The major contribution of myocardial damage to global mortalities raises debate
regarding the exploration of new therapeutic strategies for its treatment.
Therefore, our study investigated the counteracting effect of tiron against
isoprenaline (ISO)-mediated cardiac infarction in mice. Tiron was administered
to mice for 7 days prior to two consecutive injections of ISO on days 8 and 9 of the
treatment protocol. Tiron significantly reduced the levels of CK-MB, LDH, and
AST in serum samples of ISO-challenged mice. A considerable increase in the
cardiac antioxidant response was observed in tiron-treated mice, as indicated by
depletion of MDA and enhancement of antioxidant activities. Furthermore, tiron
induced a marked decrease in NLRP3, ASC, and caspase-1 levels accompanied by
weak immune reactions of IL-1β, NF-κB, TLR4, and iNOS in the infarct cardiac
tissues. Histopathological screening validated these variations observed in the cardiac specimens. Thus, tiron clearly mitigated the oxidative and inflammatory
stress by repressing the NLRP3 inflammasome and the TLR4/NF-κB/iNOS signaling
cascade.