SILAC-based proteomic analysis reveals that salidroside antagonizes cobalt chloride-induced hypoxic effects by restoring the tricarboxylic acid cycle in cardiomyocytes.

Hypoxic status alters the energy metabolism and induces cell injury in cardiomyocytes, and it further triggers the occurrence and development of cardiovascular diseases. Our previous studies have shown that salidroside (SAL) exhibits anti-hypoxic activity. However, the mechanisms remain obscure.

[L-arginine suppresses ischemia/reperfusion induced up-regulation of endothelin-1 production in a rat model of acute myocardial injury].

Objective: To examine the level of endothelin-1 (ET-1) in serum and its expression in myocardium tissue during the development of acute myocardial ischemia/reperfusion (I/R) injury in rat and the effects of L-arginine (L-Arg) administration on these indexes.

Methods: One hundred and ten Wistar rats were randomly divided into nine groups to receive: (1) sham surgery, (2)ischemia (I, by ligation of anterior descending coronary artery for 30 minutes), (3) I+reperfusion (R, by the removal of the ligature) for 0.5 hour, (4) I+R for 1 hour, (5) I+R for 2 hours; group (6) ~ (9) also received I/R treatment as in group 2 ~ 5 respectively but with L-Arg pretreatment.

Cardiotonic steroids attenuate ERK phosphorylation and generate cell cycle arrest to block human hepatoma cell growth.

Recent studies revealed the potential of Na(+)/K(+)-ATPase as a target for anticancer therapy and showed additional modes of action of cardiotonic steroids (CSs), a diverse family of naturally derived compounds, as inhibitors of Na(+)/K(+)-ATPase. The results from epidemiological studies showed significantly lower mortality rates in cancer patients receiving CSs, which sparked interest in the anticancer properties of these drugs. The present study was designed to investigate the anticancer effect of CSs (ouabain or cinobufagin) and to elucidate the molecular mechanisms of CS activity in hepatoma cell lines (HepG2 and SMMC-7721).