Fig. 7: Effect of HPC on the level of ROS and the glutathionylation of membrane Atp1b1 after tGCI in CA1. | Cell Death & Disease

Fig. 7: Effect of HPC on the level of ROS and the glutathionylation of membrane Atp1b1 after tGCI in CA1.

From: Neuroglobin mediates neuroprotection of hypoxic postconditioning against transient global cerebral ischemia in rats through preserving the activity of Na+/K+ ATPases

Fig. 7

A ROS level was evaluated with DCFH-DA in Sham, tGCI, and HPC groups with or without administration of Ngb ODNs. Representative photomicrographs show that ROS fluorescence (green) is distributed around DAPI (blue). B, C Quantitative analysis of DCFH-DA signal in the CA1 subregion. Each bar represents the mean ± S.D. *p < 0.05 vs. Sham-operated animals, #p < 0.05 vs. tGCI group, and &p < 0.05 vs. HPC group with injection of S-ODNs (n = 6 in each group). Scale bar: 125 μm. D Immunoprecipitation blots showing the glutathionylated Atp1b1 in CA1 of ischemic and hypoxic postconditioned rats. E Immunoprecipitation blots showing the glutathionylated Atp1b1 in the CA1 of Sham and HPC group with or without administration of Ngb ODNs. Glutathionylated proteins was immunoprecipitated (IP) using anti-GSH antibody. Membranous Atp1b1 was detected by Immunoblot (IB). The experiments were repeated twice (n = 3 in each group)

Back to article page