Conclusion
Treatment with alteplase can be effective in reducing cerebral infarction volume and moderating neurological deficits in ACI modeled rats within a 6-h time window, which may be correlated with the regulation of GFAP and GAP-43 expressions by alteplase.
Methods
Sprague Dawley (SD) rats (n = 50) were enrolled in a trial to establish a ACI rat model; of these, 48 rats were succeeefully modeled and were randomized into either the model or alteplase group, whereas another 24 SD rats were included in the sham-operated group. Findings: No significant difference in scores was observed between the model and alteplase groups at T1 (P > 0.05); however, rats in the alteplase group demonstrated lower scores than those in the model group at T2, T3, and T4 (P < 0.05). Rats in the model group showed a larger cerebral infarction volume than those in the alteplase group (P < 0.05), and the infarction volume on day 1, 3, 6, and 9 was higher in rats in the alteplase group than those in the sham-operated group (P < 0.05).
Objective
To investigate the effects of alteplase on neurological deficits, as well as on the expressions of glial fibrillary acidic protein (GFAP) and growth-associated protein-43 (GAP-43) in brain tissues of rats with acute cerebral infarction (ACI).