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

Author: Zhang Shuang   Li Hong   Yang Shi-Jie  

Publisher: Taylor & Francis Ltd

ISSN: 1028-6020

Source: Journal of Asian Natural Products Research, Vol.13, Iss.12, 2011-12, pp. : 1135-1145

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Abstract

Tribulosin (tigogenin 3-O-β-d-xylopyranosyl(1–2)-[β-d-xylopyranosyl (1–3)]-β-d-glucopyranosyl (1–4)-[a-l-rhamnopyranosyl(1–2)]-β-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) 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 and ERK1/2 expression increased after pretreated with tribulosin. In the presence of PKC 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 were detected. Tribulosin has protective effects on cardiac myocytes against apoptosis induced by H/R injury via PKC and ERK1/2 signaling pathway.

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