rutaecarpine/hypoxia

Rutaecarpine has been shown to exhibit wide pharmacological effects in the cardiovascular system via stimulation of calcitonin gene-related peptide (CGRP) release. In the present study, the effect of rutaecarpine on hypoxia-induced right ventricular (RV) remodeling and the underlying mechanisms were

OBJECTIVE The aim of this study is to investigate the potential roles of Rutaecarpine (Rut) in hypoxia-induced human pulmonary artery smooth muscle cells (HPASMCs) model. METHODS HPASMCs were cultured with or without hypoxia followed by Rut administration. Cytotoxicity and cell proliferation were

Our previous studies showed that rutaecarpine (Rut) protected against myocardial ischemia/reperfusion (I/R) injury, which was associated with activation of transient receptor potential vanilloid subtype 1 (TRPV1). Recently, TRPV1 activation was also reported to exert neuroprotective effects. The

It is proposed that myocardial cell apoptosis causes ventricular remodeling and heart failure. The aim of the present study was to determine the effects of rutaecarpine (Rut) on hypoxia-reoxygenation (H-R)-induced apoptosis in myocardial cell line H9c2, as well as the underlying mechanisms. Cultured

In order to develop new drugs from natural products, constituents of natural medicines were examined for their effectiveness in the KCN-induced anoxia model in mice. Methanol extract from a Chinese medicine, evodia (fruits of Evodia rutaecarpa Benth. or E. officinalis Dode), had a significant effect