Sulfated chitosan directs the recovery of ischemic stroke by attenuating the inflammatory cascade

Rapid vascularization and effective suppression of hyperinflammation are key factors in rescuing major organ damage, but there is no effective way to overcome in the treatment of cardiovascular and cerebrovascular diseases. Herein, we propose new strategies to influence the inflammatory cascade from the source of the immune response and promote tissue repair. This means that effective regulation of neutrophils is the key to the treatment of major organ injuries associated with inflammation. Sulfated chitosan (SCS), as a kind of glycosaminoglycan-like polysaccharide, can not only remarkable promote the apoptosis of neutrophils and polarize macrophages towards M2, but also enable neutrophil to produce vascular-related subsets. In ischemia hind limb and ischemic stroke models, SCS significantly shortened the acute inflammatory period represented by neutrophils and accelerated the repair period represented by M2 macrophages. Moreover, SCS dramatically inhibited the expression of MMP-9 in ischemic stroke, providing a guarantee for the rapid reconstruction of extracellular matrix. Compared with the control group, the reenlarged of the infarct volume was inhibited by approximately 20% in ischemic hemisphere. Taken together, this study highlights utilizing effects of bioactive materials itself simultaneously regulates immunity and promotes angiogenesis, which lays a foundation for the study of ischemia therapy especially for acute inflammatory associated major organ damage.