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Updated: Jul 13, 2026

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
Published on: November 21, 2025
Propofol attenuation of renal ischemia/reperfusion injury involves heme oxygenase-1
Hui-hua Wang1, Hai-yan Zhou, Cong-cong Chen
1Departments of Anesthesiology and Cardiology, the Second Affiliated Hospital, Zhejiang University Medical School, Hangzhou, China.
Aim:
To examine the protective effect of propofol in renal ischemia/reperfusion (I/R) injury and the role of heme oxygenase-1 (HO-1) in this process.
Methods:
Sprague-Dawley rats were randomly divided into 3 groups: (i) sham-operated group; (ii) I/R group; and (iii) propofol group. Bilateral renal warm ischemia for 45 min was performed. After 2, 6, and 24 h reperfusion, blood samples and kidneys were collected for assessment of renal injury, and HO-1 expressions were analyzed by immunohistochemical analysis, RT-PCR and Western blotting.
Results:
Blood urea nitrogen and serum creatinine levels in the propofol group were significantly lower than that in the I/R group at 24 h after reperfusion. The mean histological score by Palleros standard showed that propofol significantly attenuated renal I/R injury after 6 h reperfusion. Propofol increased HO-1 mRNA and protein levels 2 h after reperfusion, whereas HO-1 expressions were present at exceedingly low levels in the I/R group and the sham-operated group at same time point. Propofol also markedly increased HO-1 mRNA and protein levels than I/R at 6 and 24 h after reperfusion.
Conclusion:
These results suggest that propofol mitigates renal I/R injury in rats. This protection may be partly through the induction of the HO-1 expression.
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