TRPA1 agonist cinnamaldehyde protects against high glucose-induced oxidative stress injury

AIM To explore the effect and mechanism of cinnamaldehyde on oxidative stress injury induced by high glucose. METHODS Rat myocardial cells (H9C2) were cultured with both high glucose medium (33 mmol/L D-glucose) and low glucose medium (5.5 mmol/L D- glucose-e.g., control group). Western blotting and immunohistochemistry were used to observe the expression of TRPA1 in H9C2 cells. Then, mitochondrial superooxide fluorescence probe (mito-SOX) and TUNEL apoptosis kits were used to observe the effects of cinnamaldehyde on ROS, cell apoptosis in H9C2 and the expressions of Nrf2 and TRPA1 were observed by Western blotting. TRPA1 and Nrf2 mRNA levels were detected by fluorescence quantitative PCR. RESULTS Western blotting and immunohistochemistry confirmed that TRPA1 was expressed in H9C2 cells. Cinnamaldehyde inhibited the ROS generation from mitochondria (P<0.01) and decreased the cells apoptosis (P<0.01) under high glucose condition and these effects were reversed by pretreatment with TRPA1 blocker HC 030031. Fluorescence quantitative PCR and Western blotting indicated that cinnamaldehyde up-regulated both the protein and mRNA levels of TRPA1 and Nrf2 (P<0.01) under high glucose condition and these effects were also blocked by HC 030031 (P<0.01). CONCLUSION Cinnamaldehyde prevents the oxidative stress injury induced by high glucose as a TRPA1 agonist and this effect is associated with Nrf2 activation.