Fig. 4
From: IGF-1R promotes pain-like behavior in rats with myofascial pain syndrome via the PI3K/AKT pathway
IGF-1 induced pain behaviors and reversed by PI3K inhibitor LY294002 in control rats. (A) The mechanical withdrawal thresholds of control rats decreased significantly at 1, 2, and 4 h after intramuscular injection of IGF-1 (*P< 0.05, **P < 0.01), n = 6 rats per group. The data expressed as mean ± standard deviation (mean ± SD). (B) The mechanical withdrawal thresholds of control rats showed no significant differences after intramuscular injection of IGF-1 and LY294002 compared with the control group (P > 0.05), n = 6 rats per group. The data expressed as mean ± standard deviation (mean ± SD). (C) After intramuscular injection of IGF-1 to control rats, protein expression levels of IGF-1, IGF-1R, PI3K, p-AKT, mTOR, and RhoA were significantly increased compared to the control group (*P < 0.05, **P < 0.01). And when LY294002 was added, the protein expression levels of IGF-1 and IGF-1R remained significantly different (*P < 0.05, **P < 0.01), while the expression levels of PI3K, p-AKT, mTOR, and RhoA showed no significant differences compared to the control group (P > 0.05), n = 6 rats per group. The data expressed as mean ± standard deviation (mean ± SD).
