fig4

Neuroprotection by minocycline in murine traumatic spinal cord injury: analyses of matrix metalloproteinases

Figure 4. Microglial/macrophage activation and infiltration is reduced in minocycline treated mice. Microglia/macrophages were visualized using Iba1 immunostaining 5 days after injury. A comparison of representative sections from normal uninjured mice (A, B) and SCI mice treated with vehicle (C, D) reveals that there was increased density of cells in the SCI tissue, as well as a more amoeboid morphology characteristic of microglial/macrophage activation after SCI (D). In contrast, in minocycline treated mice (E, F), the density of microglia/macrophages appeared to be qualitatively reduced compared to vehicle controls. In minocycline treated mice (F), the microglia, while demonstrating morphological changes indicative of activation (i.e. shortened and thickened processes), did not progress as much as in the vehicle animals (D). Finally, within the epicenter of the injury in vehicle and minocycline treated animals (G and H respectively), there was an increased number of Iba1 labeled cells displaying an amoeboid morphology, with a greater density of these cells in the vehicle treated mice compared to the minocycline group. Iba1 stained sections were scored blinded for microglial/macrophage activation using a scale from 0-4, where 0 was normal cord and 4 indicated the presence of highly activated microglia/macrophages. There was a significant difference (*P < 0.05, Mann Whitney U test) in the morphology and density of Iba1 labeled cells in minocycline treated mice after SCI compared to vehicle (I, where each point represents one longitudinal section containing the central canal per mouse). SCI: spinal cord injury

Neuroimmunology and Neuroinflammation
ISSN 2349-6142 (Online) 2347-8659 (Print)

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