Propofol via Antioxidant Property Attenuated Hypoxia-Mediated Mitochondrial Dynamic Imbalance and Malfunction in Primary Rat Hippocampal Neurons

Figure 7

Hypoxia- and propofol-modulated phosphorylation of Drp1 and mitochondrial dynamics was mediated via ERK and PKA pathway. The upper panel was a representative experiment, and the lower panel was the summary of densitometric data from 5 separate experiments. GAPDH served as loading control. (a) Hypoxia induced the phosphorylation of ERK, which was abolished by propofol, α-tocopherol, ebselen, and ERK inhibitors. Data were expressed as normalized ratio of protein band density of phosphorylated ERK against ERK, which was normalized with GAPDH, and were presented as . (b) Hypoxia induced the phosphorylation of Drp1^ser616, which was abolished by propofol, α-tocopherol, ebselen, and ERK inhibitors. Data were expressed as normalized ratio of protein band density of phosphorylated Drp1 against Drp1, which was normalized with GAPDH, and were presented as . (c) Hypoxia reduced the phosphorylation of PKA, which was abolished by propofol, α-tocopherol, ebselen, and PKA activator. Data were expressed as normalized ratio of protein band density of phosphorylated PKA against PKA, which was normalized with GAPDH, and were presented as . (d) Hypoxia reduced the phosphorylation of Drp1^ser637, which was abolished by propofol, α-tocopherol, ebselen, and PKA activator. Data were expressed as normalized ratio of protein band density of phosphorylated Drp1 against Drp1, which was normalized with GAPDH, and were presented as . (e) Hypoxia-mediated mitochondrial fragmentation was attenuated by ERK inhibitors and PKA activator. Data were presented as the percentage of of treated neurons compared with that of untreated control neurons, which was set as 100%, and represents the number of independent repeats.

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