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Fig. 4 | Journal of Neuroinflammation

Fig. 4

From: Microglial NLRP3 inflammasome activation mediates IL-1β release and contributes to central sensitization in a recurrent nitroglycerin-induced migraine model

Fig. 4

Chronic treatment with MCC950 (NLRP3 inhibitor) reversed NTG-induced hyperalgesia. a Drug administered in the second experiment. In treatment groups, mice were treated with VEH or MCC950 (10 mg/kg i.p.) daily for 11 days. On days 3, 5, 7, 9 and 11, basal threshold responses were determined, then mice were injected with VEH or MCC950; 30–45 min later, mice were injected with nitroglycerin (NTG; 10 mg/kg, i.p.). Acute treatment responses were assessed 2 h following NTG administration. The saline group and NTG group were injected with saline or NTG, respectively, and the mechanical sensitivity responses were also tested before injection and 2 h after injection. b, c Basal threshold responses were significantly decreased after NTG administrations. ***p < 0.001 for the saline group compared to the NTG group. In the groups receiving MCC950-preventative treatment, basal threshold responses induced by NTG was significantly reversed. ###p < 0.001 for the MCC950+NTG group compared to the NTG group. Two-way RM ANOVA and Holm-Sidak post hoc analysis (n = 8 mice per group). d, e NTG administrations induced acute hyperalgesia. ***p < 0.001 for the saline group compared to the NTG group. Acute NTG-induced hyperalgesia were blocked by treatment with MCC950. ###p < 0.001 for the MCC950+NTG group compared to the NTG group. Two-way RM ANOVA and Holm-Sidak post hoc analysis (n = 8 mice per group)

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