Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2022 Apr 25:9:685998.
doi: 10.3389/fcvm.2022.685998. eCollection 2022.

Cardioprotective Effects and Possible Mechanisms of Luteolin for Myocardial Ischemia-Reperfusion Injury: A Systematic Review and Meta-Analysis of Preclinical Evidence

Qinyuan Pan  1 , Yang Liu  1 , Wenrui Ma  1 , Rongsheng Kan  2 , Hong Zhu  2 , Dongye Li  1   2
Affiliations

Cardioprotective Effects and Possible Mechanisms of Luteolin for Myocardial Ischemia-Reperfusion Injury: A Systematic Review and Meta-Analysis of Preclinical Evidence

Qinyuan Pan et al. Front Cardiovasc Med. .

Abstract

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.

Keywords: apoptosis; inflammation; luteolin; myocardial ischemia-reperfusion injury; oxidation.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
PRISMA flow chart of the search process.
Figure 2
Figure 2
Forest plot showing changes in myocardial infarct size. IS, infarct size; AAR, area at risk; LV, left ventricular.
Figure 3
Figure 3
Forest plots for effect of luteolin on hemodynamics including (A) LVSP, (B) LVEDP, (C) +dp/dtmax, (D) -dp/dtmax. LVSP, left ventricular systolic pressure; LVEDP, left ventricular end-diastolic pressure; +dp/dtmax, maximum rate of left ventricular pressure rise; -dp/dtmax, maximum rate of left ventricular pressure decrease.
Figure 4
Figure 4
Forest plots for (A) apoptotic rate, (B) MDA, (C) TNF-α. LAD, left anterior descending branch; MDA, malondialdehyde; TNF-α, tumor necrosis factor alpha.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Sandoval Y, Jaffe AS. Type 2 myocardial infarction: JACC review topic of the week. J Am Coll Cardiol. (2019) 73:1846–60. 10.1016/j.jacc.2019.02.018 - DOI - PubMed
    1. Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, et al. . Fourth universal definition of myocardial infarction (2018). J Am Coll Cardiol. (2018) 72:2231–64. 10.1016/j.jacc.2018.08.1038 - DOI - PubMed
    1. Jennings RB, Ganote CE. Structural changes in myocardium during acute ischemia. Circ Res. (1974) 35(Suppl 3):156–72. - PubMed
    1. Virmani R, Forman MB, Kolodgie FD. Myocardial reperfusion injury. Histopathological effects of perfluorochemical. Circulation. (1990) 81(3 Suppl):Iv57-68. - PubMed
    1. Ooi DS, Isotalo PA, Veinot JP. Correlation of antemortem serum creatine kinase, creatine kinase-MB, troponin I, and troponin T with cardiac pathology. Clin Chem. (2000) 46:338−44. - PubMed

Publication types