Vascular permeability to growth hormone in the rat central nervous system after focal spinal cord injury. Influence of a new anti-oxidant H 290/51 and age

Mustafa, A.; Sharma, Hari Shanker; Olsson, Yngve; Gordh, Torsten; Thorén, Per; Sjöquist, Per-Ove; Roos, Paul; Adem, Abdu; Nyberg, Fred

doi:10.1016/0168-0102(95)00937-o

Cited by 38 publications

(31 citation statements)

References 32 publications

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“…These observations suggest that lipid peroxidation and generation of free radicals contributes to the BSCB breakdown in SCI [285][286][287][288]. It is still not known whether BSCB disruption by free radicals within the endothelial cell membrane is associated with the receptor-mediated signal transduction mechanisms [93,287,289,290].…”

Section: Antioxidant Compound H-290/51 Is Neuroprotective In Scimentioning

confidence: 95%

Pathophysiology of Blood-Spinal Cord Barrier in Traumatic Injury and Repair

Sharma¹

2005

CPD

158

218

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Blood-spinal cord barrier (BSCB) plays an important role in the regulation of the fluid microenvironment of the spinal cord. Trauma to the spinal cord impairs the BSCB permeability to proteins leading to vasogenic edema formation. Several endogenous neurochemical mediators and growth factors contribute to trauma induced BSCB disruption. Studies carried out in our laboratory suggest that those drugs and neurotrophic factors capable to attenuate the BSCB dysfunction following trauma are neuroprotective in nature. Whereas, agents that do not exert any influence on the BSCB disruption failed to reduce cell injury. These observations are in line with the idea that BSCB disruption plays an important role in the pathophysiology of spinal cord injuries. The probable mechanism(s) of trauma induced BSCB dysfunction and its contribution to cell injuries are discussed.

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Section: Antioxidant Compound H-290/51 Is Neuroprotective In Scimentioning

confidence: 95%

Pathophysiology of Blood-Spinal Cord Barrier in Traumatic Injury and Repair

Sharma¹

2005

CPD

158

218

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“…[36]. Various parameters were measured in order to evaluate the extent of METH-induced neurotoxicity as well as the influence of ambient temperature.…”

Section: Methodsmentioning

confidence: 99%

Exacerbation of Methamphetamine Neurotoxicity in Cold and Hot Environments: Neuroprotective Effects of an Antioxidant Compound H-290/51

et al. 2015

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In this study, we examined the influence of cold and hot environments on methamphetamine (METH) neurotoxicity in both drug-naive rats and animals previously exposed to different types of nanoparticles (NPs). Since METH induces oxidative stress, we also examined how a potential chain-braking antioxidant H-290/51 (Astra-Zeneca Mölndal, Sweden) affects METH-induced neurotoxicity. Exposure of drug-naive rats to METH (9 mg/kg, s.c.) at 4°, 21° or 34°C for 3 hrs resulted in breakdown of the blood-brain barrier (BBB), brain edema and neuronal injuries, which all differed in their extent depending upon ambient temperatures. The changes were moderate at 21°C, 120–180% larger at 34°C, and almost absent at 4°C. In rats chronically treated with NPs (SiO2, Cu or Ag; 50–60 nm, 50 mg/kg, i.p. for 7 days), METH-induced brain alterations showed a 2- to 4-fold increase in brain pathologies after METH at 21°C; 4-to 6-fold increase at 34°C and 3- to 4-fold increase at 4°C. SiO2 exposure showed the most pronounced METH-induced brain pathology at all temperature ranges followed by Ag and Cu NPs. Pretreatment with a potent antioxidant compound H-290/51 (50 mg/kg, p.o. 30 min before METH) significantly reduced brain pathology in naive animals exposed to METH at 21°C and 34°C. In NPs-treated animals, however, attenuation of METH-induced brain pathology occurred only after repeated exposure of H-290/51 (−30 min, 0 min and +30 min). These observations are the first to show that NPs aggravate METH-induced brain pathology in both cold and hot environments and demonstrate that timely intervention with antioxidant H-290/51 could have neuroprotective effects.

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“…When GH defi cient adults were treated with GH for 1 month, there was a 10-fold increase in GH CSF levels compared with baseline suggesting that GH does indeed pass the blood CSF barrier [33] . Mustafa et al [34] showed that the vascular permeability to GH is very low in the CNS of normal rats and the permeability of GH is increased following a focal trauma to the cord, which is progressive in time and widespread within the CNS. In the present study, we have evaluated if GH had any benefi cial effect on the oxidative system of the H-I brain.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Human Growth Hormone on Superoxide Dismutase Activity, Glutathione and Malondialdehyde Levels of Hypoxic-Ischemic Newborn Rat Brain

Yapıcıoğlu

Satar²,

Canacankatan³

et al. 2006

Neonatology

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Objectives: We investigated the effect of human growth hormone (GH) on newborn rat brain superoxide dismutase, glutathione and malondialdehyde (MDA) levels in hypoxic-ischemic (H-I) newborn rats. Methods: Fourty-eight 7 days old newborn rats were randomized to a healthy (n: 15), H-I (n: 18) and GH administered H-I (GH-H-I, n: 15) group. Permanent, left common carotid ligation was performed in the H-I groups. In the GH-H-I group, 50 mg/kg human GH (Norditropin Simplex, Novo Nordisk A/S) was administered subcutaneously just before carotid artery ligation. Two hours after ligation, rats were subjected to 2 h of hypoxemia and then were decapitated. Right and left cerebral hemispheres (CHs) and cerebellum-brain stem (C-BS) were separated. Results: Glutathione levels of each region were not statistically different from each other in and between the groups. Superoxide dismutase levels were higher in C-BSs compared to CHs (for each comparison p < 0.01). CHs and C-BS MDA levels were similar in the control and H-I groups but MDA levels of both CHs of the GH-H-I group were significantly higher than the levels of the H-I group (p = 0.01; p = 0.024, respectively). Left CH MDA level of GH-H-I group was higher compared to left CH MDA of the control group (p = 0.045) while there was no difference between right CHs. In the GH-H-I group, left CH MDA level was higher than the C-BS (p = 0.03). MDA levels of the C-BSs did not differ between the groups (p > 0.05). Conclusion: Although we have not evaluated the effect of GH histopathologically, increased lipid peroxidation especially in the H-I (left) hemisphere of the GH treated rats might suggest that GH treatment may be harmful in H-I encephalopathy.

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Vascular permeability to growth hormone in the rat central nervous system after focal spinal cord injury. Influence of a new anti-oxidant H 290/51 and age

Cited by 38 publications

References 32 publications

Pathophysiology of Blood-Spinal Cord Barrier in Traumatic Injury and Repair

Pathophysiology of Blood-Spinal Cord Barrier in Traumatic Injury and Repair

Exacerbation of Methamphetamine Neurotoxicity in Cold and Hot Environments: Neuroprotective Effects of an Antioxidant Compound H-290/51

The Effect of Human Growth Hormone on Superoxide Dismutase Activity, Glutathione and Malondialdehyde Levels of Hypoxic-Ischemic Newborn Rat Brain

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