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Figure 3. Schematic representation of the proposed neuroprotective mechanism of OsM. OsM binds to an OSMRß/gp130 receptor complex, initiating signaling pathways via JAK-STAT and MAPK. The activated receptor interacts with the NMDA receptor complex blocking NMDA-mediated excitotoxicity. OsM-mediated down-regulation of NR2C might lead to reduced responsiveness to NMDA. OsM-mediated increase in OSMRß expression could provide a positive feedback loop while up-regulation of NS-1 and TIMP-1 would result in inhibition of t-PA and matrix-metalloproteinase activity, respectively. These proteases have been shown to have detrimental effects during excitotoxic injury. JAK, janus kinase; STAT, signal transducer and activator of transcription; MAPK, mitogen-activated protein kinase.
