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Peripheral pain is enhanced by insulin-like growth factor-1 and its receptors in a mouse model of type 2 diabetes.
Journal of Diabetes 2018 August 14
BACKGROUND: Insulin-like growth factor-1 (IGF-1) is a multidimensional neurotrophic factor. Nevertheless, it has been reported that IGF-1 may lead to hyperalgesia. This study aimed to investigate the effects of IGF-1 on the overall behaviour of diabetic mice and to explore the possible mechanisms of IGF-1-induced pain effects.
METHODS: The mice were divided into five groups: db/m group, db/db group, db/db+vehicle group, IGF-1-treated db/db group and IGF-1-JB-1-treated db/db group. Behavioural studies were conducted using the hot plate and Von Frey tests after intraplantar injection of recombinant insulin-like growth factor-1 (rIGF-1) and IGF-1 receptor (IGF-1R) antagonist. Morphological changes in the dorsal root ganglia (DRG) were observed using electron microscopy. IGF-1R expression and co-localisation with pain mediators in the DRG were detected using immunofluorescence. Changes in the expression of IGF-1R, extracellular signal regulation kinase (ERK), and ras-associated factor-1 (c-raf) in the DRG were detected by western blotting.
RESULTS: Intraplantar injection of rIGF-1 resulted in a hyperalgesic effect after two hours. This IGF-1-induced hypersensitivity was attenuated by pre-intraplantar injection of an IGF-1R antagonist. There was no significant change in neuronal structure in the db/m group, whereas the other four groups were impaired. Moreover, IGF-1R was co-localised with pain mediators in DRG of mice. Intraplantar injection of rIGF-1 resulted in the increased expression of IGF-1R, p-ERK and c-raf in DRG, and pre-intraplantar injection of an IGF-1R antagonist attenuated the level of p-ERK and c-raf.
CONCLUSIONS: IGF-1-induced acute hyperalgesia may be associated with the IGF-R/c-raf/ERK pathway. This IGF-1-induced hypersensitivity was attenuated after using an IGF-1R antagonist. This article is protected by copyright. All rights reserved.
METHODS: The mice were divided into five groups: db/m group, db/db group, db/db+vehicle group, IGF-1-treated db/db group and IGF-1-JB-1-treated db/db group. Behavioural studies were conducted using the hot plate and Von Frey tests after intraplantar injection of recombinant insulin-like growth factor-1 (rIGF-1) and IGF-1 receptor (IGF-1R) antagonist. Morphological changes in the dorsal root ganglia (DRG) were observed using electron microscopy. IGF-1R expression and co-localisation with pain mediators in the DRG were detected using immunofluorescence. Changes in the expression of IGF-1R, extracellular signal regulation kinase (ERK), and ras-associated factor-1 (c-raf) in the DRG were detected by western blotting.
RESULTS: Intraplantar injection of rIGF-1 resulted in a hyperalgesic effect after two hours. This IGF-1-induced hypersensitivity was attenuated by pre-intraplantar injection of an IGF-1R antagonist. There was no significant change in neuronal structure in the db/m group, whereas the other four groups were impaired. Moreover, IGF-1R was co-localised with pain mediators in DRG of mice. Intraplantar injection of rIGF-1 resulted in the increased expression of IGF-1R, p-ERK and c-raf in DRG, and pre-intraplantar injection of an IGF-1R antagonist attenuated the level of p-ERK and c-raf.
CONCLUSIONS: IGF-1-induced acute hyperalgesia may be associated with the IGF-R/c-raf/ERK pathway. This IGF-1-induced hypersensitivity was attenuated after using an IGF-1R antagonist. This article is protected by copyright. All rights reserved.
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