Key result
Pre-treatment with the NF-κB inhibitor pyrrolidine dithiocarbamate inhibited adriamycin-induced myocardial apoptosis and p53 expression in rats, indicating that NF-κB activation is pro-apoptotic in adriamycin-induced myocardial injury.
Why the study?
Does inhibition of NF-κB with PDTC prevent adriamycin-induced myocardial apoptosis in rats?
Does inhibition of NF-κB with PDTC prevent adriamycin-induced myocardial apoptosis in rats?
NF-κB activation plays a pro-apoptotic role in adriamycin-induced acute myocardial injury by regulating p53 expression, suggesting NF-κB inhibition as a potential cardioprotective strategy.
Nuclear factor κB (NF-κB) is activated by a wide range of inducers and is able to mediate gene transcription. We investigated the role of NF-κB in adriamycin-induced myocardial injury in rats and its mechanism of action. A total of 30 male Wistar rats were randomly divided into 3 groups: control, anthracycline antibiotic adriamycin (ADR) and ADR + pyrrolidine dithiocarbamate (PDTC). Myocardial apoptosis was detected by TUNEL assay; myocardium p53 gene expression was examined by RT-PCR analysis; location and distribution of p53 was observed by immunohistochemical assay; myocardial expression of p53 protein was assessed by Western blot analysis and activity of NF-κB was evaluated by electrophoretic mobility shift assay. The binding activity of NF-κB, myocardial apoptotic index and expression of p53 increased significantly in the ADR groups. All of these changes induced by ADR were inhibited by PDTC. It was concluded that NF-κB activation may be pro-apoptotic through regulation of the expression of p53 in adriamycin-induced myocardial injury.
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Baogui Sun (2011) studied Adriamycin-induced acute myocardial injury (n=30). Pyrrolidine dithiocarbamate (PDTC) vs. Adriamycin alone and saline control was evaluated on Myocardial apoptosis and p53 expression. Pre-treatment with the NF-κB inhibitor pyrrolidine dithiocarbamate inhibited adriamycin-induced myocardial apoptosis and p53 expression in rats, indicating that NF-κB activation is pro-apoptotic in adriamycin-induced myocardial injury.
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