ArticleScientific reports2026
Effect of tipiracil hydrochloride, thymidine phosphorylase inhibitor, on the ischemia/reperfusion injury of brain tissue in rats.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Thymidine phosphorylase (TP) expression is increased in neurons under ischemia/reperfusion (I/R) conditions. Our aim was to evaluate the effect of tipiracil hydrochloride (TPI), a selective TP inhibitor, on rat brain tissue subjected to I/R. Both common carotid arteries were occluded for 30 min in the ischemic untreated group of rats (C-IR), and ischemic groups treated with tipiracil 25 mg/g (T-IR25) or 50 mg/kg (T-IR50). In the control group (C), the arteries were not ligated. Tipiracil was given during ischemia, and after 8 h of I/R intraperitoneally. After 24 h of I/R, brain tissue was isolated for histology and immunohistochemy of TP expression. Metalloproteinases 2 and 9 (MMP-2 and -9) and tissue inhibitor of metalloproteinases (TIMP-1) were determined in serum at 3 and 24 h of reperfusion. TP expression in brain tissue was the highest in C-IR and T-IR25 compared to the C and T-IR50. No changes in serum TP levels were observed. After 24 h, there was a significant decrease in MMP-9 levels in T-IR25 compared to the C-IR and T-IR50. MMP-2 levels also decreased significantly at this time point in all groups compared to group C, which correlated with increased TIMP-1 activity in the T-IR25 and T-IR50. The inhibition of TP activity in the group receiving TPI suggests its protective effect on brain tissue under I/R conditions. The decrease in MMP activities in the treated groups suggests a protective effect of TPI on the development of neuroinflammation caused by local brain tissue ischemia.
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