Perillaldehyde reduces myocardial ischemia-reperfusion injury in rats by inhibiting MAPK1

Myocardial ischemia-reperfusion (MI/RI) injury is a type of cardiac damage that occurs during the reperfusion of myocardial tissue following a period of ischemia. While perillaldehyde (PAE) has been suggested to have anti-inflammatory properties, its effects on MI/RI remain unclear. This study aimed to evaluate the impact of PAE on MI/RI injury. To simulate MI/RI in vivo, an ischemia-reperfusion (I/R) rat model was established. The levels of lactate dehydrogenase (LDH), creatine kinase (CK) and oxidative stress-related factors were measured using commercial assay kits. The myocardial infarct size was assessed through triphenyl tetrazolium chloride (TTC) staining. The expression levels of miR-133a-3p and inflammatory factors were determined using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). Myocardial cell apoptosis was evaluated by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) staining, and the protein levels of BCL2 associated X (Bax), BCL2 apoptosis regulator (Bcl-2) and mitogen-activated protein kinase 1 (MAPK1) were analyzed by Western blot. PAE could effectively alleviate MI/RI-induced myocardial injury by reducing the levels of LDH and CK, as well as decreasing infarct size. It also mitigated the myocardial inflammatory response by lowering the levels of proinflammatory factors. Additionally, PAE reduced oxidative stress and apoptosis in myocardial cells. Further experiments showed that these protective effects of PAE were associated with the up-regulation of miR-133a-3p, which in turn decreased MAPK1 levels. In conclusion, PAE attenuated MI/RI-induced myocardial injury, inflammatory response, oxidative stress and apoptosis in rats by inhibiting MAPK1, indicating that PAE may effectively reduce myocardial damage caused by I/R injury.

Perillaldehyde; Myocardial ischemia-reperfusion injury; Inflammation; Oxidative stress; Apoptosis; MAPK1

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