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Archives of cardiovascular diseases
Volume 111, n° 10
pages 545-554 (octobre 2018)
Doi : 10.1016/j.acvd.2017.12.006
Received : 8 Mars 2017 ;  accepted : 6 December 2017
Clinical research

Mechanism of interleukin-1 receptor antagonist protection against myocardial ischaemia/reperfusion-induced injury
Mécanismes de la protection par l’antagoniste des récepteurs de l’interleukine I pour lutter contre les lésions d’ischémie myocardique/reperfusion
 

Figure 1




Figure 1 : 

Infarct size in each group. A. Cross-sectional photomicrographs of triphenyltetrazolium chloride (TTC)-stained (white) infarcted regions. B. Percentage of infarcted area in the left ventricle in ischaemia/reperfusion (I/R) and interleukin-1 receptor antagonist (IL-1ra)+I/R rats. Data are expressed as mean±standard deviation; n =3. *P <0.05, **P <0.01, ***P <0.001 versus the sham group. # P <0.05, ## P <0.01 versus the I/R group.


Figure 2




Figure 2 : 

Effects of the interleukin-1 receptor antagonist (IL-1ra) on the expression of Bax (A, B), Bcl-2 (A, C), Bax/Bcl-2 (D) and caspase-3 (E, F). At the end of 2hours of reperfusion, the whole homogenates from frozen left ventricular tissue were analysed for protein expression by western blot analyses. Data are expressed as mean±standard deviation; n =3. *P <0.05, **P <0.01, ***P <0.001 versus the sham group. # P <0.05, ## P <0.01, ### P <0.001 versus the ischaemia/reperfusion (I/R) group.


Figure 3




Figure 3 : 

Effects of interleukin-1 receptor antagonist (IL-1ra) on the expression of the inositol 1,4,5-trisphosphate receptor (IP3R). Data are expressed as mean±standard deviation; n =3. *P <0.05, **P <0.01, ***P <0.001 versus the sham group. # P <0.05, ## P <0.01 versus the ischaemia/reperfusion (I/R) group.


Figure 4




Figure 4 : 

Effects of the interleukin-1 receptor antagonist (IL-1ra) on the contractile properties of isolated ventricular cardiomyocytes. A. Resting cell length. B. Peak shortening (normalized to cell length); C. Maximal velocity of shortening (+dL/dt). D. Maximal velocity of relengthening (−dL/dt). E. Time to peak shortening (TPS). F. TR (90) (time to 90% relengthening). Data are expressed as mean±standard deviation; n =10–15 cells each. *P <0.05, ** P <0.01, ***P <0.001 versus the dimethyl sulphoxide (DMSO) group. # P <0.05, ## P <0.01, ### P <0.001 versus the ischaemia/reperfusion (I/R) group. $ P <0.05, $$ P <0.01, $$$ P <0.001 versus the IL-1ra+I/R group. % P <0.05, %% P <0.01, %%% P <0.001 versus the 2-aminoethoxydiphenyl borate (2-APB)+I/R group.


Figure 5




Figure 5 : 

Effects of the interleukin-1 receptor antagonist (IL-1ra) on the Ca2+ transients of isolated ventricular cardiomyocytes. A. Representative recordings expressed as F/F0. B. Resting intracellular Ca2+. C. Ca2+ transient amplitude (ΔFFI). D. Decay time constants of the Ca2+ transients (Tau). Data are expressed as mean±standard deviation; n =10–15 cells each. *P <0.05, **P <0.01, ***P <0.001 versus the dimethyl sulphoxide (DMSO) group. # P <0.05, ## P <0.01, ### P <0.001 versus the ischaemia/reperfusion (I/R) group. $ P <0.05, $$ P <0.01, $$$ P <0.001 versus the IL-1ra+I/R group. % P <0.05, %% P <0.01, %%% P <0.001 versus the 2-aminoethoxydiphenyl borate (2-APB)+I/R group.


Figure 6




Figure 6 : 

Effects of the interleukin-1 receptor antagonist (IL-1ra) and 2-aminoethoxydiphenyl borate (2-APB) on the expression of the inositol 1,4,5-trisphosphate receptor (IP3R) in cardiomyocytes. Data are expressed as mean±standard deviation; n =3. *P <0.05, **P <0.01, ***P <0.001 versus the dimethyl sulphoxide (DMSO) group. # P <0.05, ## P <0.01, ### P <0.001 versus the ischaemia/reperfusion (I/R) group. $ P <0.05, $$ P <0.01, $$$ P <0.001 versus the IL-1ra+I/R group. % P <0.05, %% P <0.01, %%% P <0.001 versus the 2-APB+I/R group.

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