IntroductionMyocardial ischaemia/reperfusion (I/R) injury is the leading
cause of morbidity and mortality worldwide. Despite novel advances in therapeutics, the management of myocardial I/R is still an unmet medical need.
Therefore, in the present study, we have demonstrated the protective effect
of ropivacaine (RPC) on the myocardial infarction in rats and its underlying
mechanism.Material and methodsInitially, the effect of RPC was determined on the
infarct size and histopathology of cardiac tissues. The effect of RPC was also
determined on the levels of various cardiac biomarkers such as creatine
kinase (CK), creatine kinase MB (CK-MB), alanine aminotransferase (ALT),
asparganine aminotransferase (AST), and lactate dehydrogenase (LDH), and
biomarkers of oxidative stress (MDA, SOD, and GSH) and inflammation (tumour necrosis factor-α (TNF-α), interleukin 1β (IL-1β), and IL-6). RPC effect
was also quantified on cellular apoptosis and COX-2 and iNOS expression
via western blot analysis. The RPC was further docked into the active site
of COX-2.ResultsIt has been found that RPC reduces the improves haemodynamics
of (LVSP and ± dp/dtmax, and LVEDP), infarct percentage and architecture of
cardiac tissues of rats. It also reduces the level of studies cardiac injury biomarkers together with a reduction of oxidative stress (MDA, SOD, and GSH)
and inflammation (TNF-α, IL-1β, and IL-6). Upon administration of RPC, the
rate of cellular apoptosis was found to be greatly reduced, with a reduction in COX-2 and iNOS expression. In docking analysis, RPC creates van
der Waals forces and pi-interactions with Tyr381, Arg106, Val102, Leu345,
Val509, Ser339, Leu338, Val335, Ala513, His75, and Leu517 at the catalytic
site of COX-2.ConclusionsCollectively, our results demonstrated that ropivacaine showed
significant benefit against myocardial ischaemic injury.
Aldo-keto reductase-7A protects liver cells and tissues from acetaminophen-induced oxidative stress and hepatotoxicity