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First story: It is well known that there is always immediate bleeding in spinal cord injury (SCI) and bleeding induces spinal cord destruction.The logical treatment should be early hemostasis.We chose Etamsylate as the hemostatic drug.We studied its effect on the size of lesion area,protection of neurons,and locomotion recovery.All were satisfactory.Then we studied its effect on partial transection and found that there was a reduction of area of hemorrhage and size of lesion area.Second story: One of the major pathological features of SCI is the progressive enlargement of secondary injury surround-ed by reactive astrocytic scar.The mechanism of astrocytic scar formation remains unclear.Here we reported in mice that the reactive astrocytes died by receptor-interacting protein 3 and mixed lineage kinase domain-like protein (RIP3/MLKL)mediated necroptosis,rather than apoptosis or autophagy.Inhibiting RIP1 or depleting RIP3 significantly attenuated astro-cyte death and secondary injury.Further,Toll-like receptor 4 (TLR4) and myeloid differentiation primary response gene 88 (MyD88) are highly expressed in necroptotic astrocytes.In vitro antagonizing MyD88 in astrocytes could effectively block the necroptosis of astrocytes.More importantly,our data showed that in human,necroptotic markers and TLR4/MyD88 were co-expressed in astrocytes of injured spinal cord.Taken together,these results demonstrated that reactive astrocytes under-went necroptosis during the secondary injury of SCI,and suggested that inhibiting astrocytic necroptosis may be applied to prevent secondary injury.