YS 51, 1-(β-naphtylmethyl)-6,7-dihydroxy-1,2,3,4,-tetrahydroisoquinoline, protects endothelial cells against hydrogen peroxide-induced injury via carbon monoxide derived from heme oxygenase-1

Curcumin-Induced Heme Oxygenase-1 Expression Prevents H2O2-Induced Cell Death in Wild Type and Heme Oxygenase-2 Knockout Adipose-Derived Mesenchymal Stem Cells

“…In addition, CO may activate diverse other downstream signaling pathways, including nrf-2, guanylate cyclase, p38 mitogen-activated protein kinase (MAPK), PI3K-Akt, and iNOS [98,102,104]. Finally, CO can reduce the production of ROS in cells treated with H 2 O 2 , probably by preventing the formation of hydroxyl radicals by binding to ionized iron [105]. …”

(S)YS-51, a novel isoquinoline alkaloid, attenuates obesity-associated non-alcoholic fatty liver disease in mice by suppressing lipogenesis, inflammation and coagulation

“…However, it should be noted that YS-51 has antioxidant action by induction of Mn-SOD mRNA (Seo et al, 2004) and HO-1 activation effect in endothelial cells (Heo et al, 2007;Chaea et al, 2007). Interestingly, hepatic MnSOD activity is suppressed in male rodent and human NAFLD (Krautbauer et al, 2013), and Sirt1 induces MnSOD via stimulation of Peroxisome proliferator-activated receptor-γ-co-activator-1 (PGC-1 a key regulator of energy metabolism (Pfluger et al, 2008).…”

“…Previously, we reported that a series of synthetic tetrahydroisoquinoline alkaloids (THIs) including (S)YS-51 ( Fig. 1) showed beneficial effects in septic mice and in lipopolysaccharide (LPS)-activated RAW264.7 cells by reducing HMGB1 secretion (Chaea et al, 2007;Heo et al, 2007). In particular, (S)-enantiomer was superior to the corresponding (R)-enantiomer in attenuating disseminated intravascular coagulation and multiple organ failure in LPS-treated mice (Pyo et al, 2008).…”

YS 49, 1-(α-naphtylmethyl)-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, regulates angiotensin II-stimulated ROS production, JNK phosphorylation and vascular smooth muscle cell proliferation via the induction of heme oxygenase-1

“…However, we cannot exclude the possibility that CO, a byproduct of HO-1, reduces ROS production in VSMCs activated by Ang II. In fact, we found that RuCO, a CO-donor, increased cell viability in a concentration-dependent manner by reducing ROS production in H 2 O 2 -induced endothelial and C6 glial cells (Heo, 2007;Park et al, 2007). Endogenous CO serves as a protective factor that limits excessive VSMC proliferation associated with vascular diseases (Morita et al, 1995).…”

“…Emission of the trapped oxidized DCFH was then analyzed on a FACS Flow Supply System (BD-Biosciences, San Jose, CA). We compared the relative levels of ROS (Heo et al, 2007;Park et al, 2007) produced by Ang II in the presence or absence of YS 49.…”