The current study was performed to investigate the effect of aminoguanidine (AG) on spinal cord injury (SCI) in rat. AG (75, 150 and 300mg/kg, i.p. respectively ) was administered to rats immediately following SCI. It was found that AG (150mg/kg) significantly reduced spinal cord water content and improved motor function, however, AG at the doses of 75 and 300mg/kg had no effect. Compared to SCI group without treatment, AG at the dosage of 150mg/kg induced a reduction in the permeability of blood-spinal cord barrier (BSCB) after injury 48h (from 59.8+/-5.5microl/g to 39.8+/-3.8microl/g), a 38% decrease of Malondialdehyde (MDA) values and a 1-fold increase of the Glutathione (GSH) levels at 12h after SCI. And the expression of inducible nitric oxide synthase (iNOS) protein reached a peak at 24h after injury, which was significantly attenuated by treatment with AG (150mg/kg). In addition, the expression of AQP4 protein was down-regulated by the treatment of AG (150mg/kg) at 24h after SCI, and the changes still lasted at 48h after injury. Our results indicated that AG could induce spinal cord edema clearance and improve motor function, which could be correlated with antioxidative property, the down-regulation of iNOS and AQP4 protein expression after SCI.
"Thus, we postulate that arginase-1 upregulation associated with day 4 post-injury, along with decreased expression of iNOS, was partly due to macrophages modulating nitric oxide generation and inflammatory cytokines. Because iNOS expression was previously studied in an SCI model (Fan et al., 2010; Lee et al., 2009), we focus our discussion on the expression of arginase-1 as determined by the present study. Fig. 5 "
[Show abstract][Hide abstract] ABSTRACT: The expression of arginases, enzymes that catalyze the hydrolysis of arginine to ornithine and urea, was studied in the inflammatory lesions of spinal cord injury (SCI) in rats. The level of arginase-1 expression in rat spinal cords with clip compression injury was determined by Western blot analysis and immunohistochemistry. Western blot showed that the level of arginase-1 increased in the core lesion of SCI at day 1 post injury and continued to increase through days 4 (p<0.05) and 7 (p<0.01). Immunohistochemical analysis showed that arginase-1 was constitutively expressed in neurons and glial cells in sham control spinal cords. In SCI lesions, arginase-1 was additionally detected in inflammatory cells, particularly in isolectin B4-positive macrophages and reactive astrocytes within the core lesion. These findings suggest that the increased level of arginase-1 in SCI is associated with an increase in macrophages and reactive astrocytes, possibly contributing to the modulation of inflammation during the course of SCI.
Brain research 01/2012; 1445:11-9. DOI:10.1016/j.brainres.2012.01.045 · 2.84 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Recent studies indicated that epigallocatechin gallate (EGCG) had neuroprotective effects on spinal cord injury(SCI).The current study was performed to determine the anti-edema effect of EGCG after SCI in rats. EGCG(100mg/kg, i.p.) was administered to rats immediately following SCI. It was found that EGCG(100mg/kg) could significantly reduce spinal cord water content. In addition, EGCG(100mg/kg) significantly reduced the expression of aquaporin-4(AQP4) and glial fibrillary acidic protein(GFAP) level at 24,48 and 72 hours after injury, but it did not have this effect at 12 hours after injury. The changes of AQP4 and GFAP protein induced by EGCG(100mg/kg) treatment were accompanied by a reduction of spinal cord edema. Our results indicated that EGCG (100mg/kg) could reduce spinal cord edema after SCI, which could be correlated with the down-regulation the expression of AQP4 and GFAP protein level after SCI.
Brain research 07/2013; 1527. DOI:10.1016/j.brainres.2013.06.009 · 2.84 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Salvianolic acid B (Sal B), a bioactive compound isolated from the Chinese medicinal herb danshen, is commonly used for the prevention and treatment of cardiovascular disease. The present study was performed to investigate the effect of Sal B on the blood-spinal cord barrier (BSCB) after spinal cord injury (SCI) in a rat model. Sal B (1, 10, and 50 mg/kg i.v.) was administered to rats immediately following SCI. The permeability of the BSCB and spinal cord tissue water content were evaluated. Additionally, the expression levels of tight junction proteins and heme oxygenase-1 (HO-1) were monitored by Western blot analysis. Enzyme-linked immunosorbent assay analysis of spinal cord tissue homogenates was performed 24 h post-SCI to evaluate the expression of inflammation-related cytokines. In addition, the motor recovery of SCI rats was assessed using the Basso, Beattie, and Bresnahan scoring system. Compared to the SCI group, rats treated with Sal B (10, 50 mg/kg) exhibited significantly reduced spinal cord tissue water content and BSCB permeability. Further, the motor function of rats was also greatly improved by Sal B administration. The expression of pro-inflammatory factors TNF-α and NF-κB was found to be greatly increased 24 h post-SCI, and this upregulation was significantly attenuated by Sal B treatment. The expression of ZO-1 and occludin was upregulated by Sal B (10 mg/kg) treatment after SCI, and this effect was blocked by the HO-1 inhibitor ZnPP. Taken together, our results clearly indicate that Sal B attenuates SCI by promoting the repair of the damaged BSCB, demonstrating that this molecule is a novel and promising therapeutic agent for human SCI.
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