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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Red nucleus IL-33 facilitates the early development of mononeuropathic pain in male rats by inducing TNF-α through activating ERK, p38 MAPK, and JAK2/STAT3

Fig. 2

Cellular distributions of IL-33 and ST2 in the RN of SNI rats, and the effect of IL-33 in the early development of mononeuropathic pain. A Representative images of IL-33 (Red) co-localized with RN neurons, oligodendrocytes, astrocytes, microglia or endothelial cells (Green) in naive and SNI rats. B Semiquantitative analysis of IL-33-positive cells in the RN of naive and SNI rats (neurons: F = 104.519, P < 0.001; oligodendrocytes: F = 121.789, P < 0.001; microglia: F = 251.137, P < 0.001) (n = 4 per group). C Representative images of ST2 (Red) co-localized with RN neurons, oligodendrocytes, astrocytes, microglia, or endothelial cells (Green) in naive and SNI rats. D Semiquantitative analysis of ST2-positive cells in the RN of naive and SNI rats (neurons: F = 233.032, P < 0.001; oligodendrocytes: F = 76.744, P < 0.001; microglia: F = 155.490, P < 0.001) (n = 4 per group). E Intrarubral administration of anti-IL-33 antibody at 1 week post-SNI dose-dependently (r = 0.961, P = 0.0385) attenuated SNI-induced mononeuropathic pain compared to saline control (n = 6 per group, F = 7.166, P = 0.003). F Intrarubral administration of exogenous IL-33 to naive rats dose-dependently (r = − 0.955, P = 0.0454) evoked a mechanical hypersensitivity compared to saline control (n = 6 per group, F = 35.194, P < 0.001). *P < 0.05, **P < 0.01, and ***P < 0.001. Scale bars = 50 μm

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