BC) were normal at each time point.Pathological changes occurred in the hippocampus cell of Carbon monoxide group (CO),reduction in the number of cells,disorder of cells,intercellular space expansion,nuclear fragmentation,anachromasis and pyknotic.Immunohistochemical results,the AP-1 expression level at each time point in group CO were higher than group AC and BC.On 3th day it reached a peak.The comparison at all time points among the groups in the first three days were significantly different in statistics(P<0.05).Western blot results,the expression of AP-1 was consistented with the immunohistochemical results on the time distribution trend.TUNEL results,AI in group CO was higher than those in group AC and BC at all time points,there were significant differences(P<0.05) and 7th reached the peak of apopotsis.Conclusion: Inside the hippocampus of rats,there are increasing in AP-1 . Maybe it is one of the important pathogenesis of DEACMP .
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Objective To observe the effect of erythropoietin(EPO)in rats with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Methods A total of 90 male adult SD rats were randomly divided into three groups:blank control group(BC group),air control group(AC group)and DEACMP group. Time points(1,3,7,14,21 and 28 days after acute carbon monoxide poisoning)were set for measuring the changes. Pure CO were injected into the abdominal cavity of the rats from DEACMP group for several times to estab-lish DEACMP model. Rats in AC group were injected with equal volume of air by the same way. BC group were without any treatment. Morris water maze test was used to measure the cognitive behavior. The apoptosis of pyrami-dal neurons at hippocampus was measured by TUNEL. The expression of erythropoietin(EPO)in hippocampus was measured by immunohistochemistry. Results The average escaped latency of rats in DEACMP group increased after poisoning compared with rats in other two groups(P<0.05). The apoptosis of pyramidal neurons in hippocam-pus increased from day 1 after the CO poisoning. It reached the peak at day 7 and it still had a high expression at day 28. The apoptotic index in DEACMP group increased significantly compare with that of BC group and AC group (P < 0.05). The expression of EPO in hippocampus was found increased from day 1 after the CO poisoning and reached the peak at day 3. It began to reduce at day 7. The expression in DEACMP group was higher than those of other two groups (P < 0.05). Conclusions It may be one of the causes of the DEACMP that the expression of EPO decreased in the middle and late stage after CO poisoning and its anti-apoptosis was decreased.
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Objective To observe the effect of erythropoietin(EPO)in rats with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Methods A total of 90 male adult SD rats were randomly divided into three groups:blank control group(BC group),air control group(AC group)and DEACMP group. Time points(1,3,7,14,21 and 28 days after acute carbon monoxide poisoning)were set for measuring the changes. Pure CO were injected into the abdominal cavity of the rats from DEACMP group for several times to estab-lish DEACMP model. Rats in AC group were injected with equal volume of air by the same way. BC group were without any treatment. Morris water maze test was used to measure the cognitive behavior. The apoptosis of pyrami-dal neurons at hippocampus was measured by TUNEL. The expression of erythropoietin(EPO)in hippocampus was measured by immunohistochemistry. Results The average escaped latency of rats in DEACMP group increased after poisoning compared with rats in other two groups(P<0.05). The apoptosis of pyramidal neurons in hippocam-pus increased from day 1 after the CO poisoning. It reached the peak at day 7 and it still had a high expression at day 28. The apoptotic index in DEACMP group increased significantly compare with that of BC group and AC group (P < 0.05). The expression of EPO in hippocampus was found increased from day 1 after the CO poisoning and reached the peak at day 3. It began to reduce at day 7. The expression in DEACMP group was higher than those of other two groups (P < 0.05). Conclusions It may be one of the causes of the DEACMP that the expression of EPO decreased in the middle and late stage after CO poisoning and its anti-apoptosis was decreased.
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Objective To study the effects of nuclear factor E2-related factor 2 (Nrf2) in delayed encephalopathy in rats after acute carbon monoxide poisoning. Methods One hundred and sixty-eight rats were randomly divided into three groups: forty-eight rats in the blank control group (BC group), sixty rats in the air control group (AC group) as well as in the carbon monoxide poisoning group (CO group). The DEACMP model was established by improved intraperitoneal injections. The animals were valuated at 1st ,3rd, 7th, 14th, 21th, 28th day after acute carbon monoxide poisoning. Tunnel method was used to test the pyramidal cell apoptosis in the hippocampal CA1 area. The expression of Nrf2 was tested by immunohistochemical method and Western Blot method. Result In the CO group, the apoptosis index (AI) started to increase from first day and achieved it's peak at the 7th day (20.20 ± 1.78), then began to decrease slowly. The apoptosis index was still higher than that in the other groups at 28th day. And the apoptosis index of the CO group was markedly higher than the other two groups at each time point. The Nrf2 protein started to increase from 1st day in the CO group , reached its peak at 3rd day (8.20 ± 1.08), reduced later, maintained at a high level at 28th day, and expressed significantly higher than other groups at each time point. Conclusions The Nrf2 has a linear correlation with apoptosis , and plays a dual role in DEACMP because it rapidly increased in first three days to against apoptosis. But it continuously has been excessive expressed from 7th to 28th day in promoting the apoptosis of hippocampus pyramidal cells and may be a positive factor in DEACMP.
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Objective To investigate the imaging and clinical features of Percheron artery infarction.Methods The clinical manifestations,imaging data,treatment,and prognosis of 10 patients with Percheron artery infarction were analyzed.Results All 10 patients had acute onset and had different degrees of consciousness disorders,including vertical gaze palsy (n =3),language disorder (n =3),limb weakness (n =6),and memory impairment (n =4).MRI showed bilateral thalamus infarction.Midbrain V-sign in one patient was observed.Cerebral angiography revealed that one patient had Percheron artery infarction.All 10 patients were improved and discharged,but left with varying degrees of sequelae.Conclusions Percheron artery infarction is rare in clinical practice.The diagnosis is mainly based on clinical manifestations and imaging examinations.Cerebral angiography can diagnose the disease.
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Objective To investigate the value of the Changsha version of the Montreal Cognitive Assessment Scale (MoCA) in the assessment of vascular cognitive impairment after cerebral infarction .Methods 112 cases of clinically diagnosed cerebral infarc-tion were selected and divided into the normal cognition (NC) group and vascular cognitive impairment(VCI) group .The Changsha version of MoCA and the mini-mental state examination(MMSE) were adopted to detect the cognitive function ,the correlation of two scales was analyzed and the cutoff values of the Changsha version of MoCA were preliminarily studied .Results The total scores of the Changsha version of MoCA and MMSE in the VCI group were 15 .12 ± 4 .60 and 20 .44 ± 3 .22 respectively ,which were lower than 22 .75 ± 1 .79 and 25 .21 ± 1 .74 in the NC group ,the difference had statistical significance (P< 0 .05);the total scores of the Changsha version of MoCA was positively correlated with the total scores of MMSE (r=0 .84 ,P<0 .01);the best cut-off value of the Changsha version of MoCA was 20/21 ,the sensitivity and specificity were 92% and 95% respectively .Conclusion The Changsha version of MoCA can screen VCI well and has a high screening value ,and its optimal cutoff value is 20/21 .