N'-(2,6-dimethoxybenzylidene)-3-(4-methoxyphenyl) acrylohydrazide abates oxidative stress and purinergic enzymes abnormality associated with iron-induced cardiotoxicity in Wistar rats: Experimental and computational perspectives

Abstract

The effects of N'-(2,6-dimethoxybenzylidene)-3-(4-methoxyphenyl) acrylohydrazide (KAD 9) on iron-induced cardiac injury was investigated. Evaluations of the iron chelating capability, ferric-reducing antioxidant power (FRAP), as well as DPPH free radical scavenging activity of KAD 9 were performed. The oxidative cardiac injury induced by 0.1 mM FeSO4 was treaed with varied doses of KAD 9 ex vivo. Comparing KAD 9 to conventional quercetin, the DPPH radical scavenging ability of KAD 9 significantly rises with concentration (p<0.05). The cardiac injury was generated, and this resulted in decreased malondialdehyde (MDA), catalase (CAT), ATPase, and ENTPDase activity (p<0.05). A notable increase in GSH level was seen in KAD 9 treated group. Furthermore, it was observed that KAD 9 had closer binding affinity with ATPase and ENTPDase. Due to its ability to regulate nucleotide hydrolysis and lessen oxidative stress, KAD 9 has the potential to both treat and protect against oxidative cardiac injury.