Planta Med. 2011 Mar 7. [Epub ahead of print]
Standardized Extracts from Hawthorn Leaves and Flowers in the Treatment of Cardiovascular Disorders - Preclinical and Clinical Studies.
Koch E, Malek FA.
Preclinical Research, Dr. Willmar Schwabe GmbH & Co. KG, Karlsruhe, Germany.
Extracts from different parts of hawthorn plants ( CRATAEGUS SPP.) are used worldwide for the treatment of cardiovascular diseases. So far, almost all clinical studies have been conducted with standardized hydroalcoholic extracts from leaves and flowers. These trials with more than 4000 patients have provided evidence for clinical benefits in the therapy of mild chronic heart failure. Besides cardiotonic effects, recent pharmacological investigations indicate that hawthorn extracts also possess cardio- and vasoprotective properties. Thus, these extracts may also be employed in the prophylactic and therapeutic treatment of such conditions as endothelial dysfunction, atherosclerosis, coronary heart disease, or prevention of restenosis/reocclusion following peripheral endovascular treatment. In this review the pharmacological and clinical data relating to these standardized extracts are summarized.
Space Med Med Eng (Beijing). 2005 Jun;18(3):157-60.
Regulative effects of hawthorn leave flavonoids on cytotoxicity, NO and Ca2+ in hypoxia-treated human umbilical vein endothelial cells.
Lan WJ, Ge YK, Zheng XX.
Department of Biomedical Engineering, Zhejiang University, Hangzhou Zhejiang.
To evaluate the potential effect of HLF (Hawthorn leave flavonoids, w/w, 80% flavonoids) against thrombus formation, effect of HLF on hypoxia-treated human umbilical vein endothelial cell (HUVECs) was studied.
The levels of cytotoxicity and NO upon HUVECs were studied by flow cytometry. Moreover, the level of calcium ion in HUVECs was examined through laser scanning confocal microscopy.
Data from this study showed that HLF at concentrations of 5 micrograms/ml and 10 micrograms/ml decreased the cytotoxicity of hypoxia to HUVECs (P<0.05, P<0.01). The intracellular levels of NO and calcium ion were downregulated by HLF at concentrations of 5 micrograms/ml (P<0.01; P<0.01) and 10 micrograms/ml (vs control, P<0.01; P<0.01) too.
Results observed suggest that HLF protect HUVECs from hypoxia partly through its regulative effect on NO and calcium ion levels.
Phytomedicine. 2009 May;16(5):462-9. Epub 2009 Jan 7.
Cardiovascular effects in vitro of aqueous extract of wild strawberry (Fragaria vesca, L.) leaves.
Mudnic I, Modun D, Brizic I, Vukovic J, Generalic I, Katalinic V, Bilusic T, Ljubenkov I, Boban M.
Department of Pharmacology, University of Split School of Medicine, Split, Croatia.
In contrast to the strawberry fruits, strawberry leaves as a source of bioactive compounds with potentially beneficial biological effects have been largely overlooked. In this study we examined direct, dose-dependent effects of wild strawberry (Fragaria vesca, L.) leaves aqueous extract, in two experimental models and animal species, the isolated guinea pig hearts and rat aortic rings. Vasodilatory potential of the wild strawberry leaves extract was compared with vasodilatory activity of aqueous extract of hawthorn (Crataegus oxycantha, L) leaves with flowers, which can be regarded as a reference plant extract with a marked vasodilatory activity. The extracts were analysed by their "phenolic fingerprints", total phenolic content and antioxidative capacity. Their vasodilatory activity was determined and compared in the isolated aortic rings from 24 rats that were exposed to the extracts doses of 0.06, 0.6, 6, and 60 mg/100ml. Both extracts induced similar, dose-dependent vasodilation. Maximal relaxation was 72.2+/-4.4% and 81.3+/-4.5%, induced by the strawberry and hawthorn extract, respectively. To determine vasodilatory mechanisms of the wild strawberry leaves extract, endothelium-denuded and intact rings exposed to nitric oxide (NO) synthase inhibitor L-NAME or cyclooxygenase inhibitor indomethacin were used. Removal of the endothelium prevented and exposure to L-NAME or indomethacin strongly diminished the vasodilatatory response to the extract. In the isolated hearts (n=12), the wild strawberry extract was applied at concentrations of 0.06, 0.18, 0.6, and 1.8 mg/100ml. Each dose was perfused for 3.5 min with 15 min of washout periods. Heart contractility, electrophysiological activity, coronary flow and oxygen consumption were continuously monitored. The extract did not significantly affect heart rate and contractility, main parameters of the cardiac action that determine oxygen demands, while coronary flow increased up to 45% over control value with a simultaneous decrease of oxygen extraction by 34%. The results indicate that the aqueous extract of wild strawberry leaves is a direct, endothelium-dependent vasodilator, action of which is mediated by NO and cyclooxygenase products and which potency is similar to that of the hawthorn aqueous extract.
