RESUMO
Objective To observe the expression and distribution of insulin-like growth factor-1 receptor (IGF-1R) in orbital adipose tissues of patients with thyroid-associated ophthalmopathy (TAO), and to explore the effect of insulin-like growth factor-1 (IGF-1) on the proliferation and differentiation of orbital preadipocytes. Methods We harvested the orbital adipose tissues from 6 patients with TAO (TAO group) and 5 controls (control group); the patients were treated in Changzheng Hospital, Second Military Medical University from Sep. 2014 to Jan. 2015. The expression and distribution of IGF-1R in the orbital adipose tissues were examined by Western blotting analysis, real-time PCR and immunohistochemistry. The orbital preadipocytes were extracted in two groups, and the effects of different concentrations of IGF-1 (0 nmol/L, 1 nmol/L, 5 nmol/L, 10 nmol/L, and 20 nmol/L) on cell proliferation were examined by CCK8. The differentiation of cells and the expression of IGF-1R were observed by oil red O staining and Western blotting; the effect of different concentrations of IGF-1 (0 nmol/L, 1 nmol/L, 5 nmol/L, 10 nmol/L, and 20 nmol/L) on preadipocyte differentiation was detected by real-time PCR. Results The expressions of IGF-1R protein and mRNA in orbital adipose tissues in TAO group were significantly higher than those in the control group (P<0. 01). The proliferation of orbital preadipocytes was promoted in both groups, and the cell proliferation in TAO group was significantly higher than that in control group when treated with 1-20 nmol/L IGF-1 (P<0. 05, P<0. 01). The expression of IGF-1R in the TAO group was significantly higher than that in the control group before and after differentiation. Compared with IGF-1 absent group, 1-20 nmol/L IGF-1 significantly promoted the expression of PPARγ mRNA in orbital preadipocytes in TAO group (P<0. 01). Oil red O staining results showed that the lipid droplet synthesis was significantly increased with the increase of IGF-1 concentration (P<0. 05, P<0. 01). Conclusion IGF-1R is highly expressed in the adipose tissue and preadipocytes in patients with TAO, and IGF-1 can promote the proliferation and differentiation of preadipocytes in patients with TAO.
RESUMO
Objective To investigate the effect of aspirin (Asp) on cognitive function and the insulin-like growth factor-1 receptor/phosphorylated insulin-like growth factor-1 receptor (IGF-1R/p-IGF-1R) expression in the hippocampus of rats with diabetic encephalopathy, so as to analyze the protective mechanism of aspirin on brain. Methods Diabetes mellitus (DM) was induced by intraperitoneal injection of streptozotocin (STZ, 60 mg/kg body mass). Rats were randomly assigned to four groups (n = 10 animals per group), i. e. control, control + Asp, DM, and DM + Asp groups. One week after the injection of STZ, the animals in Con + Asp and DM + Asp groups were gavaged with aspirin (10 mg/ [kg · d]) for 14 weeks. Meanwhile, the control group received the same dose of noromal saline for 14 weeks, and then the cognitive function was observed by Morris water maze (MWM) test in all rats. The expressions of IGF-1R and p-IGF-1R proteins in the hippocampus of rats were examined by Western blotting analysis. Results The cognitive function of diabetic rats was improved after treated with aspirin; the escape latency of MWM test in DM + Asp group was significantly shorter than that in DM group (P< 0.01) ; the number of platform crossing and time spent in the target quadrant in the MWM test were significantly more in DM + Asp group compared with those in DM group (P<0.01 or P<0.05). H-E result showed that the neurons in DM + Asp group were increased compared with that in DM group. The hippocampal expression of p-IGF-1R protein in DM group was significantly lower than that in the control group (P<0.01) and aspirin treatment significantly increased p-IGF-1R expression (P<0.01). However, the IGF-1R protein levels in the hippocampus showed no significant difference between different groups. Conclusion Aspirin may protect the brain of rats with diabetic encephalopathy by regulating the IGF-1R signaling pathway.