Safwa Mahmoud Soror
Dept. Head
Suppression of NLRP3 inflammasome orchestrates the protective efficacy of tiron against isoprenaline-induced myocardial injury
• 2024
Publication Information
Authors
Ateya M. Ibrahim7,8, Reham M. Ibrahim9, Hala Anwer9,
Ostan Mihaela10*, Rada Olga10, Khairiah M. Alwutayed11,
Rasha H. Al-Serwi12, Mohamed El-Sherbiny13, Safwa M. Sorour14
and Dalia H. El-Kashef15
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publication.type
Local
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Abstract
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
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