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Fig. 6 | Journal of Neuroinflammation

Fig. 6

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

Fig. 6

Schematic depicting mechanism by which hypoxic preconditioning protects neuron against tGCI in the hippocampal CA1 through inhibition of MLKL-dependent necroptosis. The expression of RIP3 and the interaction of RIP1-RIP3 were increased in CA1 after reperfusion of tGCI. In addition, tGCI enhanced the expression of IL-1R1, which in turn, increased the RIP3-p-MLKL interaction, promoted the plasma membrane translocation of p-MLKL and the influx of Ca2+, ultimately inducing neuronal necroptosis. Hypoxic preconditioning downregulated the expression of IL-1R1, disrupted the interaction between IL-1R1 and the necrosome, attenuated the expression and the plasma membrane translocation of p-MLKL, thus decreasing the Ca2+ influx and alleviating neuronal death in CA1 after tGCI. HPC hypoxic preconditioning

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Journal of Neuroinflammation

ISSN: 1742-2094