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Myocardial infarction is a devastating event, especially when reperfusion does not occur. The inflammatory response has been implicated in the pathogenesis of left ventricular remodeling after myocardial infarction. This study focused on the anti-apoptotic and anti-inflammatory effects of Sesamin on ligation of the left anterior descending artery in experimental mouse model and the potential mechanism underlying the activation of JNK pathway and NF-κB pathway.
Ligation of the left anterior descending artery was used to induce MI in an experimental mouse model. After 1 week, H&E and PSR staining for histopathological changes of cardiac tissue were observed. Cellular signaling, caspase 3 activity, and nuclear factor kappa B (NF-κB) transcription were detected by Western blotting. The inflammatory response was evaluated by real-time quantitative RT-PCR and immunofluorescence staining.
Sesamin alleviated significantly MI-induced cardiac damage, indicated by the histopathological examination. The myocardial apoptosis in the border zone was dramatically reduced by sesamin, resulting from the altered expression of apoptotic factors. Moreover, treatment with sesamin also mitigated the inflammatory response, decreased expression of cytokines and the inactivation of NF-κB (nuclear factor κB) signalling. Sesamin decreased the levels of p-JNK protein, which in turn inactivated pro-apoptotic signaling events by restoring the balance between mitochondrial pro-apoptotic Bcl-2 and Bax proteins.
Sesamin alleviate MI-induced cardiac dysfunction through decrease of myocardial apoptosis and inflammatory response.