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ABSTRACT: To explore the protective effects of intranasal (IN) dosing of nerve growth factor (NGF) on brain injury induced by organophosphorus compounds (OP) in rats.
The OP-treated Sprague-Dawley rats received an intraperitoneal injection of atropine sulphate and pralidoxime at 1 min after intoxication. Then NGF or saline was dosed via the olfactory pathway. All rats were sacrificed 24 hours after OP exposure. Damaged nerve cells were estimated on corpus striatum strained with hematoxylin-eosin (H&E) method. And the activity of acetylcholinesterase (AchE) and the concentrations of malondialdehyde (MDA) and reduced glutathione hormone (GSH) in corpus striatum were measured by colorimetric method.
As assessed by H&E staining, a large number of degenerated and necrotic nerve cells were observed in corpus striatum in rats from in IN saline group. But in IN NGF group, the number of degenerated neurons was smaller than in IN NS group. Following OP exposure, the activity of AchE decreased in corpus striatum in both IN saline and IN NGF groups (0.46 ± 0.11 vs 0.35 ± 0.09 U/mg prot). No significant differences existed between two groups. But the concentrations of MDA in corpus striatum of IN NGF group rats reduced markedly by 25.14% (4.02 ± 0.85 vs 5.37 ± 1.33 nmol/mg prot) and the level of GSH increased sharply by 15.73% (52.82 ± 2.80 vs 45.64 ± 4.88 mg/g prot) as compared with IN saline group (P < 0.05).
Intranasal dosing of NGF may improve neuropathology and protect rats against OP-induced oxidative damage in corpus striatum.
Zhonghua yi xue za zhi 09/2012; 92(33):2366-9.
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Mao-Gang Chen,
Wu-Sheng Zhu,
Qin Yin,
Bo-Na Wu,
Qi-Zhang Wang,
Min-Min Ma,
De-Zhi Liu,
Yong-Kun Li,
Chao-Lai Liu,
Xian-Jun Huang,
Zhao-Yao Chen,
Wan-Xiang Wang, Ge-Lin Xu,
Xin-Feng Liu
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ABSTRACT: To investigate the association of plasma homocysteine and OSA (obstructive sleep apnea) syndrome in ischemic stroke (IS).
A total of 92 male IS patients were classified by apnea hypopnea index (AHI) into 2 groups: non-OSA group (AHI < 5/h) and OSA group (AHI > or = 5). All patients were tested for plasma homocysteine when polysomnography was finished at (14 +/- 2) d after the onset of IS.
The mean level of homocysteine was significantly higher in the OSA group than that in the non-OSA group (17 +/- 5 vs 11 +/- 3 micromol/L, P < 0.01). Pearson correlation analysis revealed a positive correlation between the homocysteine level and the severity of AHI (r = 0.482, P < 0.01). Further multiple linear regression analysis showed that AHI and folate were independent predictors of homocysteine level (R2 = 0.553, P < 0.01, beta for AHI = 0.671, beta for folate = -0.256).
The severity of OSA is significantly associated with an elevated level of homocysteine in IS patients. And this association is independent of other causative factors of an elevated level of homocysteine.
Zhonghua yi xue za zhi 07/2011; 91(25):1753-6.
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ABSTRACT: To analyze the predictors of Wingspan in-stent restenosis (ISR) for the treatment of symptomatic intracranial arterial stenosis.
Between January 2007 and November 2009, 42 patients with symptomatic intracranial arterial stenosis registered in Nanjing stroke registry program (NSRP) were treated with Wingspan stent system. Clinical and follow-up results were retrospectively analyzed. They were divided into the non-restenosis and restenosis groups according to their follow-up imaging data. ISR was defined as > 50% stenosis within 5 mm or adjacent to stent or an absolute luminal loss > 20%. The analysis of stepwise multivariate Cox regression was performed to evaluate the independent predictive factors.
