Blockade of Interleukin-6 Receptor Suppresses Reactive Astrogliosis and Ameliorates Functional Recovery in Experimental Spinal Cord Injury

摘要: Endogenous neural stem/progenitor cells (NSPCs) have recently been shown to differentiate exclusively into astrocytes, the that are involved in glial scar formation after spinal cord injury (SCI). The microenvironment of cord, especially inflammatory cytokines dramatically increase acute phase at site, is considered be an important cause inhibitory mechanism neuronal differentiation following SCI. Interleukin-6 (IL-6), which has demonstrated induce NSPCs undergo astrocytic selectively through JAK/STAT pathway vitro, also play a critical role as proinflammatory cytokine and associated with secondary tissue damage In this study, we assessed efficacy rat anti-mouse IL-6 receptor monoclonal antibody (MR16-1) treatment SCI mice. Immediately contusive modified NYU impactor, mice were intraperitoneally injected single dose MR16-1 (100 microg/g body weight), lesions histologically, functional recovery was evaluated. not only suppressed diffentiation-promoting effect signaling vitro but inhibited development astrogliosis vivo. decreased number invading severity connective formation. addition, observed significant treated compared control These findings suggest neutralization represents attractive option for