Antibodies against disulfidebond A oxidoreductase-like protein (DsbA-L) and CTRP9 were bought from Santa Cruz Biotechnology (Santa Cruz, CA, USA); antibodies against CHOP, GRP-78, TNF-[alpha], Caspase-3, Caspase-9, Caspase-12, and GAPDH were from Cell Signaling Technology (Beverly, MA, USA).
CTRP9 significantly suppressed ERS in diabetic hearts as demonstrated by significantly reduced GRP-78 and CHOP expression compared with treating with KH buffer, together with significantly increased DsbA-L expression (Figures 2(a), 2(c), 2(d), and 2(e)).
TG treatment led to significantly increased ERS and inflammatory response, as demonstrated by enhanced CHOP, GRP-78, and TNF-[alpha] expression, together with greatly reduced cellular protein levels of DsbA-L (Figures 3(a), 3(b), 3(e), 3(f), and 3(g)).
DsbA-L knockdown induced ERS in H9c2 cells as shown by significantly increased CHOP and GRP-78 expression (Figures 4(a), 4(e), and 4(f)).
Representative images (a) and bar graphs of cardiac TNF-[alpha] (b), CHOP (c), GRP-78 (d), and DsbA-L (e) determined by Western blots.