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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: The spinal microglial IL-10/β-endorphin pathway accounts for cinobufagin-induced mechanical antiallodynia in bone cancer pain following activation of α7-nicotinic acetylcholine receptors

Fig. 7

Blockade effects of the specific p38 mitogen-activated protein kinase (MAPK) activation inhibitor SB203580 (a, b), JNK MAPK activation inhibitor SP600125 (c, d), and ERK1/2 MAPK activation inhibitor UO126 (e, f) on cinobufagin-stimulated gene overexpression of IL-10 and the β-endorphin precursor proopiomelanocortin (POMC) in primary cultures of spinal microglia. Cultured primary microglial cells, originated from the spinal cords of 1-day-old neonatal rats, incubated with each MAPK inhibitor for 1 hour followed by cinobufagin (100 μM) for 2 h. The mRNA expression of IL-10 and POMC was measured using qRT-PCR. The data are presented as means ± SEM (n = 3 independent repeats with duplicates). The asterisk and number sign denote statistical significance (p < 0.001) compared to the control group and cinobufagin group, respectively, by one-way ANOVA followed by the post hoc Student–Newman–Keuls test

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