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Andersson, Rolf G. G.
Alternative names
Publications (10 of 48) Show all publications
Karlsson, J.-E., El-Saadi, W., Ali, M., Puskar, W., Skogvard, P., Engvall, J. E., . . . Jynge, P. (2015). Mangafodipir as a cardioprotective adjunct to reperfusion therapy: a feasibility study in patients with ST-segment elevation myocardial infarction. European Heart Journal - Cardiovascular Pharmacotherapy, 1(1), 39-45
Open this publication in new window or tab >>Mangafodipir as a cardioprotective adjunct to reperfusion therapy: a feasibility study in patients with ST-segment elevation myocardial infarction
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2015 (English)In: European Heart Journal - Cardiovascular Pharmacotherapy, ISSN 2055-6837, Vol. 1, no 1, p. 39-45Article in journal (Refereed) Published
Abstract [en]

Aims The aim of the present study was to examine the feasibility of applying the catalytic antioxidant mangafodipir [MnDPDP, manganese (Mn) dipyridoxyl diphosphate] as a cardioprotective adjunct to primary percutaneous coronary intervention (pPCI) in patients with ST-segment elevation (STE) myocardial infarction (STEMI). Both MnDPDP and a metabolite (Mn dipyridoxyl ethyldiamine) possess properties as mitochondrial superoxide dismutase mimetics and iron chelators, and combat oxidative stress in various tissues and conditions.

Methods and results

The study tested MnDPDP (n ¼ 10) vs. saline placebo (n ¼ 10), given as a brief intravenous (i.v.) infusion prior to balloon inflation during pPCI in patients with STEMI. Mangafodipir waswell tolerated and did not affect heart rate or blood pressure. Despite longer ischaemic time (205 vs. 144 min, P ¼ 0.019) in theMnDPDPgroup, plasma biomarker releaseswere identical for the two groups. With placebo vs.MnDPDP, mean STE resolutions were 69.8 vs. 81.9% (P ¼ 0.224) at 6 h and 73.1 vs. 84.3% (P ¼ 0.077) at 48 h. Cardiac magnetic resonance revealed mean infarct sizes of 32.5 vs. 26.2% (P ¼ 0.406) andmeanleft ventricular (LV) ejection fractions of 41.8 vs. 47.7% (P ¼ 0.617) with placebovs.MnDPDP.More LVthrombi were detected in placebo hearts (5 of 8) than MnDPDP-treated hearts (1 of 10; P ¼ 0.011).

Conclusions Mangafodipir is a safe drug for use as an adjunct to reperfusion therapy. A tendency to benefit of MnDPDP needs confirmation in a larger population. The study revealed important information for the design of a Phase II trial.

 

Place, publisher, year, edition, pages
European Society of Cardiology, 2015
Keywords
Cardiac reperfusion injury; Primary PCI; STEMI; Oxidative stress; Mitochondrial superoxide dismutase
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:liu:diva-116549 (URN)10.1093/ehjcvp/pvu021 (DOI)
Available from: 2015-03-27 Created: 2015-03-27 Last updated: 2017-03-01
Laskar, A., Andersson, R. & Li, W. (2013). Fodipir and Its Dephosphorylated Derivative Dipyridoxyl Ethyldiamine Are Involved in Mangafodipir-Mediated Cytoprotection against 7 beta-Hydroxycholesterol-Induced Cell Death. Pharmacology, 92(3-4), 182-186
Open this publication in new window or tab >>Fodipir and Its Dephosphorylated Derivative Dipyridoxyl Ethyldiamine Are Involved in Mangafodipir-Mediated Cytoprotection against 7 beta-Hydroxycholesterol-Induced Cell Death
2013 (English)In: Pharmacology, ISSN 0031-7012, E-ISSN 1423-0313, Vol. 92, no 3-4, p. 182-186Article in journal (Refereed) Published
Abstract [en]

