Pregabalin as a neuroprotector after spinal cord injury in rats

Ha, Kee-Yong; Kim, Young-Hoon; Rhyu, Kee-Won; Kwon, Soon-Eok

doi:10.1007/s00586-008-0653-6

Cited by 60 publications

(54 citation statements)

References 32 publications

(49 reference statements)

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“…Through our previous study, we were able to verify the possibility of pregabalin as a neuroprotector after SCI (14). In that study, we only presented the anti-apoptotic and anti-inflammatory effects by histopathology.…”

Section: Discussionmentioning

confidence: 99%

Pregabalin as a Neuroprotector after Spinal Cord Injury in Rats: Biochemical Analysis and Effect on Glial Cells

Carragee

Cheng

et al. 2011

J Korean Med Sci

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As one of trials on neuroprotection after spinal cord injury, we used pregabalin. After spinal cord injury (SCI) in rats using contusion model, we observed the effect of pregabalin compared to that of the control and the methylprednisolone treated rats. We observed locomotor improvement of paralyzed hindlimb and body weight changes for clinical evaluation and caspase-3, bcl-2, and p38 MAPK expressions using western blotting. On histopathological analysis, we also evaluated reactive proliferation of glial cells. We were able to observe pregabalin's effectiveness as a neuroprotector after SCI in terms of the clinical indicators and the laboratory findings. The caspase-3 and phosphorylated p38 MAPK expressions of the pregabalin group were lower than those of the control group (statistically significant with caspase-3). Bcl-2 showed no significant difference between the control group and the treated groups. On the histopathological analysis, pregabalin treatment demonstrated less proliferation of the microglia and astrocytes. With this animal study, we were able to demonstrate reproducible results of pregabalin's neuroprotection effect. Diminished production of caspase-3 and phosphorylated p38 MAPK and as well as decreased proliferation of astrocytes were seen with the administration of pregabalin. This influence on spinal cord injury might be a possible approach for achieving neuroprotection following central nervous system trauma including spinal cord injury.

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Section: Discussionmentioning

confidence: 99%

Pregabalin as a Neuroprotector after Spinal Cord Injury in Rats: Biochemical Analysis and Effect on Glial Cells

Carragee

Cheng

et al. 2011

J Korean Med Sci

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“…To quantitate extents of apoptosis, we recorded numbers of TUNEL positive cells in each group. Finally, overall mean counts for each set of specimens in each group were calculated, and mean group values were compared [13].…”

Section: Determination Of Apoptosis In Spinal Cordmentioning

confidence: 99%

Does dexmedetomidine reduce secondary damage after spinal cord injury? An experimental study

et al. 2009

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The aim of this experimental study was to investigate the possible protective effect of dexmedetomidine (DEX) on traumatic spinal cord injury (SCI). Twentytwo New Zealand rabbits were divided into three groups: sham (no drug or operation, n = 6), Control [SCI ? single dose of 1 mL saline intraperitoneally (i.p), after trauma; n = 8] and DEX (SCI ? 1 lg/kg dexmedetomidine in 1 mL, i.p, after trauma, n = 8). Laminectomy was performed at T10 and balloon angioplasty catheter was applied extradurally. Four and 24 h after surgery, rabbits were evaluated by an independent observer according to the Tarlov scoring system. Blood, cerebrospinal fluid (CSF), tissue samples from spinal cord were taken for biochemical and histopathological evaluations. After 4 h of SCI, all animals in control or DEX treated groups became paraparesic. On the other hand, 24 h after SCI, partial improvements were observed in both control and DEX treated groups. Traumatic SCI leads to increase in the lipid peroxidation and decreases enzymatic or nonenzymatic endogenous antioxidative defense systems. Again, SCI leads to apoptosis in spinal cord. DEX treatment slightly prevented lipid peroxidation and augmented endogenous antioxidative defense systems in CSF or spinal cord tissue, but failed to prevent apoptosis or neurodeficit after traumatic SCI. Therefore, it could be suggested that treatment with dexmedetomidine does not produce beneficial results in SCI.

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“…As of this writing, pregabalin is one of two prescription medications currently approved by the FDA (Food and Drug Administration) for the treatment of FMS. The use of pregabalin in FMS treatment is further supported by the drug’s ability to decrease excitotoxic neurodegeneration induced by the mechanisms described above [47], perhaps in part through its role as an opener of ATP-sensitive potassium ion (KATP) channels [48] that mediate neuroprotection [49]. …”

Section: Proposed Pharmaceuticalsmentioning

confidence: 99%

Combined use of pregabalin and memantine in fibromyalgia syndrome treatment: A novel analgesic and neuroprotective strategy?

Recla

Sarantopoulos

2009

Medical Hypotheses

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Fibromyalgia syndrome (FMS) is a chronic widespread pain syndrome that is estimated to affect 4 to 8 million U.S. adults. The exact molecular mechanisms underlying this illness remain unclear, rendering most clinical treatment and management techniques relatively ineffective. It is now known that abnormalities in both nociceptive and central pain processing systems are necessary (but perhaps not sufficient) to condition the onset and maintenance of FMS. These same systemic abnormalities are thought to be responsible for the loss of cephalic gray matter density observed in all FMS patients groups studied to date. The current scope of FMS treatment focuses largely on analgesia and does not clearly address potential neuroprotective strategies. This article proposes a combined treatment of pregabalin and memantine to decrease the pain and rate of gray matter atrophy associated with FMS. This dual-drug therapy targets the voltage-gated calcium ion channel (VGCC) and the N-methyl D-aspartate receptor (NMDAR) (respectively), two primary components of the human nociceptive and pain processing systems.

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Pregabalin as a neuroprotector after spinal cord injury in rats

Cited by 60 publications

References 32 publications

Pregabalin as a Neuroprotector after Spinal Cord Injury in Rats: Biochemical Analysis and Effect on Glial Cells

Pregabalin as a Neuroprotector after Spinal Cord Injury in Rats: Biochemical Analysis and Effect on Glial Cells

Does dexmedetomidine reduce secondary damage after spinal cord injury? An experimental study

Combined use of pregabalin and memantine in fibromyalgia syndrome treatment: A novel analgesic and neuroprotective strategy?

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