Abstract:

Objective  To investigate the effect and mechanism of ulinastatin on learning and cognitive function of hippocampus after ischemiareperfusion injury in rats． Methods  The focal ischemia reperfusion model was established by thread embolism of middle cerebra1 artery. The animals were sacrificed at 24h after the reperfusion． Morphological examination of the CA1 region of hippocampus was perfromed with H&E staining. The expression of nuclear factor kappa B p65 protein(NF-κB p65) was measured by Western blot. The levels of tumor necrosis factor α(TNF-α)and interleukin 10 (IL-10) were determined by enzymelinked immunosorbent assay. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were determined by biochemical colorimetry. Morris water maze test was done after the administration of ulinastatin for the other  30 Wistar rats. Results  The pyramidal cells of hippocampus of rats were  protected by ulinastatin.  After the administration of ulinastatin, the expression of NF-κB p65 in the hippocampus, serum level of IL-10 and SOD increased, while the serum level of TNF-α, and the level of MDA in brain tissue homogenate decreased decreased. Meanwhile, ulinastatin could decrease the latency of escaping, increase the percentage of swimming distance in the platform quadrant and number of entries in the target area. Conclusions  Ulinastatin can improve the learning and memory ability of focal brain ischemiareperfusion injury model rats. Antiinflammatory and antioxidant effects are attributed to the basic mechanism.

Key words: Ulinastatin; Reperfusion injury; Hippocampus; Inflammatory factors; Antioxidant effect