ns-7 has been researched along with Arterial-Occlusive-Diseases* in 2 studies
2 other study(ies) available for ns-7 and Arterial-Occlusive-Diseases
| Article | Year |
|---|---|
Reversal by NS-7, a neuroprotective compound, of the decrease in transcription factor CREB mRNA expression in rat brain after permanent middle cerebral artery occlusion.
The effect of a neuroprotective agent NS-7 on changes in mRNA expressions for cyclic AMP responsive element binding protein (CREB) and several neurotrophins was examined in the rat cerebral cortex after permanent middle cerebral artery occlusion (MCAO). Significant reduction in mRNA expressions for CREB was observed at 24h after MCAO. NS-7 (0.5mg/kg), when injected at 6h after MCAO, significantly reversed the decreased expression for CREB mRNA. In addition, the mRNA expression for basic fibroblast growth factor (bFGF) was also significantly enhanced by NS-7 in MCA-occluded but not in sham-operated rats. On the other hand, the mRNAs for interluekin-6 and inducible-type nitric oxide synthase were markedly induced in the cerebral cortex of MCA-occluded rats, which was not significantly reversed by NS-7. Therefore, it is suggested that the reversal of decrease in CREB mRNA and concomitant increase in mRNA expression for bFGF may contribute to the neuroprotective action of NS-7. Topics: Animals; Arterial Occlusive Diseases; Brain; Brain-Derived Neurotrophic Factor; Cerebral Arteries; Cyclic AMP Response Element-Binding Protein; Fibroblast Growth Factor 2; Male; Neuroprotective Agents; Proto-Oncogene Proteins c-bcl-2; Pyrimidines; Rats; Rats, Sprague-Dawley; RNA, Messenger | 2001 |
Inhibition of ischemia-induced fodrin breakdown by a novel phenylpyrimidine derivative NS-7: an implication for its neuroprotective action in rats with middle cerebral artery occlusion.
The effect of a novel neuroprotective compound, NS-7 [4-(4-fluorophenyl)-2-methyl-6-(5-piperidinopentyloxy)pyrimidine hydrochloride], on ischemia-induced fodrin breakdown was examined both in vitro and in vivo. The fodrin breakdown was measured by western blot followed by a densitometric analysis. In slices of the rat cerebral cortex, a pronounced fodrin breakdown was observed under hypoxic and hypoglycemic conditions. The enhancement of fodrin breakdown was completely blocked by omission of extracellular Ca2+ and significantly inhibited by calpain inhibitors such as E-64 and calpain inhibitor-I, thereby suggesting that the fodrin breakdown induced by hypoxia/hypoglycemia is due to the activation of Ca2+-stimulated neutral protease calpain. NS-7 (1-30 microM) produced a concentration-dependent inhibition of hypoxia/hypoglycemia-induced fodrin breakdown. In rats with unilateral middle cerebral artery occlusion (MCAO), a pronounced fodrin breakdown was observed in the cerebral cortex and striatum, although the time course for the development of the fodrin breakdown was much slower in the cerebral cortex than in the striatum. NS-7 (0.5 mg/kg i.v.), when injected immediately after MCAO, suppressed not only the fodrin breakdown but also the infarction in the cerebral cortex. From these results it is suggested that inhibition of calpain activation is implicated in the neuroprotective action of NS-7. Topics: Animals; Arterial Occlusive Diseases; Brain Ischemia; Calcium; Calpain; Carrier Proteins; Cerebral Cortex; Cerebral Infarction; Enzyme Activation; Glucose; Hypoglycemia; Hypoxia; Male; Microfilament Proteins; Neostriatum; Nerve Tissue Proteins; Neuroprotective Agents; Organ Culture Techniques; Oxygen; Piperazines; Pyrimidines; Rats; Rats, Sprague-Dawley | 1997 |