Anti-inflammatory effect of trans-anethol in a rat model of myocardial ischemia-reperfusion injury
Marwa Matboli, Amany Helmy Hasanin, Shaimaa Hamady, Eman Khairy, Reham Hussein Mohamed, Yasmin M. Aboul-Ela, Mona Raafat, Sara Abdel Gawad Elsebay, Hossam Y. Emam, Rania Shamekh, Sara H. A. Agwa
Abstract
Myocardial ischemia‑reperfusion injury (MI/R) is considered a main risk factor for global cardiac mortality and morbidity, for which no effective treatment exists. Both inflammation and epigenetic regulation play a pivotal role in the early stage of MI/R. The present study aimed at investigating the prospective anti-inflammatory role of trans-anethole (TNA) in targeting MI/R and its related mechanism in upregulating the expression of the inflammatory and cardiac-related gene (VAV3), and its epigenetic regulators (lncRNA-JRKL-AS1 and miR-1298) that were retrieved from in-silico data analysis in an ischemia/reperfusion (I/R) rat model. MATERIALS & METHODS: TNA was administered in 3 doses (50, 100, and 200 mg/kg), 15 min prior to coronary ligation in male Wistar rats. The left ventricular end-diastolic pressure and dP/dtmax were assessed. Histopathological, biochemical, and molecular analyses were performed to assess the effects of TNA pre-treatment on the I/R rats model. RESULTS: TNA alleviated the I/R-induced cardiac injury pathologically and improved the cardiac function tests and enzymes. At the molecular level, TNA upregulated the expression level of the retrieved RNA-based panel (VAV3 mRNA/miR-1298/lncRNA JRKL-AS1). At the protein level, TNA decreased the cardiac content of the pro-inflammatory cytokine TNF-α. CONCLUSION: TNA has demonstrated a potential ability to alleviate the cardiac injury and attenuate the inflammatory response following ischemia-reperfusion in the rat model through modulation of the expression of RNA panel (VAV3 mRNA/miR-1298/lncRNA JRKL-AS1) and TNF- α protein.