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目的 探讨桂皮醛对高糖介导的心肌细胞氧化应激损伤的作用及机制。方法 大鼠心肌细胞（H9C2）以高糖培养基（33mmol/L D-葡萄糖）培养，以低糖培养基（5.5 mmol/L D-葡萄糖）作为对照。首先利用Western blot和免疫组织化学证实瞬时受体电位通道A1亚型（TRPA1）在H9C2心肌细胞中的表达；在此基础上分别利用线粒体超氧化物荧光探针（mitoSOX）及TUNEL细胞凋亡试剂盒观察桂皮醛对高糖环境下H9C2细胞线粒体活性氧(ROS)水平以及细胞凋亡的影响，以Western blot法观察Nrf2和TRPA1的表达；利用荧光定量PCR观察TRPA1及Nrf2 mRNA水平。结果 TRPA1在H9C2细胞中有表达，桂皮醛可显著抑制高糖介导线粒体ROS生成（P<0.01），并可减少心肌细胞的凋亡（P<0.01），而上述作用可被TRPA1的阻断剂HC030031所阻断。桂皮醛可上调TRPA1、Nrf2的蛋白及mRNA表达（P<0.01），而通过HC030031抑制TRPA1可显著减弱桂皮醛的上述作用（P<0.01）。结论 桂皮醛可防止高糖介导的心肌细胞氧化应激损伤，而该作用可能与其激活TRPA1，上调Nrf2有关。
Objective To investigate the effect and mechanism of cinnamaldehyde on high glucose-induced oxidative stress injury in cardiomyocytes. Methods Rat myocardial cells (H9C2) were cultured in high glucose medium (33 mmol / L D-glucose) and low glucose medium (5.5 mmol / L D-glucose) as controls. First, the expression of transient receptor potential channel subtype A1 (TRPA1) in H9C2 cardiomyocytes was confirmed by Western blot and immunohistochemistry. On the basis of this, mitochondrial superoxide fluorescent probe (mitoSOX) and TUNEL apoptosis reagent To observe the effect of cinnamaldehyde on mitochondrial reactive oxygen species (ROS) and apoptosis in H9C2 cells under high glucose conditions. The expression of Nrf2 and TRPA1 was detected by Western blot. The levels of TRPA1 and Nrf2 mRNA were detected by real-time PCR. Results The expression of TRPAl was detected in H9C2 cells. Cinnamaldehyde significantly inhibited ROS production (P <0.01) and decreased cardiomyocyte apoptosis (P <0.01), which was blocked by TRPAl Agent HC030031 blocked. Cinnamaldehyde up-regulated the protein and mRNA expression of TRPA1 and Nrf2 (P <0.01). Inhibition of TRPA1 by HC030031 significantly attenuated the effects of cinnamaldehyde (P <0.01). Conclusion Cinnamaldehyde can prevent oxidative stress injury induced by high glucose in cardiomyocytes, which may be related to the activation of TRPAl and upregulation of Nrf2.