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Meta-Analysis
. 2022 May 2;17(5):e0267968.
doi: 10.1371/journal.pone.0267968. eCollection 2022.

The role and mechanism of tetramethylpyrazine for atherosclerosis in animal models: A systematic review and meta-analysis

Affiliations
Meta-Analysis

The role and mechanism of tetramethylpyrazine for atherosclerosis in animal models: A systematic review and meta-analysis

SiJin Li et al. PLoS One. .

Abstract

Background: Atherosclerosis(AS) is widely recognized as a risk factor for incident cardiovascular and cerebrovascular diseases. Tetramethylpyrazine (TMP) is the active ingredient of Ligusticum wallichii that possesses a variety of biological activities against atherosclerosis.

Objective: This systematic review and meta-analysis sought to study the impact of and mechanism of tetramethylpyrazine for atherosclerosis in animal models.

Methods: A systematic search was conducted of PubMed, Embase, Cochrane Library, Web of Science database, Chinese Biomedical (CBM) database, China National Knowledge Infrastructure (CNKI), WanFang data, and Vip Journal Integration Platform, covering the period from the respective start date of each database to December 2021. We used SYRCLE's 10-item checklist and Rev-Man 5.3 software to analyze the data and the risk of bias.

Results: Twelve studies, including 258 animals, met the inclusion criteria. Compared with the control group, TMP significantly reduced aortic atherosclerotic lesion area, and induced significant decreases in levels of TC (SMD = -2.67, 95% CI -3.68 to -1.67, P < 0.00001), TG (SMD = -2.43, 95% CI -3.39 to -1.47, P < 0.00001), and LDL-C (SMD = -2.87, 95% CI -4.16 to -1.58, P < 0.00001), as well as increasing HDL-C (SMD = 2.04, 95% CI 1.05 to 3.03, P = 0.001). TMP also significantly modulated plasma inflammatory responses and biological signals associated with atherosclerosis. In subgroup analysis, the groups of high-dose TMP (≥50 mg/kg) showed better results than those of the control group. No difference between various durations of treatment groups or various assessing location groups.

Conclusion: TMP exerts anti-atherosclerosis functions in an animal model of AS mediated by anti-inflammatory action, antioxidant action, ameliorating lipid metabolism disorder, protection of endothelial function, antiplatelet activity, reducing the proliferation and migration of smooth muscle cells, inhibition of angiogenesis, antiplatelet aggregation. Due to the limitations of the quantity and quality of current studies, the above conclusions need to be verified by more high-quality studies.

Trial registration number: PROSPERO registration no.CRD42021288874.

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Flow diagram of the study identification and selection process.
Fig 2
Fig 2. Risk of bias and quality assessment.
Fig 3
Fig 3. The methodological quality of the included studies was assessed.
Fig 4
Fig 4. Forest plot of TMP on aortic lesion area.
Fig 5
Fig 5. Forest plot of TMP on TC.
Fig 6
Fig 6. Forest plot of TMP on TG.
Fig 7
Fig 7. Forest plot of TMP on LDL-C.
Fig 8
Fig 8. Forest plot of TMP on HDL-C.
Fig 9
Fig 9. Subgroup analyses of the aortic lesion area.
(A) The different doses of TMP on the effect size of the outcome measure; (B) the duration of treatment on the effect size of the outcome measure.; (C) the different locations of the aortic lesion of TMP on the effect size of the outcome measure. #P < 0.05 vs. control groups; &P > 0.05 vs. control groups.
Fig 10
Fig 10. A schematic representation of mechanisms of TMP for AS.

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References

    1. Kuznetsova T, Prange KHM, Glass CK, de Winther MPJ. Transcriptional and epigenetic regulation of macrophages in atherosclerosis. Nat Rev Cardiol. 2020;17(4):216–228. doi: 10.1038/s41569-019-0265-3 . - DOI - PMC - PubMed
    1. Conte SM, Vale PR. Peripheral Arterial Disease. Heart Lung Circ. 2018;27(4):427–432. doi: 10.1016/j.hlc.2017.10.014 . - DOI - PubMed
    1. Andersson C, Vasan RS. Epidemiology of cardiovascular disease in young individuals. Nat Rev Cardiol. 2018;15(4):230–240. doi: 10.1038/nrcardio.2017.154 . - DOI - PubMed
    1. Benjamin EJ, Muntner P, Alonso A, Bittencourt MS, Callaway CW, Carson AP, et al.. American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart Disease and Stroke Statistics-2019 Update: A Report From the American Heart Association. Circulation. 2019;139(10):e56–e528. doi: 10.1161/CIR.0000000000000659 . - DOI - PubMed
    1. Michos ED, McEvoy JW, Blumenthal RS. Lipid Management for the Prevention of Atherosclerotic Cardiovascular Disease. N Engl J Med. 2019;381(16):1557–1567. doi: 10.1056/NEJMra1806939 . - DOI - PubMed

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