Objective: Mangafodipir exerts pharmacological effects, including vascular relaxation and protection against oxidative stress and cell death induced by oxysterols. Additionally, mangafodipir has been proposed for cardiovascular imaging. The primary metabolites of mangafodipir, manganese dipyridoxyl ethyldiamine (MnPLED) and its constituent dipyridoxyl diphosphate (Dp-dp) also known as fodipir, are pharmacologically active. However, whether they affect oxysterol-induced cytotoxicity is currently unknown. In this study, we examine whether the mangafodipir metabolite affects 7 beta-hydroxycholesterol (7 beta-OH)-induced cell death and identify the underlying mechanisms. Methods: U937 cells were pretreated or not with mangafodipir substrate (Ms; 200 pm), MnPLED (100 mu mol/l) or Dp-dp (100 mu mol/l) for 8 h and then exposed to 7 beta-OH (28 mu mol/l) for 18 h. Results: Our results revealed that pretreatment with MnPLED or Dp-dp protected against 7 beta-OH-induced cellular reactive oxygen species (ROS) production, apoptosis, and lysosomal membrane permeabilization (LMP). MnPLED and Dp-dp, in par with Ms, confer protection against 7 beta-OH-induced cytotoxicity by reducing cellular ROS and stabilization of the lysosomal membrane. Conclusion: These results suggest that fodipir is the pharmacologically active part in the structure of mangafodipir, which prevents 7 beta-OH-induced cell death by attenuating cellular ROS and by preventing LMP. In addition, MnPLED, which is the dephosphorylated product of fodipir, exerts a similar protective effect against 7 beta-OH-induced cytotoxicity. This result indicates that dephosphorylation of fodipir does not affect its pharmacological actions. Altogether our result confirms the cytoprotective effect of mangafodipir and justifies its potential use as a cytoprotective adjuvant.

Place, publisher, year, edition, pages
KARGER, ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND, 2013
Keywords
Atherosclerosis, Apoptosis, Mangafodipir, Oxidative stress, Oxysterols
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-102098 (URN)10.1159/000354601 (DOI)000326770700008 ()
Note

Funding Agencies|Swedish Heart Lung Foundation||Torsten and Ragnar Soderberg Foundation||Stroke Foundation||Olle Engkvist Foundation||Swedish Gamla Tjanarinnor Foundation||Linkoping University Linkoping University Hospital Research Foundation||Medical Research Council of Southeast Sweden||

Available from: 2013-11-29 Created: 2013-11-29 Last updated: 2017-12-06
Laskar, A., Andersson, R. G. & Li, W. (2013). Fodipir (Dp-dp) and its dephosphorylated derivative PLED are involved in mangafodipir mediated cyto-protection against 7β-hydroxycholesterol induced cell death.
Open this publication in new window or tab >>Fodipir (Dp-dp) and its dephosphorylated derivative PLED are involved in mangafodipir mediated cyto-protection against 7β-hydroxycholesterol induced cell death
2013 (English)Manuscript (preprint) (Other academic)
Abstract [en]

Mangafodipir exerts pharmacological effects, including vascular relaxation and protection against oxidative stress and cell death induced by oxysterols. Additionally, mangafodipir has been proposed for cardiovascular imaging. The primary metabolite of mangafodipir, manganese dipyridoxyl ethyldiamine (MnPLED) and its constituent, dipyridoxyl diphosphate (Dp-dp) also known as fodipir, are pharmacologically active. However, whether they affect oxysterol induced cytotoxicity is currently unknown. In this study, we examine whether the mangafodipir metabolite affects 7β-hydroxycholesterol (7βOH) induced cell death and identify the underlying mechanisms. U937 cells were pre-treated or not with mangafodipir substrate (Ms) (200 μm), MnPLED (100 μM) or Dp-dp (100 μM) for 8 hours and then exposed to 7βOH (28 μM) for 18 hours. Our results revealed that pre-treatment with MnPLED or Dp-dp protected against 7βOH induced cellular reactive oxygen species (ROS) production, apoptosis, and lysosomal membrane permeabilization (LMP). MnPLED and Dpdp in par with Ms, confer protection against 7βOH induced cytotoxicity by reducing  cellular ROS and stabilization of lysosomal membrane. These results suggest that, fodipir is the active part in mangafodipir, which shows the noted effects and its activity is conserved in MnPLED. These results further confirm the cyto-protective effect of mangafodipir and justify its potential use as a cyto-protective adjuvant.

