Pelargonidin-3-O-glucoside prevents isoproterenol-induced myocardial infarction via modulating cardiac and inflammatory markers expression in experimental rats.

Abstract

IntroductionThis study examined the cardioprotective effects of Pelargonidin-3-O-glucoside (Pg3G) against myocardial infarction induced by isoproterenol (ISO) in male Wistar rats.MethodsAnimals were divided into four groups each groups contain six animals. Group 1 control; Group 2 Pg3G treated control; Group 3 ISO-control; Group 4 Pg3G + ISO treated rats. At the end of the experiment period the animals were sacrificed and collected the serum, heart tissue used for the experimental work.ResultsAccording to the network pharmacology analysis, Prostaglandin-endoperoxide Synthase 2 (PTGS2), Matrix metallo proteins -9 (MMP-9), and tumour necrosis factor-alpha (TNF-α) were identified as potential targets among the 97 common targets between Pg3G and myocardial injury. Further, we investigated that prominent cardiac indicator such creatine kinase (CK), CK-MB, cardiac troponin T (cTnT), and cardiac troponin I (cTnI) were not elevated by ISO in the presence of Pg3G administration. Additionally, Pg3G administration decreased the pro-inflammatory cytokines generated by ISO, including as interleukin-6 (IL-6), interleukin-1 beta (IL-1β), and TNF-α, suggesting its anti-inflammatory qualities. Additionally, Pg3G increased levels of reduced glutathione (GSH) and restored the activity of important antioxidant enzymes that were depleted by ISO-induced oxidative stress, including glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD).DiscussionPg3G capacity to reduce ISO-induced inflammatory, fibrotic, and cardiac toxicity markers in myocardial tissue was demonstrated by gene expression investigations. Therefore, Pg3G may be considered for ISO-induced cardiac injury since it provides significant cardioprotection by reducing oxidative stress, inflammation, and fibrosis.