Diosgenin-Induced Protection Against Myocardial Ischaemia-Reperfusion Injury Is Mediated by Mitochondrial Katp Channels in a Rat Model Publisher Pubmed



Badalzadeh R¹ ; Yousefi B^{2, 3} ; Tajaddini A³ ; Ahmadian N⁴ Show Affiliations
Source: Perfusion (United Kingdom) Published:2015

Abstract

Objective: This study was aimed to evaluate the effects of diosgenin on myocardial ischaemia-reperfusion injury and the potential involvement of mitochondrial KATP (mitoKATP) channel and nitric oxide (NO) system blockades in this field. Materials and methods: After isolation of hearts of male Wister rats, the study was conducted on control and diosgenin- receiving hearts in the presence or absence of 5-HD and L-NAME (as antagonists of mitoKATP channel and NO system, respectively) in an isolated buffer-perfused heart model. Global ischaemia was induced by 30-min occlusion of aortic flow followed by 90-min reperfusion. Cardiac haemodynamics were recorded throughout the experiment using a PowerLab data acquisition system. Results: The levels of creatine kinase (CK-MB) and lactate dehydrogenase (LDH) in the coronary effluents were estimated colourimetrically. Diosgenin pre-administration significantly decreased the release of LDH and CK-MD into the coronary effluent as compared the with the control group (P<0.05). The left ventricular developed pressure (LVDP) and contractility (±dP/dt) were significantly improved and restored to pre-ischaemic values in the diosgenin-receiving group (P<0.05). There were no significant differences in left ventricular end-diastolic pressure, coronary flow and heart rate between the control and diosgenin-treated groups during the pre-ischaemic and reperfusion periods. Blocking the mitoKATP channels by 5-HD completely eliminated the positive effect of the diosgenin on the LVDP and ±dP/dt (P<0.05). However, blocking the NO system by L-NAME slightly reduced the diosgenin effects and the inhibitory effect of L-NAME was less than 5-HD. Conclusion: The results showed that diosgenin may have cardioprotective effects against myocardial reperfusion injury through activating the mitoKATP channels. © The Author(s) 2015.