Bassim I Mohammad¹*
Myocardial injury caused by ischemia followed by reperfusion mediates a complex series of inflammatory response that reduces the benefit of medical interventions, such as percutaneous coronary intervention, and coronary bypass surgery. The objective of this study was to investigate the potential cardioprotective effect of tetrahydroisoquinoline against myocardial I/R, and the mechanistic pathway of this effect. A total of 32 adult (4 – 6 months) male Albino-Webster mice were randomly divided into 4 equal groups: (1) sham-control group, (2) ischemia and reperfusion (I/R) operated group, (3) vehicle-treated group, and (4) tetrahydroisoquinoline (TIQ)-treated group receiving TIQ 10 mg/kg once daily shortly before I/R. ELISA technique was performed to measure myocardial and plasma levels of cytokines (IL-1β, IL-6, and TNF-α), chemokine (MCP-1), and cTn-I. In addition, the activity of ICAM-1 was analyzed by Western blot. Further, the ischemia changes and myocytes injury were examined by histopathological assessment using hematoxylin and eosin (H&E) stain. The results demonstrated that treatment with TIQ markedly improved left ventricular function (LVF) in mice, and reduced plasma level of cTn-I as marker of cardiac injury. Moreover, the effects of TIQ was associated with attenuations in both chemokine and cytokines expression following I/R, that accompanied by down-regulation of activation of ICAM-1 pathway. In conclusions, this study revealed that treatment with TIQ was able to improve LV function after I/R. This improvement was associated with reductions of inflammatory response and activity of ICAM-1, as mechanistic link of its action.
Keywords: Tetrahydroisoquinoline; ICAM-1; Ischemia/Reperfusion