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Structural apelin analogues: mitochondrial ROS inhibition and cardiometabolic protection in myocardial ischaemia reperfusion injury.

Pisarenko O, Shulzhenko V, Studneva I, Pelogeykina Y, Timoshin A, Anesia R, Valet P, Parini A, Kunduzova O - Br. J. Pharmacol. (2015)

Bottom Line: Treatment of cardiomyocytes with AI and AII decreased cell apoptosis concentration-dependently.Prevention of oxidative damage by AI and AII was associated with the improvement of functional and metabolic recovery after I/R in the heart.These data provide the evidence for the potential of the structural apelin analogues in selective reduction of mitochondrial ROS generation and myocardial apoptosis and form the basis for a promising therapeutic strategy in the treatment of oxidative stress-related heart disease.

View Article: PubMed Central - PubMed

Affiliation: Russian Cardiology Research-and-Production Complex, Moscow, Russia.

No MeSH data available.


Related in: MedlinePlus

Effects of peptides on ROS formation and cell membrane damage during reperfusion of rat isolated heart. (A) DMPO–OH adduct concentrations in the myocardial effluent. *P < 0.05, significantly different from control; #P < 0.05, significantly different from the value before ischaemia. (B) LDH leakage from perfused rat heart before and after global ischaemia. Data shown are the mean ± SEM of six to eight experiments and expressed in IU·g−1 dry weight for 5 min Langendorff perfusion before or after global ischaemia. *P < 0.05, significantly different from value before ischaemia, #P < 0.05, significantly different from control (C) on early reperfusion.
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fig02: Effects of peptides on ROS formation and cell membrane damage during reperfusion of rat isolated heart. (A) DMPO–OH adduct concentrations in the myocardial effluent. *P < 0.05, significantly different from control; #P < 0.05, significantly different from the value before ischaemia. (B) LDH leakage from perfused rat heart before and after global ischaemia. Data shown are the mean ± SEM of six to eight experiments and expressed in IU·g−1 dry weight for 5 min Langendorff perfusion before or after global ischaemia. *P < 0.05, significantly different from value before ischaemia, #P < 0.05, significantly different from control (C) on early reperfusion.

Mentions: The effluent DMPO–OH concentrations did not differ significantly between the groups before ischaemia (Figure 2A), thus indicating that infusion of peptides does not initiate ROS formation. A significant increase in DMPO–OH concentration was observed at the first, third and fifth minutes of reperfusion in the control group, compared with the steady-state value. Pre-ischaemic administration of A13, A12, AI or AII decreased DMPO–OH formation during reperfusion compared with control. This effect was statistically significant for all peptides at the third and fifth minutes of reperfusion. In this case, DMPO–OH concentrations did not differ from the pre-ischaemic values. The DMPO–OH adduct could be formed from a decomposition of the superoxide radical adduct DMPO–OOH or from direct trapping of OH. radicals generated in the Haber–Weiss and the Fenton reactions (Tosaki et al., 1990). Thus the detection of DMPO–OH adduct in the coronary effluent did not directly reflect ROS formation in the heart and the data obtained indicated that the peptides reduced the release of ROS-generating systems and hydrogen peroxide from myocardial tissue.


Structural apelin analogues: mitochondrial ROS inhibition and cardiometabolic protection in myocardial ischaemia reperfusion injury.

Pisarenko O, Shulzhenko V, Studneva I, Pelogeykina Y, Timoshin A, Anesia R, Valet P, Parini A, Kunduzova O - Br. J. Pharmacol. (2015)

Effects of peptides on ROS formation and cell membrane damage during reperfusion of rat isolated heart. (A) DMPO–OH adduct concentrations in the myocardial effluent. *P < 0.05, significantly different from control; #P < 0.05, significantly different from the value before ischaemia. (B) LDH leakage from perfused rat heart before and after global ischaemia. Data shown are the mean ± SEM of six to eight experiments and expressed in IU·g−1 dry weight for 5 min Langendorff perfusion before or after global ischaemia. *P < 0.05, significantly different from value before ischaemia, #P < 0.05, significantly different from control (C) on early reperfusion.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4459014&req=5

fig02: Effects of peptides on ROS formation and cell membrane damage during reperfusion of rat isolated heart. (A) DMPO–OH adduct concentrations in the myocardial effluent. *P < 0.05, significantly different from control; #P < 0.05, significantly different from the value before ischaemia. (B) LDH leakage from perfused rat heart before and after global ischaemia. Data shown are the mean ± SEM of six to eight experiments and expressed in IU·g−1 dry weight for 5 min Langendorff perfusion before or after global ischaemia. *P < 0.05, significantly different from value before ischaemia, #P < 0.05, significantly different from control (C) on early reperfusion.
Mentions: The effluent DMPO–OH concentrations did not differ significantly between the groups before ischaemia (Figure 2A), thus indicating that infusion of peptides does not initiate ROS formation. A significant increase in DMPO–OH concentration was observed at the first, third and fifth minutes of reperfusion in the control group, compared with the steady-state value. Pre-ischaemic administration of A13, A12, AI or AII decreased DMPO–OH formation during reperfusion compared with control. This effect was statistically significant for all peptides at the third and fifth minutes of reperfusion. In this case, DMPO–OH concentrations did not differ from the pre-ischaemic values. The DMPO–OH adduct could be formed from a decomposition of the superoxide radical adduct DMPO–OOH or from direct trapping of OH. radicals generated in the Haber–Weiss and the Fenton reactions (Tosaki et al., 1990). Thus the detection of DMPO–OH adduct in the coronary effluent did not directly reflect ROS formation in the heart and the data obtained indicated that the peptides reduced the release of ROS-generating systems and hydrogen peroxide from myocardial tissue.

Bottom Line: Treatment of cardiomyocytes with AI and AII decreased cell apoptosis concentration-dependently.Prevention of oxidative damage by AI and AII was associated with the improvement of functional and metabolic recovery after I/R in the heart.These data provide the evidence for the potential of the structural apelin analogues in selective reduction of mitochondrial ROS generation and myocardial apoptosis and form the basis for a promising therapeutic strategy in the treatment of oxidative stress-related heart disease.

View Article: PubMed Central - PubMed

Affiliation: Russian Cardiology Research-and-Production Complex, Moscow, Russia.

No MeSH data available.


Related in: MedlinePlus