The use of
cisplatin is severely limited by the risk of developing cardiovascular complications.
Sinapic acid may reduce
cisplatin's side effects. The
anti oxidant, anti-inflammatory, and
peroxynitrite-scavenging properties of
sinapic acid could provide protection against the
cardiotoxicity caused by
cisplatin. To induce toxicity in rats,
cisplatin was administered for a period of 5 weeks. Animal electrocardiograms were obtained after
cisplatin toxicity had taken effect. Blood samples and heart tissues were then harvested from the anesthetized animals. The ELISA technique was used to evaluate the level of proinflammatory
cytokines and oxidative and nitrosative stress indicators in the heart tissue and serum. A real-time PCR was used to analyze GPX4 and NF-κB expression in the heart tissue.
Hematoxylin-
eosin and Masson's trichrome were also utilized. Electrocardiograms data showed an increase in QRS and QT intervals. Biochemically,
cisplatin increased oxidative, nitrosative, and proinflammatory
cytokine levels. Animals exposed to
cisplatin had histopathological findings in the heart tissue, according to the results of histological assessment.
Sinapic acid reduced
TNF-alpha,
interleukin-6,
malondialdehyde, and
ischemia-modified albumin.
Sinapic acid also reduced oxidative and nitrosative stress. Furthermore,
Sinapic acid restored lengthy QT and QRS.
Cisplatin-treated rats had higher NF-κB activation than controls. This effect was successfully inhibited by
sinapic acid. Histopathologically, tissues treated with
sinapic acid were less damaged than tissues treated with
cisplatin. In conclusion, our results suggest that
sinapic acid exhibited a protective effect against the
cardiotoxicity induced by
cisplatin. These effects may be caused by the overexpression of GPX4 and the downregulation of
NF-KB, as well as
antioxidant and anti-inflammatory properties.