Keywords
Atherogenic, Apoptosis, Mangafodipir, Oxidative stress, Oxysterols
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-91996 (URN)
Available from: 2013-05-07 Created: 2013-05-07 Last updated: 2013-05-07Bibliographically approved
Kurz, T., Grant, D., Andersson, R., Robertson, T., De Cesare, M. & Karlsson, J. O. (2012). Effects of MnDPDP andICRF-187 on Doxorubicin-Induced Cardiotoxicityand Anticancer Activity1. Translational Oncology, 5(4), 252-259
Open this publication in new window or tab >>Effects of MnDPDP andICRF-187 on Doxorubicin-Induced Cardiotoxicityand Anticancer Activity1
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2012 (English)In: Translational Oncology, ISSN 1944-7124, E-ISSN 1936-5233, Vol. 5, no 4, p. 252-259Article in journal (Refereed) Published
Abstract [en]

Oxidative stress participates in doxorubicin (Dx)–induced cardiotoxicity. The metal complex MnDPDP and its metaboliteMnPLED possess SOD-mimetic activity, DPDP and PLED have, in addition, high affinity for iron. Mice wereinjected intravenously with MnDPDP, DPDP, or dexrazoxane (ICRF-187). Thirty minutes later, mice were killed, theleft atria were hung in organ baths and electrically stimulated, saline or Dx was added, and the contractility wasmeasured for 60 minutes. In parallel experiments, 10 μM MnDPDP or MnPLED was added directly into the organbath. The effect of MnDPDP on antitumor activity of Dx against two human tumor xenografts (MX-1 and A2780)was investigated. The in vitro cytotoxic activity was studied by co-incubating A2780 cells with MnDPDP, DPDP,and/or Dx. Dx caused a marked reduction in contractile force. In vivo treatment with MnDPDP and ICRF-187 attenuatedthe negative effect of Dx. When added directly into the bath, MnDPDP did not protect, whereas MnPLEDattenuated the Dx effect by approximately 50%. MnDPDP or ICRF-187 did not interfere negatively with the antitumoractivity of Dx, either in vivo or in vitro. Micromolar concentrations of DPDP but not MnDPDP displayed anin vitro cytotoxic activity against A2780 cells. The present results show that MnDPDP, after being metabolized toMnPLED, protects against acute Dx cardiotoxicity. Both in vivo and in vitro experiments show that cardioprotectiontakes place without interfering negatively with the anticancer activity of Dx. Furthermore, the results suggest thatthe previously described cytotoxic in vivo activity of MnDPDP is an inherent property of DPDP.

Translational Oncology (2012) 5, 252–259

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-80755 (URN)10.1593/tlo.11304 (DOI)000311488600005 ()
Note

funding agencies|Medical Research Council of Southeast Sweden|FORSS-85191|PledPharma AB||

Available from: 2012-08-29 Created: 2012-08-29 Last updated: 2017-12-07
Karlsson, J. O., Adolfsson, K., Thelin, B., Jynge, P., Andersson, R. & Falkmer, U. G. (2012). First Clinical Experience with the Magnetic Resonance Imaging Contrast Agent and Superoxide Dismutase Mimetic Mangafodipir as an Adjunct in Cancer Chemotherapy-A Translational Study. Translational Oncology, 5(1), 32-38
Open this publication in new window or tab >>First Clinical Experience with the Magnetic Resonance Imaging Contrast Agent and Superoxide Dismutase Mimetic Mangafodipir as an Adjunct in Cancer Chemotherapy-A Translational Study
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2012 (English)In: Translational Oncology, ISSN 1944-7124, E-ISSN 1936-5233, Vol. 5, no 1, p. 32-38Article in journal (Refereed) Published
Abstract [en]

