Vinegar/Tetramethylpyrazine Induces Nutritional Preconditioning Protecting the Myocardium Mediated by VDAC1.
Vinegar/Tetramethylpyrazine Induces Nutritional Preconditioning Protecting the Myocardium Mediated by VDAC1.
复制标题
醋/四甲基吡嗪诱导营养预处理，保护 VDAC1 介导的心肌
DOI：
10.1155/2021/6670088
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发表时间：
2021
影响因子：
--
通讯作者：
He M
中科院分区：
文献类型：
--
作者：
He H;Wang L;Qiao Y;Zhou Q;Yang B;Yin L;Yin D;He M
醋对健康有好处。川芎嗪(TMP)是决定其风味、品质和功能的主要成分。我们推测食醋/TMP预处理可通过低剂量、长期补充“营养预适应”来保护心肌，减轻缺氧/复氧(A/R)所致的心肌损伤。为了验证这一假说，采用高效液相色谱法检测食醋中TMP的含量；采用小鼠心脏和大鼠心肌细胞建立A/R损伤模型，从多项酶学指标、功能指标或细胞分子生物学指标评价食醋/TMP预处理对心肌的保护作用及其机制。结果表明，食醋中含有TMP，其含量与储藏时间成正比。食醋/TMP可改善A/R损伤小鼠离体心血流动力学参数，降低乳酸脱氢酶(LDH)和肌酸磷酸激酶活性，缩小心肌梗死范围，减少心肌细胞凋亡。同样，醋/TMP预处理可提高心肌细胞存活率，降低LDH活性，减少心肌细胞抗A/R损伤后的凋亡。醋液/TMP预处理还能维持A/R损伤心肌细胞的线粒体功能，包括提高耗氧率和细胞外酸化速率，减少活性氧产生，减少线粒体膜电位损失，线粒体膜通透性转换孔开放，细胞色素c释放。然而，醋/TMP的保护作用伴随着VDAC1在心肌中的表达下调，并被上调VDAC1表达的腺病毒pAD/VDAC1逆转。综上所述，本研究首次证明食醋/TMP可通过下调VDAC1的表达，抑制氧化应激，防止线粒体功能障碍，从而对鼻咽癌产生心肌保护作用，即VDAC1是靶细胞，线粒体是靶细胞器。TMP是食醋中最重要的心肌保护物质之一。
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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