ISR was found in 15 patients (15/42, 35.7%) with 16 lesions (16/43, 37.2%) at a median follow-up period of 7 months (range: 4 - 23). Diabetes (HR = 0.281; 95%CI = 0.088 - 0.898; P = 0.032) and stent diameter (HR = 0.213; 95%CI = 0.049 - 0.918; P = 0.038) were two independent predictors for ISR.
Diabetes and stent diameter may be two independent predictors for ISR after a treatment of Wingspan system.
Zhonghua yi xue za zhi 05/2011; 91(19):1303-7.
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ABSTRACT: To evaluate the effect of lesion length on in-stent restenosis (ISR) after intracranial stenting.
Between March 2004 and September 2009, 65 patients with symptomatic intracranial arterial stenosis were successfully implanted with single bare metal balloon-mounted stent. All received a conventional angiographic follow-up. The patients were divided into three groups according to lesion length: short lesions (< 5 mm), medium lesions (5-10 mm) and long lesions (> 10 mm). ISR was defined as > 50% stenosis within stent or absolute luminal loss > 20%. The influence of different lesion lengths on ISR was evaluated. Furthermore, the independent predictive factors for ISR were selected.
There were short lesions (n = 28), medium lesions (n = 29) and long lesions (n = 8). The median interval of angiographic follow-up was 7 months with a range of 5-30 months. Of 65 patients, 19 (29.2%) had ISR. The ISR rates were 14.3%, 37.9% and 50% in short lesions, medium lesions and long lesions respectively (P = 0.045). Multivariate Cox regression analysis showed that lesion length (HR = 1.210; 95%CI = 1.011-1.446; P = 0.037) and diabetes (HR = 2.630; 95%CI = 1.032-6.705; P = 0.043) were associated with ISR.
Lesion length and diabetes are two independent predictors for ISR after intracranial stenting.
Zhonghua yi xue za zhi 08/2010; 90(29):2040-3.
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ABSTRACT: To investigate the relationship between cerebral microbleeds (CMB), cardiovascular risk factors, and plasma fibrinogen in patients with acute ischemic stroke.
Sixty-eight patients with acute ischemic stroke from June 2008 to March 2009 were enroued prospectively. All patients received cranial magnetic resonance imaging at the first week, and T2(*)-weighted gradient echo MRI sequence was performed to detect CMB. Plasma fibrinogen, uric acid levels and other biochemical parameters were measured on the next day of admission. All data were selected from Nanjing Stroke Registry Program.
Among a total 68 patients, 29 (43%) patients had 109 lesions of cerebral microbleeds on gradient-echo MRI. Age, hypertension, fibrinogen and uric acid were significantly associated with the presence of CMB (P = 0.004, 0.024, 0.020, 0.027 respectively). Through a logistic regression analysis, age, hypertension and plasma fibrinogen were significantly associated with the presence of cerebral microbleeds [(P = 0.02, OR = 1.10, 95%CI 1.02 to 1.19; P = 0.003, OR = 9.35, 95%CI 2.17 to 40.23; P = 0.019, OR = 1.01, 95%CI 1.00 to 1.02].
There is a high prevalence of CMB in patients with acute ischemic stroke. And it has a strong relationship with high plasma fibrinogen.
Zhonghua yi xue za zhi 02/2010; 90(7):451-3.
