- Nicotinamide Reduces the Infarct Volume in a Rat Model of Transient Middle Cerebral Artery Occlusion.
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Min Sup Lee, Young Jun Ahn, Ki Young Choi, Gu Kang, Seong Sik Kang, Il Young Cheong, Kun Jai Lee, Keun Woo Kim
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Korean J Pathol. 2006;40(2):93-102.
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 Abstract
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- BACKGROUND
Cerebral ischemia depletes ATP and causes irreversible tissue injury. Nicotinamide is a precursor of NAD+ and it is also a poly (ADP-ribose) polymerase (PARP) inhibitor that increases the neuronal ATP concentration and so protects against stroke. Therefore we examined whether nicotinamide could protect against cerebral ischemia by using a model of transient middle cerebral artery occlusion (MCAO) (reperfusion 2 h post ischemia) in Sprague-Dawley rats.
METHODS
Nicotinamide (500 mg/kg) or normal saline was administered intraperitoneally 24 and 0 h before and after MCAO, respectively. The infarction volumes were determined with triphenyltetrazolium chloride staining 24 h after reperfusion. The nitrotyrosine, PAR polymer and PARP-1 expressions were examined by immunohistochemistry with using brain slices obtained from the rats that were sacrificed at 0, 15, 30, 60 and 120 min after reperfusion.
RESULTS
The infarction volumes were significantly attenuated (21.8%, p<0.05). The nitrotyrosine expressions were increased at 0, 15 and 30 min, and those expressions for PARP polymer and PARP-1 were increased at 60 and 120 min, respectively. Nicotinamide partly reduced the expressions for nitrotyrosine and PAR polymer except for PARP-1.
CONCLUSIONS
These results suggest that nicotinamide may attenuate ischemic brain injury through its antioxidant activity and the inhibition of PARP-1.
- Minocycline Attenuates the Development of Allodynia: An Immunohistochemical Study on CD11b, GFAP and c-Fos in the Spinal Dorsal Horn in SD Rat.
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Gu Kang, Ki Young Choi, Min Sup Lee, Young Jun Ahn, Seong Sik Kang, Il Young Cheong, Wanjoo Chun, Sung Soo Kim
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Korean J Pathol. 2004;38(5):311-318.
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Abstract
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- BACKGROUND
Minocycline, a semisynthetic second-generation tetracycline, is an antibiotic that has excellent ability to penetration into the CNS via the brain-blood barrier.
Minocycline has emerged as a potent inhibitor of microglial activation, and it is an effective neuroprotective agent in experimental brain ischemia. Glial cell activation and proliferation are known to be associated with neuropathic pain in the peripheral nerve injuries.
METHODS
The fifty percent threshold of withdrawal responses was measured in the hindpaws of SD rats following tight ligation of left fifth lumbar spinal nerve. Rats were sacrificed at 1, 3, 5, and 7 days and at 0.5, 1, 2, and 4 h post ligation (n=5/group/time point). Immunohistochemistry for GFAP, CD11b and c-Fos was done on the spinal cord at the level of the fifth lumbar nerve. Minocycline (45 mg/kg) and normal saline (300-400 microL) were administered intraperitoneally, 1 day and 1 h before the operations, and every day postoperatively until the rats were sacrificed.
RESULTS
Treatment with minocycline reduced allodynia and the expressions of CD11b at 5 days and c-Fos at 1 and 2 h post operation compared with the saline treatment (control).
CONCLUSIONS: It was thought that minocycline reduced the allodynia induced by tight ligation of the fifth lumbar spinal nerve in rats through the inhibition of microglial activation and c-Fos expression.
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