ArticleOxidative medicine and cellular longevity2021
Vinegar/Tetramethylpyrazine Induces Nutritional Preconditioning Protecting the Myocardium Mediated by VDAC1.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Role of vinegar in cardiovascular health: A narrative review.Journal of biological methods · 2025Review
- Transcriptome Sequencing of Bacillus sp. TTMP20 and Analysis of the Effect of BDH Gene on Tetramethylpyrazine Synthesis.Current microbiology · 2024Article
- Fruit vinegar as a promising source of natural anti-inflammatory agents: an up-to-date review.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2024Review
- Tanshinone IIA confers protection against myocardial ischemia/reperfusion injury by inhibiting ferroptosis and apoptosis via VDAC1.International journal of molecular medicine · 2023Article
- Synergistic Fermentation with Functional Microorganisms Improves Safety and Quality of Traditional Chinese Fermented Foods.Foods (Basel, Switzerland) · 2023Review
- Targeting calcium-mediated inter-organellar crosstalk in cardiac diseases.Expert opinion on therapeutic targets · 2022Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
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Abstract
Vinegar is good for health. Tetramethylpyrazine (TMP) is the main component of its flavor, quality, and function. We hypothesized that vinegar/TMP pretreatment could induce myocardial protection of "nutritional preconditioning (NPC)" by low-dose, long-term supplementation and alleviate the myocardial injury caused by anoxia/reoxygenation (A/R). To test this hypothesis, TMP content in vinegar was detected by HPLC; A/R injury model was prepared by an isolated mouse heart and rat cardiomyocyte to evaluate the myocardial protection and mechanism of vinegar/TMP pretreatment by many enzymatic or functional, or cellular and molecular biological indexes. Our results showed that vinegar contained TMP, and its content was in direct proportion to storage time. Vinegar/TMP pretreatment could improve hemodynamic parameters, decrease lactate dehydrogenase (LDH) and creatine phosphokinase activities, and reduce infarct size and apoptosis in the isolated hearts of mice with A/R injury. Similarly, vinegar/TMP pretreatment could increase cell viability, decrease LDH activity, and decrease apoptosis against A/R injury of cardiomyocytes. Vinegar/TMP pretreatment could also maintain the mitochondrial function of A/R-injured cardiomyocytes, including improving oxygen consumption rate and extracellular acidification rate, reducing reactive oxygen species generation, mitochondrial membrane potential loss, mitochondrial permeability transition pore openness, and cytochrome c releasing. However, the protective effects of vinegar/TMP pretreatment were accompanied by the downregulation of VDAC1 expression in the myocardium and reversed by pAD/VDAC1, an adenovirus that upregulates VDAC1 expression. In conclusion, this study is the first to demonstrate that vinegar/TMP pretreatment could induce myocardial protection of NPC due to downregulating VDAC1 expression, inhibiting oxidative stress, and preventing mitochondrial dysfunction; that is, VDAC1 is their target, and the mitochondria are their target organelles. TMP is one of the most important myocardial protective substances in vinegar.
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