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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Inhibition of MLKL-dependent necroptosis via downregulating interleukin-1R1 contributes to neuroprotection of hypoxic preconditioning in transient global cerebral ischemic rats

Fig. 1

Hypoxic preconditioning prevents the tGCI-induced upregulation of phosphorylated MLKL in CA1. A Immunohistochemistry of MLKL in rat brains. Representative images show Sham group (a, b), 24 h after reperfusion of tGCI groups (c, d) and HPC groups (e, f), respectively. B Quantitative analyses of MLKL-immunoreactivities in CA1. C Immunohistochemistry of p-MLKL (Ser345) in the rat brains. Representative images show Sham group (a, b), 168 h after reperfusion of tGCI groups (c, d) and HPC groups (e, f), respectively. D Quantitative analyses of p-MLKL-immunoreactivities in CA1. E, F Representative immunoblots showing the expression of MLKL and p-MLKL (Ser345) in CA1, respectively. The histogram presents the quantitative analyses of MLKL and p-MLKL (Ser345) levels. Data are expressed as percentage of value of Sham animals. Each bar represents the mean±S.D. *p<0.05 vs. Sham animals and #p<0.05 vs. tGCI groups at the same time point. G Representative photomicrographs with fluorescent staining of p-MLKL (Ser345) (red), NeuN/Iba-1/GFAP (green) and DAPI (blue) in CA1. HPC hypoxic preconditioning

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Journal of Neuroinflammation

ISSN: 1742-2094