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Updated: Oct 2, 2026
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Involvement of heme oxygenase-1 in delayed cardioprotection induced by monophosphoryl lipid A in rats
1Department of Pharmacology, Xiang-Ya Medical College, Central South University, Changsha 410078, China.
Aim:
To explore whether the heme oxygenase-1 (HO-1) pathway is involved in the delayed cardioprotection induced by monophosphoryl lipid A (MLA).
Methods:
Sprague-Dawley rats were pretreated with MLA 24 h before the experiment. Ischemia-reperfusion injury was induced by 60 min coronary artery occlusion followed by 3 h reperfusion. Infarct size, the serum creatine kinase (CK) activity, the serum content of nitric oxide (NO), and expression of HO-1 mRNA and protein in the heart were measured.
Results:
Pretreatment with MLA (500 microg/kg, ip) markedly reduced infarct size and CK release and increased the serum content of NO (P < 0.01). The effects of MLA were completely abolished by pretreatment with L-nitroarginine methyl ester (L-NAME 10 mg/kg, ip), an inhibitor of NO synthase (P < 0.01), or Zinc protoporphyrin IX (45 micromol/kg, ip), an inhibitor of HO (P < 0.01). MLA caused a significant increase in the expression of HO-1 mRNA and protein, an effect which was not affected by L-NAME (P > 0.05).
Conclusion:
The results suggest that the HO-1/NO pathway is involved in the delayed cardioprotection induced by MLA.