Arztl Forsch. 1959 Sep 10;13:475-6.
[The effect of the Crataegus extract esbericard on the venous pressure and the venous tone in man].
[Article in German]
FOLDI M, KOVACH AG, SOLTI F, ISKUM M.
J Cardiovasc Pharmacol. 2009 Mar;53(3):253-60.
Crataegus special extract WS 1442 causes endothelium-dependent relaxation via a redox-sensitive Src- and Akt-dependent activation of endothelial NO synthase but not via activation of estrogen receptors.
Anselm E, Socorro VF, Dal-Ros S, Schott C, Bronner C, Schini-Kerth VB.
Département de Pharmacologie et Physico-Chimie, UMR 7175, Université Louis Pasteur de Strasbourg, Strasbourg, France.
This study determined whether the Crataegus (Hawthorn species) special extract WS 1442 stimulates the endothelial formation of nitric oxide (NO), a vasoprotective factor, and characterized the underlying mechanism.
METHODS AND RESULTS:
Vascular reactivity was assessed in porcine coronary artery rings, reactive oxygen species (ROS) formation in artery sections by microscopy, and phosphorylation of Akt and endothelial NO synthase (eNOS) in endothelial cells by Western blot analysis. WS 1442 caused endothelium-dependent relaxations in coronary artery rings, which were reduced by N-nitro-L-arginine (a competitive inhibitor of NO synthase) and by charybdotoxin plus apamin (two inhibitors of endothelium-derived hyperpolarizing factor-mediated responses). Relaxations to WS 1442 were inhibited by intracellular ROS scavengers and inhibitors of Src and PI3-kinase, but not by an estrogen receptor antagonist. WS 1442 stimulated the endothelial formation of ROS in artery sections, and a redox-sensitive phosphorylation of Akt and eNOS in endothelial cells.
WS 1442 induced endothelium-dependent NO-mediated relaxations of coronary artery rings through the redox-sensitive Src/PI3-kinase/Akt-dependent phosphorylation of eNOS.
Int J Dev Neurosci. 2009 Dec;27(8):799-803. Epub 2009 Aug 25.
Hawthorn extract reduces infarct volume and improves neurological score by reducing oxidative stress in rat brain following middle cerebral artery occlusion.
Elango C, Jayachandaran KS, Niranjali Devaraj S.
Department of Biochemistry, University of Madras, Guindy Campus, Chennai 600 025, Tamil Nadu, India.
In our present investigation the neuroprotective effect of alcoholic extract of Hawthorn (Crataegus oxycantha) was evaluated against middle cerebral artery occlusion induced ischemia/reperfusion injury in rats. Male Sprague-Dawley rats were pretreated with 100 mg/kg body weight of the extract by oral gavage for 15 days. The middle cerebral artery was then occluded for 75 min followed by 24 h of reperfusion. The pretreated rats showed significantly improved neurological behavior with reduced brain infarct when compared to vehicle control rats. The glutathione level in brain was found to be significantly (p<0.05) low in vehicle control rats after 24 h of reperfusion when compared to sham operated animals. However, in Hawthorn extract pretreated rats the levels were found to be close to that of sham. Malondialdehyde levels in brain of sham and pretreated group were found to be significantly lower than the non-treated vehicle group (p<0.05). The nitric oxide levels in brain were measured and found to be significantly (p<0.05) higher in vehicle than in sham or extract treated rats. CONCLUSION: Our results suggest that Hawthorn extract which is a well known prophylactic for cardiac conditions may very well protect the brain against ischemia-reperfusion. The reduced brain damage and improved neurological behavior after 24 h of reperfusion in Hawthorn extract pretreated group may be attributed to its antioxidant property which restores glutathione levels, circumvents the increase in lipid peroxidation and nitric oxide levels thereby reducing peroxynitrite formation and free radical induced brain damage.
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