Table 2.
Disease | Used Animals | Mechanism of Therapeutic Action of Gelsolin | Ref. |
---|---|---|---|
Lung injuries | Mice, rats | decrease of acute inflammatory response, binding of inflammatory mediators, limitation of neutrophil migration, inhibition of neutrophil adhesion to endothelial surface, improvement of pulmonary microvascular functions | [38,83] |
Burns and thermal injuries | Mice | decrease of acute neuroinflammatory response, binding of inflammatory mediators, decrease of elevated caspase-3 activity, improvement of peripheral T lymphocyte functions, regulation of oxidative response, shortening of bleeding time | [42,84] |
Sepsis | Mice, rats | binding of free circulating actin released from damaged cells, decrease of acute inflammatory response, binding of inflammatory mediators | [85,86] |
Pneumonia | Mice | decrease of acute inflammatory response, binding of inflammatory mediators, improvement of bacterial clearance by macrophages via NOS3-dependent mechanism | [87] |
Alzheimer’s disease | Mice | decrease of apoptosis, regulation of oxidative response, limitation of Aβ fibrillogenesis and Aβ-induced neurotoxicity | [88,89] |
MS/EAE | Mice | decrease of acute neuroinflammatory response, binding of inflammatory mediators, regulation of oxidative response | [35] |
Diabetes | Mice | depolymerization of F-actin | [36] |
Abbreviations: MS: multiple sclerosis; EAE: experimental autoimmune encephalomyelitis.