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ABSTRACT: The aim of the present study was to assess the dose-effectiveness of intranasal (IN) vascular endothelial growth factor (VEGF)in the treatment of experimental stroke. Sprague-Dawley rats were randomized into four groups as IN low (100 microg/ml), IN middle (200 microg/ml) and IN high (500 microg/ml) VEGF-treated group, and IN saline-treated group (n=12), given recombinant human VEGF 165 or saline intranasally. Focal cerebral ischemia was induced by transient (90 min) middle cerebral artery occlusion (MCAO) method. Behavioral neurological deficits were assessed 1, 7 and 14 d after the onset of MCAO. Rats were sacrificed at 14 d, the brain sections were stained and an image analysis system was used to calculate the infarct volume. Microvessels were labeled by FITC-dextran and the segment lengths, diameters and number of microvessels were measured by Image Pro-Plus Version 6.0 software. Fourteen days post MCAO, infarct volume significantly reduced (P<0.01) in rats which received the middle dose of IN VEGF when compared to IN saline. And middle dose of VEGF significantly improved behavioral recovery (P<0.01). No significant difference in the behavioral recovery and infarct volume was observed between the saline-treated group and the low or high VEGF-treated groups (P>0.05). Compared to IN saline, middle and high doses of VEGF significantly increased the segment length, diameter and number of microvessels (P<0.01). No significant difference in the segment length, diameter and number of microvessels was observed between the IN saline-treated group and the low VEGF-treated group (P>0.05). The middle dose of IN VEGF was most effective on reducing infarct volume, improving behavioral recovery and enhancing angiogenesis in stroke brain, which can be used in the following treatments to further evaluate the effect of VEGF.
Neuroscience Letters 06/2009; 461(3):212-6. · 2.11 Impact Factor
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ABSTRACT: To investigate the effects of montelukast on atherosclerosis and monocyte chemoattractant protein-1 expression in a hypercholesterolemic rabbit model.
Thirty four male New Zealand white rabbits were randomized into four groups including normal control group (n = 6), placebo group (n = 8), atorvastatin group (1.5 mgxkg(-1)xd(-1), beginning at 8(th) weeks for 4 weeks, n = 10) and montelukast group (1 mgxkg(-1)xd(-1), beginning at 8(th) weeks for 4 weeks, n = 10). Rabbits except those in normal control group were fed a high cholesterol diet for 12 weeks. Serum lipids were measured at 0, 8 and 12 weeks after intervention. The intima/media ratio, percentages of macrophages or smooth muscle cells in intima and the expression of MCP-1 mRNA were examined.
Atherosclerosis was evidenced in placebo group and atorvastatin or montelukast treatment significantly reduced neointima (0.32 +/- 0.12 and 0.34 +/- 0.10 vs. 1.12 +/- 0.36, P < 0.05) and macrophage content [(9.8 +/- 4.6)% and (11.2 +/- 3.7)% vs. (34.6 +/- 8.8)%, P < 0.05], increased SMC content [(18.6 +/- 6.9)% and (19.2 +/- 8.6)% vs. (5.2 +/- 2.3)%, P < 0.05] and inhibited expression of MCP-1 mRNA (0.42 +/- 0.08 and 0.40 +/- 0.06 vs. 2.36 +/- 0.48, P < 0.01). Montelukast had similar anti-atherogenetic effects as atorvastatin but had no influence on plasma lipids.
Montelukast could attenuate atherosclerosis in this hypercholesterolemic rabbit model which might be attributed to its anti-inflammatory effects.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 03/2009; 37(3):257-61.
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ABSTRACT: Basic fibroblast growth factor (bFGF) is a very important mitogenic factor with proved neurogenesis effects in the central nervous system. Intranasal administration can bypass blood-brain barrier and deliver drugs into the brain directly. We investigated whether intranasal administration of bFGF at later time points after ischemia could promote adult neurogenesis and improve neurologic functions. Rats received bFGF or saline intranasally once daily for 6 consecutive days, starting at 1 day after transient middle cerebral artery occlusion (MCAO). Bromodeoxyuridine (BrdU) was injected at 5 and 6 days after MCAO. Rats were killed at 7 or 28 days after MCAO. Neurogenesis was assessed by immunostaining for BrdU and cell type-specific markers. Neurological functions were evaluated by the modified Neurological Severity Scores. Compared with the control animals, intranasal administration of bFGF improved behavioral recovery without affecting infarct size, and enhanced proliferation of progenitor cells in the subventricular zone and the subgranular zone of the dentate gyrus (DG). Furthermore, the new proliferated cells could differentiate into neurons (BrdU+NeuN+ cells) in the striatum and DG at 28 days after MCAO. Intranasal administration of bFGF offers a non-invasive alternative for the treatment of stroke.