Preclinical research suggests that the clinically approved magnetic resonance imaging contrast agent mangafodipir may protect against adverse events (AEs) caused by chemotherapy, without interfering negatively with the anticancer efficacy. The present translational study tested if pretreatment with mangafodipir lowers AEs during curative (adjuvant) FOLFOX6 chemotherapy in stage III colon cancer (Dukes C). The study was originally scheduled to include 20 patients, but because of the unforeseen withdrawal of mangafodipir from the market, the study had to be closed after 14 patients had been included. The withdrawal of mangafodipir was purely based on commercial considerations from the producer and not on any safety concerns. The patients were treated throughout the first 3 of 12 scheduled cycles. Patients were randomized to a 5-minute infusion of either mangafodipir or placebo (7 in each group). AEs were evaluated according to the National Cancer Institutes (NCI) Common Terminology Criteria for Adverse Events and the Sanofi-NCI criteria. The primary end points were neutropenia and neurosensory toxicity. There were four AEs of grade 3 (severe) and one AE of grade 4 (life threatening) in four patients in the placebo group, whereas there were none in the mangafodipir group (P andlt; .05). Of the grade 3 and 4 events, two were neutropenia and one was neurosensory toxicity. Furthermore, white blood cell count was statistically, significantly higher in the mangafodipir group than in the placebo group (P andlt; .01) after treatment with FOLFOX. This small feasibility study seems to confirm what has been demonstrated preclinically, namely, that pretreatment with mangafodipir lowers AEs during adjuvant 5-fluorouracil plus oxaliplatin-based chemotherapy in colon cancer patients.

Place, publisher, year, edition, pages
NEOPLASIA PRESS, 1150 W MEDICAL CENTER DR, MSRB III, RM 9303, ANN ARBOR, MI 48109-0648 USA, 2012
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-79112 (URN)10.1593/tlo.11277 (DOI)000304817600005 ()
Note

Funding Agencies|Medical Research Council of Southeast Sweden|FORSS-85191|PledPharma AB||

Available from: 2012-06-29 Created: 2012-06-29 Last updated: 2017-12-07Bibliographically approved
Karlsson, J. O., Kurz, T., Flechsig, S., Nasstrom, J. & Andersson, R. (2012). Superior Therapeutic Index of Calmangafodipir in Comparison to Mangafodipir as a Chemotherapy Adjunct. TRANSLATIONAL ONCOLOGY, 5(6), 492-502
Open this publication in new window or tab >>Superior Therapeutic Index of Calmangafodipir in Comparison to Mangafodipir as a Chemotherapy Adjunct
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2012 (English)In: TRANSLATIONAL ONCOLOGY, ISSN 1944-7124, Vol. 5, no 6, p. 492-502Article in journal (Refereed) Published
Abstract [en]

Mangafodipir is a magnetic resonance imaging contrast agent with manganese superoxide dismutase (MnSOD) mimetic activity. The MnSOD mimetic activity protects healthy cells against oxidative stress-induced detrimental effects, e. g., myelosuppressive effects of chemotherapy drugs. The contrast property depends on in vivo dissociation of Mn2+ from mangafodipir-about 80% dissociates after injection. The SOD mimetic activity, however, depends on the intact Mn complex. Complexed Mn2+ is readily excreted in the urine, whereas dissociated Mn2+ is excreted slowly via the biliary route. Mn is an essential but also a potentially neurotoxic metal. For more frequent therapeutic use, neurotoxicity due to Mn accumulation in the brain may represent a serious problem. Replacement of 4/5 of Mn2+ in mangafodipir with Ca2+ (resulting in calmangafodipir) stabilizes it from releasing Mn2+ after administration, which roughly doubles renal excretion of Mn. A considerable part of Mn2+ release from mangafodipir is governed by the presence of a limited amount of plasma zinc (Zn2+). Zn2+ has roughly 10(3) and 10(9) times higher affinity than Mn2+ and Ca2+, respectively, for fodipir. Replacement of 80% of Mn2+ with Ca2+ is enough for binding a considerable amount of the readily available plasma Zn2+, resulting in considerably less Mn2+ release and retention in the brain and other organs. At equivalent Mn2+ doses, calmangafodipir was significantly more efficacious than mangafodipir to protect BALB/c mice against myelosuppressive effects of the chemotherapy drug oxaliplatin. Calmangafodipir did not interfere negatively with the antitumor activity of oxaliplatin in CT26 tumor-bearing syngenic BALB/c mice, contrary calmangafodipir increased the antitumor activity. Translational Oncology (2012) 5, 492-502

