The effect of aminoguanidine on compression spinal cord injury in rats. Brain Res

Department of Orthopaedics, The First Affiliated Hospital, China Medical University, Shenyang 110001, Liaoning Province, China.
Brain research (Impact Factor: 2.84). 04/2010; 1342:1-10. DOI: 10.1016/j.brainres.2010.04.038
Source: PubMed


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.

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    • "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 "
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    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.
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    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.
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    ABSTRACT: This study investigated the protective effect of two nitric oxide synthase inhibitors N(omega)-Nitro-L-arginine methyl ester (L-NAME, 100 mg/kg i.p.) and aminoguanidine (AG, 400 mg/kg i.p.), and an antioxidant acetyl-L-carnitine (ALC, 250 mg/kg i.p., once daily for five days) against radiation-induced damage in Wistar rats. Blood samples were collected 6 hrs after whole-body irradiation with 8 Gy. Plasma concentrations of nitrite+nitrate (NOx) and malondialdehyde (MDA) were measured by high-performance liquid chromatography. A single injection of L-NAME one hour before exposure effectively prevented the radiation-induced elevation of plasma NO(x) and it reduced 2.6-fold the risk for death during the subsequent 30-day period. Pretreatment with ALC prevented the radiation-induced increase in plasma MDA and it had similar effect on mortality as L-NAME did. Presumably due to its short half-life, the partially iNOS-selective inhibitor and antioxidant AG given in a single dose before exposure did not attenuate MDA and NO(x) and it failed to significantly improve the 30-day survival. In conclusion, pretreatment with both the nonspecific NOS inhibitor L-NAME and the antioxidant ALC markedly reduce mortality to radiation sickness in rats. The radioprotective effect may be directly related to effective attenuation of the radiation-induced elevation of NO production by L-NAME and of oxidative stress by ALC.
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