Xiangjun Wu,
Hui Ye,
Qiao Cai,
Yuanxiang Ke,
Danying Wang
Department of Pediatrics, Taizhou First People's Hospital, Taizhou 318020, People's Republic of China;
For correspondence:- Danying Wang
Email: zjchs7@163.com
Accepted: 29 September 2019
Published: 30 October 2019
Citation:
Wu X, Ye H, Cai Q, Ke Y, Wang D.
Effect of early exogenous supplementation of rhIGF-1 on oxygen-induced retinopathy in a mice model of prematurity, and on expressions of IGF-1 and VEGF. Trop J Pharm Res 2019; 18(10):2019-2024
doi:
10.4314/tjpr.v18i10.3
© 2019 The authors.
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Abstract
Purpose: To investigate the effect of early exogenous supplementation of recombinant human insulin-like growth factor (rhIGF-1) on oxygen-induced mouse model of retinopathy of prematurity (ROP).
Methods: Three groups of healthy SPF grade C57BL/6 mice were used in this study, with 20 mice in each group. Hyperoxia saline (HS) and hyperoxia rhIGF-1 (HrGF) groups were placed in a closed oxygen chamber for one week and returned to the normal environment on the 15th day. The hyperoxia rhIGF-1 (HrGF) group was intraperitoneally injected with rhIGF-1 (1.5 mg/kg), while mice in high-oxygen saline (HS) group received normal saline. The air group (AG) was untreated. Changes in retinal blood vessel distributions, expression levels of serum IGF-1 and VEGF, and retinal IGF-1 and VEGF were determined.
Results: On day 20, pronounced neo-vascularization was observed, but the distribution was disordered. Serum IGF-1 levels in AG and HrGF were significantly higher than that in HS group, but VEGF level was lower in HS mice (p < 0.05). VEGF level in hyperoxia rhIGF-1 group on days 11 and 15 decreased, relative to control value, while retinal IGF-1 and VEGF in AG and hyperoxia rhIGF-1 mice were elevated, relative to corresponding values in HS mice (p < 0.05).
Conclusion: Early exogenous supplementation of rhIGF-1 exerts a therapeutic effect on ROP. Thus, rhIGF-1 may be a potential drug regimen for ROP in clinics.
Keywords: Oxygen-induced retinopathy, rhIGF-1, Premature infants, IGF-1, VEGF