Anti-inflammatory Influence of Trans-anethole on The Cardiac Regenerative Capacity in Myocardial Ischemia/Reperfusion Injuries


Hamed M. O. A., El-Desouky M. A., Matboli M., Elhakim H. K. A., Mahran N. A.

EGYPTIAN JOURNAL OF CHEMISTRY, cilt.67, sa.3, ss.309-321, 2024 (ESCI) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 67 Sayı: 3
  • Basım Tarihi: 2024
  • Doi Numarası: 10.21608/ejchem.2023.235111.8585
  • Dergi Adı: EGYPTIAN JOURNAL OF CHEMISTRY
  • Derginin Tarandığı İndeksler: Emerging Sources Citation Index (ESCI), Scopus, CAB Abstracts
  • Sayfa Sayıları: ss.309-321
  • Karadeniz Teknik Üniversitesi Adresli: Hayır

Özet

Reperfusion injury of an ischemic heart is considered one of the risk factors of cardiac mortality associated with high inflammation, limiting the innate ability of the body to heal even with the use of external interventions. Trans-anethole (TA) is an efficient anti-inflammatory agent that protects the heart and increases its capacity to regenerate. 3 doses of TA (50, 100, and 200 mg/Kg) were administered 60 minutes before ischemia/reperfusion injury induction. Cardiac left ventricle tissue and blood samples were used for histopathological and immunohistochemical examination and assessment of the expression of mRNA FOXC1- miR-1248 - lncRNA TSIX and cardiac enzymes. TA administration negated biochemical, molecular, and histopathological alterations induced by ischemia-reperfusion injuries. The present findings revealed a reduction in LDH, CKMB, and cardiac troponin. The microscopic examination revealed regression in the presence of cardiac edema, hemorrhage, cellular inflammatory infiltration, and fibrosis, along with an elevated number of C kit + cells in the cardiac tissue specimens. Also, TA showed an increase in the relative expression of miR-1248 with a decrease in mRNA FOXC1 and lncRNA TSIX. The study's findings suggest that mRNA FOXC1, miR-1248, and lncRNA TSIX possess high potential as diagnostic biomarkers, exhibiting perfect sensitivity and specificity.