title: Ferilnic nirate produces delayed preconditioning against myocardial ischemia and reperfusion injury in rats.
abstract: To determine whether ferilnic nirate (FLNT) can precondition the rat heart against myocardial ischemia/reperfusion (I/R) damage and its mechanism, two groups of experiments were conducted. In the first group of experiments, rats were divided among four treatment groups: sham group; solvent with I/R (I/R control group); FLNT pretreatment with I/R (I/R FLNT group); and late ischemic preconditioning group (LPC group). In the second group of experiments without I/R, rats were divided into two treatment groups: control group and FLNT group. The results indicated that myocardial infarct size and the levels of creatine kinase and lactate dehydrogenase in the sera of the I/R FLNT group were significantly lower and the level of nitric oxide molecule and Mn-containing superoxide dismutase were significantly elevated in the heart tissue compared with I/R control group. The protein expression ratio of Bcl-2/Bax in heart tissue was significantly elevated in the I/R FLNT group. These results demonstrate FLNT is able to precondition rat hearts against myocardial ischemia/reperfusion damage to a similar level as that achieved via the late phase of ischemic preconditioning. The mechanism may involve the up-regulation of nitric oxide and the strengthening of anti-oxidant and anti-apoptosis cellular functions.
authors.affiliation: Department of Pharmacology, General Hospital of Beijing Military Command, Beijing, China.
authors.forename: Jing-feng
authors.initials: JF
authors.lastname: Xu
authors.forename: Zhan-qing
authors.initials: ZQ
authors.lastname: Wang
authors.forename: Jin-ping
authors.initials: JP
authors.lastname: Wang
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D003373:Coumaric Acids / Q000494:pharmacology / Q000627:therapeutic use*; D006321:Heart / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009203:Myocardial Infarction / Q000473:pathology; D017202:Myocardial Ischemia / Q000097:blood / Q000517:prevention & control*; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000517:prevention & control*; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism; D009566:Nitrates / Q000494:pharmacology / Q000627:therapeutic use*; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D020011:Protective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; D015415:Biomarkers; D003373:Coumaric Acids; C553416:N-2-(ferulamidoethyl)nitrate; D009566:Nitrates; D020011:Protective Agents; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D009569:Nitric Oxide; D008315:Malondialdehyde; D052247:Nitric Oxide Synthase Type II; D013482:Superoxide Dismutase