2015Medical & Pharmaceutical Journal of Chinese People's Liberation ArmyRequires access

Interleukin 33 in Protecting Myocardial Ischemia and Reperfusion Injury by Down Regulation of HMGB1 Expression in Rats

MA Rui-son

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Abstract

Objective To investigate the protective effect of interleukin-33( IL-33) on myocardial ischemia and reperfusion injury( I / R) by down regulation of high mobility group protein1( HMGB1) expression in rats. Methods The 32 adult male SD rats were randomly divided into sham operation group( SO group,n = 10),I / R group( n = 10),IL-33 group( n = 6) and HMGB1 antibodies group( HMGB1 Ab group,n = 6). The rats in SO group underwent chest cutting operation,and a suture was passed through the myocardium beneath the left anterior descending( LAD) without ligation; while the I / R models were established in rats in the rats in other 3 groups,and the rats in IL-33 and HMGB1 Ab groups were treated with IL-33 10μg and IL-33 10μg + HMGB1 neutralizing antibody respectively by vena caudalis injection 30 min before the model establishment. The levels of serum lactate dehydrogenase( LDH) and creatine kinase( CK),and expressions of tumor necrosis factor-α( TNF-α),IL-6,HMGB1,total Caspase-3,cleaved Caspase-3,Bcl-2 and Bax in all groups were detected,and HMGB1 mRNA levels in SO,I / R and IL-33 groups were quantificationally detected. Results After reperfusion for 4 h,IL-33 could significantly decrease LDH and CK levels and the TNF-α,IL-6,HMGB1 and Bax expressions,and Caspase-3 activation( P 0. 05),but increase the Bcl-2 expression( P 0. 05);while HMGB1 could weaken protective effect of IL-33( P 0. 05). Conclusion IL-33 may inhibit myocardial inflammatory reaction and apoptosis by inhibiting HMGB1 expression in myocardial tissues so as to protect I / R myocardium.

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Objective To investigate the protective effect of interleukin-33( IL-33) on myocardial ischemia and reperfusion injury( I / R) by down regulation of high mobility group protein1( HMGB1) expression in rats. Methods The 32 adult male SD rats were randomly divided into sham operation group( SO group,n = 10),I / R group( n = 10),IL-33 group( n = 6) and HMGB1 antibodies group( HMGB1 Ab group,n = 6). The rats in SO group underwent chest cutting operation,and a suture was passed through the myocardium beneath the left anterior descending( LAD) without ligation; while the I / R models were established in rats in the rats in other 3 groups,and the rats in IL-33 and HMGB1 Ab groups were treated with IL-33 10μg and IL-33 10μg + HMGB1 neutralizing antibody respectively by vena caudalis injection 30 min before the model establishment. The levels of serum lactate dehydrogenase( LDH) and creatine kinase( CK),and expressions of tumor necrosis factor-α( TNF-α),IL-6,HMGB1,total Caspase-3,cleaved Caspase-3,Bcl-2 and Bax in all groups were detected,and HMGB1 mRNA levels in SO,I / R and IL-33 groups were quantificationally detected. Results After reperfusion for 4 h,IL-33 could significantly decrease LDH and CK levels and the TNF-α,IL-6,HMGB1 and Bax expressions,and Caspase-3 activation( P 0. 05),but increase the Bcl-2 expression( P 0. 05);while HMGB1 could weaken protective effect of IL-33( P 0. 05). Conclusion IL-33 may inhibit myocardial inflammatory reaction and apoptosis by inhibiting HMGB1 expression in myocardial tissues so as to protect I / R myocardium.

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Available abstract

Objective To investigate the protective effect of interleukin-33( IL-33) on myocardial ischemia and reperfusion injury( I / R) by down regulation of high mobility group protein1( HMGB1) expression in rats. Methods The 32 adult male SD rats were randomly divided into sham operation group( SO group,n = 10),I / R group( n = 10),IL-33 group( n = 6) and HMGB1 antibodies group( HMGB1 Ab group,n = 6). The rats in SO group underwent chest cutting operation,and a suture was passed through the myocardium beneath the left anterior descending( LAD) without ligation; while the I / R models were established in rats in the rats in other 3 groups,and the rats in IL-33 and HMGB1 Ab groups were treated with IL-33 10μg and IL-33 10μg + HMGB1 neutralizing antibody respectively by vena caudalis injection 30 min before the model establishment. The levels of serum lactate dehydrogenase( LDH) and creatine kinase( CK),and expressions of tumor necrosis factor-α( TNF-α),IL-6,HMGB1,total Caspase-3,cleaved Caspase-3,Bcl-2 and Bax in all groups were detected,and HMGB1 mRNA levels in SO,I / R and IL-33 groups were quantificationally detected. Results After reperfusion for 4 h,IL-33 could significantly decrease LDH and CK levels and the TNF-α,IL-6,HMGB1 and Bax expressions,and Caspase-3 activation( P 0. 05),but increase the Bcl-2 expression( P 0. 05);while HMGB1 could weaken protective effect of IL-33( P 0. 05). Conclusion IL-33 may inhibit myocardial inflammatory reaction and apoptosis by inhibiting HMGB1 expression in myocardial tissues so as to protect I / R myocardium.

Key concepts: HMGB1, Lactate dehydrogenase, Creatine kinase, Medicine, Interleukin, Ischemia, Reperfusion injury, Ligation

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