Tribulosin suppresses apoptosis via PKC epsilon and ERK1/2 signaling pathway during hypoxia/reoxygenation in neonatal rat ventricular cardiac myocytes

Tribulosin (tigogenin 3-O-beta-D-xylopyranosyl(1-2)-[beta-D-xylopyranosyl (1-3)]-beta-D-glucopyranosyl (1-4)-[a-L-rhamnopyranosyl(1-2)]-beta-D-galactopyranoside), a component of gross saponins of Tribulus terrestris, has been shown to produce cytoprotective effects in heart. Yet, the precise mechanisms are not fully understood. We examined the mechanisms of tribulosin on myocardial protection. Ventricular myocytes were isolated from the heart of neonatal rats and were exposed to 3 h of hypoxia followed by 2 h reoxygenation. Apoptosis was induced by hypoxia/reoxygenation (H/R), and the expression of protein kinase C epsilon (PKC epsilon) and extracellular signal-regulated kinase 1 and 2 (ERK1/2) in cultured neonatal rat cardiac myocytes was detected. The results indicated that treatment with tribulosin in the culture medium protected cardiac myocytes against apoptosis induced by H/R. PKC epsilon and ERK1/2 expression increased after pretreated with tribulosin. In the presence of PKC epsilon inhibitor co-treated with tribulosin, the expression of ERK1/2 was decreased in H/R cardiac myocytes. While preconditioned with PD98059, ERK1/2 inhibitor, no effects on the expression of PKC epsilon were detected. Tribulosin has protective effects on cardiac myocytes against apoptosis induced by H/R injury via PKC epsilon and ERK1/2 signaling pathway.