Place, publisher, year, edition, pages
NEOPLASIA PRESS, 1150 W MEDICAL CENTER DR, MSRB III, RM 9303, ANN ARBOR, MI 48109-0648 USA, 2012
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-88464 (URN)10.1593/tlo.12238 (DOI)000313359800014 ()
Note

Funding Agencies|Medical Research Council of Southeast Sweden|FORSS-85191|PledPharma AB||

Available from: 2013-02-07 Created: 2013-02-07 Last updated: 2014-12-03
Persson, I. A., Persson, K., Hägg, S. & Andersson, R. G. (2011). Effects of cocoa extract and dark chocolate on angiotensin-converting enzyme and nitric oxide in human endothelial cells and healthy volunteers--a nutrigenomics perspective.. Journal of Cardiovascular Pharmacology, 57(1), 44-50
Open this publication in new window or tab >>Effects of cocoa extract and dark chocolate on angiotensin-converting enzyme and nitric oxide in human endothelial cells and healthy volunteers--a nutrigenomics perspective.
2011 (English)In: Journal of Cardiovascular Pharmacology, ISSN 0160-2446, E-ISSN 1533-4023, Vol. 57, no 1, p. 44-50Article in journal (Refereed) Published
Abstract [en]

Evidence suggests that cocoa from the bean of Theobroma cacao L. has beneficial effects on cardiovascular disease. The aim of this study was to investigate if cocoa extract and dark chocolate influence angiotensin-converting enzyme (ACE) and nitric oxide (NO) in human endothelial cells (in vitro) and in healthy volunteers (in vivo). ACE activity was analyzed with a commercial radioenzymatic assay and measured in human endothelial cells from umbilical veins (HUVEC) after 10 minutes of incubation with cocoa extract. NO was measured after 24 hours of incubation. ACE activity and NO were measured at baseline and after 30, 60, and 180 minutes in 16 healthy volunteers after a single intake of 75 g of dark chocolate containing 72% cocoa. Significant inhibition of ACE activity (P < 0.01) and significant increase of NO (P < 0.001) were seen in HUVEC. In the study subjects, a significant inhibition of ACE activity (mean 18%) 3 hours after intake of dark chocolate was seen, but no significant change in NO was seen. According to ACE genotype, significant inhibition of ACE activity was seen after 3 hours in individuals with genotype insertion/insertion and deletion/deletion (mean 21% and 28%, respectively). Data suggest that intake of dark chocolate containing high amount of cocoa inhibits ACE activity in vitro and in vivo.

