Study summary · research use only
Cerebrolysin reduces excitotoxicity by modulation of cell-death proteins in delayed hours of ischemic reperfusion injury
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study used adult male Wistar rats subjected to ischemic reperfusion injury and primary cortical culture cells exposed to glutamate to examine cerebrolysin, a mixture of neuropeptides. Rats received cerebrolysin (0.15 or 0.30 mg/kg) or vehicle intraperitoneally at 3, 6, and 12 h after reperfusion and were assessed at 24 h; cortical cells received cerebrolysin (2.5 or 5 mg/ml) or vehicle at 3, 6, and 12 h post-glutamate exposure, with viability assessed at 24 h. The authors report that cerebrolysin reduced neuronal cell death in both models, that this effect at 6 h was enhanced by pretreatment with the NR2B antagonist RO25-6981, and that cerebrolysin reduced upregulation of extrasynaptic NR2B along with expression of the cell-death proteins JNK, PTEN, Calpain, Caspase-3, and SREBP1.
Abstract
Recent preclinical and clinical reports suggest that cerebrolysin shows neuroprotective properties similar to endogenous neurotrophic factors in neurodegenerative disorders including ischemic stroke. However, little is known about its underlying antiexcitotoxic action. Adult male Wistar rats were intraperitoneally treated with cerebrolysin (0.15 or 0.30 mg/kg) or vehicle at 3, 6 and 12 h after ischemic reperfusion and were assessed 24 h after reperfusion in ischemic rats. We added cerebrolysin (2.5 or 5 mg/ml) or vehicle in primary cortical culture cells at 3, 6 and 12 h of post-glutamate exposure and performed cell viability assays at 24 h. Our in-vivo and in-vitro findings showed that cerebrolysin substantially reduced neuronal cell death in delayed hours of post ischemic- and glutamate-insult conditions respectively. Further, we have assessed the influence of NR-2 A/-2B receptor antagonism on neuroprotective action of cerebrolysin at 6 h in in-vivo as well as in-vitro conditions. Neuroprotective effect of cerebrolysin at 6 h of reperfusion was enhanced by pretreatment of NR2B antagonist RO25-6981.We found that cerebrolysin restrained upregulation of extrasynaptic NR2B responsible for triggering apoptotic pathways. Cerebrolysin reduced expression of important cell death proteins such as, JNK, PTEN, Calpain and Caspase-3 components. Importantly, we also found that cerebrolysin reduced SREBP1 expression, which gets activated only after 6 h of ischemia. These results demonstrate that cerebrolysin reduces excitotoxicity and protect neuronal cells in delayed hours of ischemic reperfusion injuries by decreasing cell death proteins.
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