| Objective: Acute brain injuries can activate bidirectional crosstalk between the injured brain and the immune system. The immune system, particularly T lymphocytes and cytokines, has been implicated in the progression of brain injury after intracerebral hemorrhage(ICH). Co-stimulatory molecules B7-1(CD80)/B7-2(CD86) binding cognate receptor provides a secondary signaling to T cell activation. The aim of our study was to explore the effects of anti-B7-1 antibody on the development and prognosis of cerebral hemorrhage and to investigate the possible underlying mechanism.Methods: The procedure for inducing ICH by collagenase injection in mice has been described previously. The sham groups and the ICH groups through mouse inner canthus veniplex injection were treated with stroke-physiological saline solution and antiB7-1 antibody, respectively, at 10 minutes and 24 h after ICH. All animals were sacrificed at 72 h after surgery except the behavior group. Immune function was assessed via Splenocyte proliferation assay and oganism index, respectively. IFN-γ and IL-4 were detected by enzyme-linked immuno sorbent assay(ELISA). The cerebral edema was evaluated via brain water content. The levels of autophagy and apoptosis related proteins were measured by Western blotting analysis. In addition, Functional outcome was studied with poleclimbing test and morris water maze.Results: The treatment with anti-B7-1 antibody significantly lowered immune function, and reduced the latency of water maze on 18 and 20 days, the ratio of IFN-γ/IL-4 on day 3 after cerebral hemorrhage.Conclusion: Blocking B7-1(CD80)/CD28 signaling pathway can promote spatial memory recovery. The underlying mechanisms may be the effect of anti-B7-1 antibody combining B7-1(CD80) in regulating inflammatory and immune responses, including reverse Th1/Th2 imbalance, and slight downs-regulation of IFN-γ and edema rather than regulating programmed cell death through autophagy and apoptosis. |
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