“…Then, what is the mechanism by which 2-MCA reduces damage in I/R rat hearts? We believe that the mechanism underlying this beneficial effect on I/R-injury may be closely related to its anti-oxidant and anti-inflammatory action of 2-MCA (Reddy et al, 2004;Guo et al, 2006) via induction of HO-1. This conclusion was based on the results that (1) 2-MCA increased HO-1 expression in endothelial cells, which was significantly inhibited by SnPPIX, a HO-1 inhibitor, (2) the reduced expression of VCAM-1 by 2-MCA in TNF-␣-activated endothelial cells was also inhibited by SnPPIX and HO-1siRNA transfection, (3) administration of 2-MCA resulted in increase of HO-1 in cardiac tissues (normal as well as I/R heart) in vivo.…”