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Fig. 7 | Molecular Neurodegeneration

Fig. 7

From: Reactive astrocytes undergo M1 microglia/macrohpages-induced necroptosis in spinal cord injury

Fig. 7

Effects of depleting M1 microglia/macrophages or transplantation of M1 macrophages on astrocytic death and functional recovery. a Western-blotting ofRIP3, MLKL and HMGB1 at 5 days post-injury in GdCl3- or PBS- treated mice. GdCl3 treatment significantly blocked the induction of RIP3, MLKL and HMGB1 by SCI. *P <0.05. n = 3. b Double-staining of GFAP and PI at 5 days post-injury in GdCl3 or PBS treated mice. GdCl3 treatment significantly reduced the percent of PI-labeled astrocytes. Bar = 50 μm. *P <0.05. n = 3. c, d Quantification of cavity area at 14 days post-injury and evaluation of locomotion recovery in GdCl3 and PBS treated mice. GdCl3 treatment significantly reduced cavity size and enhanced functional recovery. BMS stands for for Basso mouse scale. Bars = 200 μm. *P <0.05. n = 3. e, f Western-blotting of RIP3, MLKL and HMGB1, and double-staining of GFAP and PI in injured spinal cord at 5 days after transplantation of M0 macrophages or M1 macrophages. M1 macrophages significantly increased the expression of RIP3, MLKL and HMGB1, and the number of PI-labeled astrocytes, as compared to DMEM control. Bar = 50 μm. **P <0.01, *P <0.05. n = 3. g, h Quantification of cavity area and locomotion recovery after transplantation of DMEM, M0 macrophages or M1 macrophages. Transplantation of M1 macrophages significantly expanded the area of spinal cavity and impeded function recovery. BMS stands for for Basso mouse scale. *P <0.05. n = 3. Bars = 200 μm

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