Protective Effects of Rutaecarpine in Cardiac Anaphylactic Injury is Mediated by CGRP

Abstract

Previous investigations have indicated that rutaecarpine activates the vanilloid receptor to evoke calcitonin gene-related peptide (CGRP) release. CGRP has been shown to alleviate cardiac anaphylactic injury. In the present study, the effect of rutaecarpine on cardiac anaphylaxis was examined. Challenge of presensitized guinea-pig hearts with a specific antigen caused marked decreases in coronary flow (CF), left ventricular pressure (LVP) and its derivatives (+/- dp/dt(max)), an increase in heart rate, and prolongation of the P-R interval. Rutaecarpine (0.3 or 1 microM) markedly increased the content of calcitonin gene-related peptide (CGRP) in the coronary effluent and decreased the content of tumor necrosis factor-alpha (TNF-alpha) in myocardial tissues concomitantly with a significant improvement of cardiac function and alleviation of the extension of the P-R interval. Rutaecarpine at the concentration of 1 microM also inhibited the sinus tachycardia. The protective effects of rutaecarpine on cardiac anaphylaxis were abolished by CGRP (8-37), a selective CGRP receptor antagonist. These results suggest that the protective effects of rutaecarpine on cardiac anaphylactic injury are related to inhibition of TNF-alpha production by stimulation of CGRP release.

Development and validation of an UPLC-ESI-MS/MS method for determination of dehydroevodiamine, limonin, evodiamine, and rutaecarpine in Evodiae Fructus

“…Alkaloids are traditionally regarded as the major bioactive compounds in EF not only because a number of types of alkaloids were isolated from the herb,[121314] but also pharmacological and clinical studies indicated that alkaloids from EF had antipolysarcous,[15] cardiotonic,[1617] central stimulative,[18] vasodilatory,[1920] and anticancer activities. [212223] Evodiamine and rutaecarpine were specified as the biomarkers for quality assessment on EF in Chinese Pharmacopoeia (CP) (edition 2005),[24] and another compound, limonin, was used combined with evodiamine and rutaecarpine in CP (edition 2010)[1] for better assessment on this herb.…”

Rutaecarpine Induces Chloride Secretion across Rat Isolated Distal Colon

“…In addition, Fructus evodiae (fruit of E. rutaecarpa) is also used for the treatment of headache, thoracicoabdominal pain, vomiting, colds, and reduced blood circulation (Fei et al, 2003). Pharmacological studies indicate that Rut has various bioactivities, such as causing vasodilatation by mechanisms of an endothelium-dependent manner coupled with the synthesis or release of nitric oxide (Wang et al, 1996), inhibiting vasoconstriction induced by anaphylaxis (Yu et al, 2005), inducing positive inotropic and chronotropic actions (Kobayashi et al, 2001), protecting the myocardium mediated by calcitonin gene-related peptide (Hu et al, 2002;Yi et al, 2004), increasing intracellular Ca 2ϩ concentration in endothelium (Wang et al, 1996), suppressing platelet plug formation in mesenteric venules (Sheu et al, 2000), inhibiting prostaglandin production in RAW264.7 macrophages (Woo et al, 2001), relaxation of rabbit and human internal anal sphincter (Jiang et al, 2000), gastroprotective effect against injury induced by aspirin and stress (Wang et al, 2005), anti-Helicobacter pylori (Tominaga et al, 2002), blockade of delayed rectifier K ϩ current in NG108-15 neuronal cells (Wu et al, 2001), inhibiting cytochrome P450 in human liver microsomes (Ueng et al, 2002(Ueng et al, , 2006Iwata et al, 2005), and inhibition of COX-2 (Moon et al, 1999).…”

Development and validation of HPLC methods for the analysis of phenethylamine and indoloquinazoline alkaloids inEvodiaspecies

“…Rutaecarpine has been found to exert several pharmacological effects, such as vasodilatatory [6,7], antithrombotic [8], cardioprotective [9], and anti-inflammatory [10] activities. Rutaecarpine is also able to inhibit UV A-induced increased generation of reactive oxygen species, suggesting a possible application in the prevention of UV Ainduced photoaging [11].…”