Objective To investigate the clinical efficacy of reteplase in the treatment of elderly patients with cerebral infarction. Methods A total of 64 elderly patients with cerebral infarction from September 2018 to March 2019 were randomly divided into study group and control group. The study group were treated with reteplase, and the control group with alteplase. After the treatment, the two groups were evaluated using National Institute of Health Stroke Scale (NIHSS), and adverse reactions were recorded. The recovery of the patients′ neurological function was measured by the modified Rankin scale (MRS), and survival rate was analyzed during three months of follow-up. Serum superoxide dismutase (SOD) and malondialdehyde (MDA) were assessed by ELISA before and after thrombolytic therapy. The data were statistically analyzed by SPSS statistics 20.0. The comparison between the two groups was performed by t/χ² test. Survival analysis was estimated by Kaplan-Meier method and tested by Log-rank test. Results NIHSS score was lower in study group than in the control group (P<0.05) at 3d, 7d, 30 d of thrombolysis, and the overall effective rate was higher in the former than in the latter [(93.55%(29/31) vs 77.78%(21/27);χ²=10.631, P=0.001]. After 3 months of treatment, no obvious disability was observed in 62.5%(20/32) of the study group, which was significantly higher than 43.75%(14/32) of the control group (χ²=6.816, P=0.009). The 3-month survival rate of the study group was higher than that of the control group (P<0.05). Adverse reactions such as bleeding occurred in both groups, but with no significant difference between the two groups (P>0.05). Compared with before treatment, SOD significantly increased and MDA significantly decreased (P<0.05) in both groups after treatment. SOD increased more significantly and MDA decreased more significantly in the study group than in the control group (P<0.05). Conclusion Reteplase treatment can improve the prognosis of patients with cerebral infarction without increasing the incidence of adverse reactions, and its mechanism may be related to inhibition of oxidative stress reaction.