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Involvement of heme oxygenase-1 in delayed cardioprotection induced by monophosphoryl lipid A in rats.

  
@article{APS7118,
	author = {Rong LU and Jun PENG and Feng YE and Han-Wu DENG and Yuan-Jian LI},
	title = {Involvement of heme oxygenase-1 in delayed cardioprotection induced by monophosphoryl lipid A in rats.},
	journal = {Acta Pharmacologica Sinica},
	volume = {23},
	number = {1},
	year = {2016},
	keywords = {},
	abstract = {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.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/7118}
}