Crocetin is one of the major active constituents of saffron extract, and it is a
carotenoid compound that prevents
reactive oxygen species and has anti-
inflammation and anti-apoptosis characteristics. This study aims to investigate whether
crocetin repairs myocardial damage in vivo after
ischemia reperfusion (I/R) and the mechanisms underlying its cardioprotective effects. Male Wistar rats were randomly allocated into three groups:
Sham, I/R, CRO.
Crocetin (50mg/kg/day, i.g.) or
sodium carboxymethylcellulose (CMC-Na) was intragastrically administered to Wistar rats for 7 days before operation.
Myocardial ischemia reperfusion injury (MIRI) was induced by occluding the left anterior descending (LAD) coronary artery for 45min and subsequent reperfusion for 3h. The cardioprotective effects of
crocetin were evaluated by biochemical values, histopathological observations and the antiapoptotic relative
proteins and gene expressions. In the rat model, pretreatment with 50mg/kg
crocetin reduced the cardiac injury, oxidative stress and
inflammation compared with that of the non-treated rats, as shown by the decreased levels of
infarct size,
creatine kinase-MB (CK-MB),
malondialdehyde (MDA), and
tumor necrosis factor-alpha (TNF-α) activity and the increased levels of total
superoxide dismutase (T-SOD) and
inflammation cytokines interleukin-10 (IL-10) activity.
Crocetin activation also decreases the
terminal deoxynucleotidyl transferase-mediated dUTP-
biotin nick end labeling (TUNEL) staining positive percentage and Bax expression, elevated Bcl-2 and
endothelial nitric oxide synthase (eNOS) expression and
nitrite (NO) production, these indicating that
crocetin can suppress the apoptosis damage. These results indicate that
crocetin can provide protection against MIRI in rats by inhibiting ROS production, blocking
inflammation, and reducing myocardium apoptosis.