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To investigate whether interleukin-33 (IL-33) protect myocardium from ischemia and reperfusion (I/R) injury by suppressing excessive autophagy.
32 Male Sprague-Dawley rats (200-250 g) were randomly divided into 4 groups: Sham operate group (n=10), I/R group (I/R, n=10), IL-33+I/R group (IL-33+I/R, n=6), anti-ST2+I/R group (anti-ST2+I/R, n=6). Rats I/R model (ischemia for 30 min, reperfusion for 4h) was used. The serum levels of creatine kinase (CK) and lactate dehydrogenase (LDH), the myocardial levels of malondialdehyde (MDA) and superoxide dismutase (SOD) and myocardial infarct size were measured. The B-cell leukemia (Bcl-2), beclin-1 and LC3 levels in myocardial tissue were measured by western blot.
Compared with I/R group, the IL-33 group had significantly lower cardiac injury (lower serum CK (1959.67±203.10 vs. 4147.67±199.00 U/L) and LDH (977.05±117.92 vs. 1736.19±171.72 U/L) levels and myocardial infarct size (18.23±5.68% vs. 71.8±8.58%)), a lower oxidative stress (lower MDA (6.50±0.81 vs. 12.94±1.81 nmol/mg) level and higher SOD (169.06±10.68 vs. 84.30±9.51 U/mg) level), a lower Bcl-2 (0.29±0.08 vs. 0.15±0.03) level and a lower autophagy (lower beclin-1 (0.16±0.02 vs. 0.42±0.06) level and smaller LC3-II/I ratio (0.148±0.04 vs. 4.17±0.72)). All of effects of IL-33 could be inhibited by anti-ST2.
our study suggests that 1) IL-33 can protect against myocardial I/R injury by inhibiting excessive autophagy; 2) IL-33 inhibits excessive autophagy via suppressing ROS generation and increasing Bcl-2 expression; 3) The content of endogenous IL-33 is too low to affect autophagy induced by I/R injury.