Abstract

The present study aimed to investigate the role of plasminogen activator inhibitor‑1 (PAI‑1) in drug‑induced early cognitive impairment and the underlying mechanism concerning microRNA (miR)‑30b. A mouse model of cognitive impairment was established by intraperitoneal injection of scopolamine (2 mg/kg body weight) for 13 days. Behavioral performance was assessed using the Morris water maze (MWM) test. The mRNA expression levels of PAI‑1 and miR‑30b were detected using quantitative polymerase chain reaction (qPCR). The protein expression levels of PAI‑1 in the hippocampus and blood were determined using western blot analysis and enzyme‑linked immunosorbent assays. The MWM test demonstrated that, on days 3 and 4, the escape latency was significantly elevated in the model mice in comparison with control group (P<0.05). In addition, the length of swimming path was significantly increased (P<0.05), while the number of times of crossing the platform location was significantly reduced in the model mouse group (P<0.05) in comparison with the control group. qPCR demonstrated that the mRNA expression levels of PAI‑1 in the model mice was significantly elevated in the hippocampus and blood in comparison with the control group (P<0.01). Furthermore, western blot analysis and enzyme‑linked immunosorbent assay demonstrated that the protein expression levels of PAI‑1 were significantly elevated in the hippocampus and blood in the model group, in comparison with the control group (P<0.05). Notably, the levels of miR‑30b in the hippocampus and blood were significantly decreased in the model mice in comparison with the control group (P<0.01). To conclude, the expression levels of PAI‑1 were significantly elevated in mice with scopolamine‑induced cognitive impairment, which may be associated with the downregulation of miR‑30b. The findings from the present study suggest that miR‑30b may