received the same dose of normal saline. At day 19 and 24, 8 mice were put to death, whose eyeballs were extirpated and ADP enzyme staining and stretched preparation of retina for observing retinal blood vessels division. HE dyeing was used for counting retinal vascular endothelial cells. Weightgrowth in each groupof mice was monitored every day. Statistical methods were carried out by t-test, ANOVA analysis and LSDmultiple comparison. Results Body weight gain was compared in each group. Body weight of the controlgroup growed faster than hyperoxia rhIGF-1 group and hyperoxia saline group with statistical significance(P<0.05, t=3.572, 7.553). It showed that hyperoxia has an inhibitory effect on weight gain in mice. P19mice in the hyperoxia rhIGF-1 group gained weight faster than the hyperoxia saline group with statistical
significance (P<0.05, t=3.980). It showed that rhIGF-1 could promote the weight gain of mice in high-oxygen
environment. The hyperoxia rhIGF-1 group was less than hyperoxia saline group in vascular endothelial cells
extending into the inner boundary membrane of retina with statistical significance (P<0.05). Retinal vessel
was normal at P19 and peripheral vascular occlusion was not obvious and peripheral vascular coverage was
high. At P24, neovascularization on retina was not obvious. Conclusion Exogenous complementing of
rhIGF-1 early can effectively promote weight growth of mice, and may mitigate the damage for the retina
caused by hyperoxia, and is expected to be a prophylaxis and treatment method for ROP
2020, Vol. 8 