Neuroscience Letters 10/2008; 446(1):30-5. · 2.11 Impact Factor
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ABSTRACT: Basic fibroblast growth factor (bFGF) is a neurotrophic and vasoactive factor, and has therapeutic potential for some central nervous system (CNS) disorders. In this study, we used the intranasal pathway to administer bFGF in adult rats, and evaluated its neuroprotective benefits and effects on endogenous neural stem cells. The bFGF levels after intranasal administration in normal rats were determined by western blot. Transient focal ischemia was achieved by occlusion of the right middle cerebral artery for 2 h. bFGF was given intranasally 2 h after reperfusion and daily thereafter on 3 successive days. Dividing progenitor cells were labeled with bromodeoxyuridine (BrdU) on day 3 of reperfusion. Rats were killed the next day after BrdU labeling. bFGF levels were significantly raised in the olfactory bulb (OB) and striatum following intranasal administration. Intranasal bFGF treatment improved neurological function and reduced infarct volume after cerebral ischemia/reperfusion, while no influence was observed on the blood pressure. And the BrdU incorporation was enhanced in the ipsilateral subventricular zone (SVZ) and striatum following intranasal administration of bFGF. These results demonstrated that bFGF can be directly delivered into brain following intranasal administration, and protects against cerebral ischemia/reperfusion. The protective effects may be attributed to the reduction of infarct volume and enhancement of endogenous progenitors in brain. Therefore, intranasal administration of bFGF may provide an alternative treatment for brain ischemia and some other CNS disorders.
Neuroscience Letters 06/2008; 437(2):93-7. · 2.11 Impact Factor
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ABSTRACT: Compelling evidence has shown that extracellular signal-regulated kinase (ERK) is widely expressed in many tissues, including the brain. In the present work, we investigated the temporospatial alterations of ERK1 immunoreactivity in hippocampus and perifocal cortex, and the expression involved in NGF/VEGF-induced neuroprotective effect. We demonstrated that ERK1 expression was first increased in hippocampal CA3/DG 1 h after reperfusion, then it was also increased 6 h after reperfusion in other brain regions, with a peak at day 1-3, and then gradually decreased to basal level at day 14. The expression of caspase-3 was strongly increased 1 h after reperfusion, with peak demonstrated at 3d. NGF/VEGF significantly inhibited the expression of ERK1 and caspase-3. These results suggest that ERK1 signaling pathway may be involved in neuronal cell death and NGF/VEGF-induced neuroprotective effect and there appeared an association between ERK and caspase-3. Inhibition of the ERK signaling pathway might therefore provide an efficient way to prevent neuronal cell death after ischemic cerebral injuries.
Neuroscience Letters 04/2008; 434(2):212-7. · 2.11 Impact Factor
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ABSTRACT: This study is aimed to evaluate the brain distribution of transforming growth factor-beta1 (TGF-beta1) following intranasal administration and the subsequent biological effects of TGF-beta1. Adult rats were given recombinant human TGF-beta1 (rhTGF-beta1) or vehicle solution intranasally. TGF-beta1 concentrations were significantly raised in several brain regions and the trigeminal nerve following intranasal delivery. The elevation appeared within 30 min and was sustained for at least 6 h, reaching its greatest level at 60 min. A concentration gradient in the central nervous system (CNS) regions was produced during the first 2 h after intranasal administration, with the OB presenting a significantly higher concentration than any other CNS regions. The nasally administered TGF-beta1 subsequently regulated gene expressions of its two receptors (TGF-beta receptor types I and II) in vivo, but did not affect mRNA level of TGF-beta1 itself. Our results suggest that TGF-beta1 can be transported into the CNS via the olfactory and trigeminal pathways, and may consequently exert its biological effects by regulating gene expressions of its receptors. Intranasal administration of neurotrophic factors may offer a potential strategy for treating some CNS disorders.
Brain Research Bulletin 10/2007; 74(4):271-7. · 2.82 Impact Factor
