Key result
Luteolin administration significantly reduced myocardial infarct size (SMD -2.50) and ameliorated hemodynamics compared to control groups in preclinical models of myocardial ischemia-reperfusion injury.
Why the study?
Effective clinical therapies for myocardial ischemia-reperfusion injury are lacking, leading researchers to investigate whether luteolin confers cardioprotective effects.
Does luteolin reduce myocardial infarct size and improve hemodynamics in preclinical models of myocardial ischemia-reperfusion injury?
Systematic Review (n=415)
Does luteolin reduce myocardial infarct size and improve hemodynamics in preclinical models of myocardial ischemia-reperfusion injury?
Standardized Mean Difference: -2.5 (95% CI -3.47–-1.52)
p-value: p=<0.00001
Luteolin demonstrates cardioprotective effects against myocardial ischemia-reperfusion injury in preclinical models by reducing infarct size and improving hemodynamics, likely through anti-apoptotic, anti-oxidative, and anti-inflammatory mechanisms.
Luteolin reduces infarct size and improves hemodynamics in preclinical MIRI; leaves open clinical translation pending human trials.
Background At present, effective clinical therapies for myocardial ischemia-reperfusion injury (MIRI) are lacking. We investigated if luteolin conferred cardioprotective effects against MIRI and elucidated the potential underlying mechanisms. Method Four databases were searched for preclinical studies of luteolin for the treatment of MIRI. The primary outcomes were myocardial infarct size (IS) and intracardiac hemodynamics. The second outcomes were representative indicators of apoptosis, oxidative stress, and inflammatory. The Stata and RevMan software packages were utilized for data analysis. Results Luteolin administration was confirmed to reduce IS and ameliorate hemodynamics as compared to the control groups ( p < 0.01). IS had decreased by 2.50%, 2.14%, 2.54% in three subgroups. Amelioration of hemodynamics was apparent in two different myocardial infarct models (model of left anterior descending branch ligation and model of global heart ischemia), as left ventricular systolic pressure improved by 21.62 and 35.40 mmHg respectively, left ventricular end-diastolic pressure decreased by 7.79 and 4.73 mmHg respectively, maximum rate of left ventricular pressure rise increased by 737.48 and 750.47 mmHg/s respectively, and maximum rate of left ventricular pressure decrease increased by 605.66 and 790.64 mmHg/s respectively. Apoptosis of cardiomyocytes also significantly decreased, as indicated by thelevels of MDA, an oxidative stress product, and expression of the inflammatory factor TNF-α ( p < 0.001). Conclusion Pooling of the data demonstrated that luteolin exerts cardioprotective effects against MIRI through different signaling pathways. As possible mechanisms, luteolin exerts anti-apoptosis, anti-oxidation, and anti-inflammation effects against MIRI.
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Pan et al. (2022) conducted a systematic review in Myocardial ischemia-reperfusion injury (MIRI) (n=415). Luteolin vs. Normal saline, vehicle, or no treatment was evaluated on Myocardial infarct size (IS/AAR ratio) (SMD -2.50, 95% CI -3.47 to -1.52, p=<0.00001). Luteolin administration significantly reduced myocardial infarct size (SMD -2.50) and ameliorated hemodynamics compared to control groups in preclinical models of myocardial ischemia-reperfusion injury.
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