Fig. 9.
Putative molecular mechanisms of argon combined with hypothermia-mediated neuroprotection. Argon combined with hypothermia activated phosphoinositide-3-kinase (PI-3K)/Akt pathway, enhanced heme oxygenase (HO)-1 and Bcl-2 expression and reduced phospho-glycogen synthase kinase (p-GSK)-3β Tyr216 expression. This leads to reduced tissue damage and inflammation in neonatal rat after hypoxia–ischemia brain injury. NF-κB = nuclear factor-κB.

Putative molecular mechanisms of argon combined with hypothermia-mediated neuroprotection. Argon combined with hypothermia activated phosphoinositide-3-kinase (PI-3K)/Akt pathway, enhanced heme oxygenase (HO)-1 and Bcl-2 expression and reduced phospho-glycogen synthase kinase (p-GSK)-3β Tyr216 expression. This leads to reduced tissue damage and inflammation in neonatal rat after hypoxia–ischemia brain injury. NF-κB = nuclear factor-κB.

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