Keywords
cocoa, dark chocolate, angiotensin-converting enzyme, genotyping, nitric oxide
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-66332 (URN)10.1097/FJC.0b013e3181fe62e3 (DOI)000286178000007 ()20966764 (PubMedID)
Available from: 2011-03-11 Created: 2011-03-11 Last updated: 2017-12-11Bibliographically approved
Persson, I.-L. A., Persson, K., Hägg, S. & Andersson, R. G. (2010). Effects of green tea, black tea and Rooibos tea on angiotensin-converting enzyme and nitric oxide in healthy volunteers. Public Health Nutrition, 13(5), 730-737
Open this publication in new window or tab >>Effects of green tea, black tea and Rooibos tea on angiotensin-converting enzyme and nitric oxide in healthy volunteers
2010 (English)In: Public Health Nutrition, ISSN 1368-9800, E-ISSN 1475-2727, Vol. 13, no 5, p. 730-737Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: Tea has been reported to reduce cardiovascular mortality, but the underlying mechanisms are largely unknown. The aim of the current project was to investigate the effect of green tea (Japanese Sencha), black tea (Indian Assam B.O.P.) and Rooibos tea (South Africa) on angiotensin-converting enzyme (ACE) and nitric oxide (NO). DESIGN: Seventeen healthy volunteers received a single oral dose of 400 ml green tea, black tea or Rooibos tea in a randomized, three-phase, crossover study. ACE activity and NO concentration were measured (at 0, 30, 60 and 180 min) in all phases. ACE activity was analysed by means of a commercial radioenzymatic assay. Nitrite was analysed as a marker of NO concentration. In addition, ACE genotype was determined using a PCR method. RESULTS: Oral intake of a single dose of Rooibos tea significantly inhibited ACE activity after 30 min (P < 0.01) and after 60 min (P < 0.05). A significant inhibition of ACE activity was seen with green tea for the ACE II genotype 30 min after intake of the tea (P < 0.05) and for the ACE ID genotype 60 min after intake (P < 0.05). A significant inhibition of ACE activity was also seen with Rooibos tea for the ACE II genotype 60 min after intake (P < 0.05). No significant effect on NO concentration was seen. CONCLUSIONS: These results suggest that green tea and Rooibos tea may have cardiovascular effects through inhibition of ACE activity.

Keywords
Tea, Angiotensin-converting enxyme, Nitric oxide
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-55073 (URN)10.1017/S1368980010000170 (DOI)000277379500018 ()20144258 (PubMedID)
Available from: 2010-04-28 Created: 2010-04-28 Last updated: 2017-12-12
Laskar, A., Miah, S., Andersson, R. G. & Li, W. (2010). Prevention of 7beta-hydroxycholesterol-induced cell death by mangafodipir is mediated through lysosomal and mitochondrial pathways. European Journal of Pharmacology (640), 124-128
Open this publication in new window or tab >>Prevention of 7beta-hydroxycholesterol-induced cell death by mangafodipir is mediated through lysosomal and mitochondrial pathways
2010 (English)In: European Journal of Pharmacology, ISSN 0014-2999, E-ISSN 1879-0712, no 640, p. 124-128Article in journal (Refereed) Published
Abstract [en]

Mangafodipir, a MRI contrast agent, has been used as a viability marker in patients with myocardial infarction and showed vascular relaxation effect. It confers myocardial protection against oxidative stress. However mechanisms underlying such protection have not yet been investigated. In this investigation we first studied whether mangafodipir inhibits apoptosis induced by 7beta-hydroxycholesterol (7betaOH), a cytotoxic cholesterol oxidation product found in atherosclerotic lesions in humans and in heart of ethanol-fed rats. We then focused on whether mangafodipir influences the production of reactive oxygen species, lysosomal and mitochondrial membrane permeabilities in the cell model. Our results revealed that pre-treatment with mangafodipir (400microM) protected against cellular reactive oxygen species production, apoptosis, and permeabilization of lysosomal and mitochondrial membranes induced by 7betaOH. In conclusion, a novel effect of mangafodipir on 7betaOH-induced apoptosis is via reduction of cellular reactive oxygen species and stabilization of lysosomal and mitochondrial membranes. This is the first report to show the additional cytoprotective effect of mangafodipir, which may suggest possible use of the drug.

Keywords
Atherosclerosis, Apoptosis, Mangafodipir, Oxidized lipid, Oxidative stress
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-57355 (URN)10.1016/j.ejphar.2010.04.046 (DOI)20452343 (PubMedID)
Available from: 2010-06-17 Created: 2010-06-17 Last updated: 2017-12-12
Persson, I., Persson, K. & Andersson, R. (2009). Effect of Vaccinium myrtillus and Its Polyphenols on Angiotensin-Converting Enzyme Activity in Human Endothelial Cells. Journal of Agricultural and Food Chemistry, 57(11), 4626-4629
Open this publication in new window or tab >>Effect of Vaccinium myrtillus and Its Polyphenols on Angiotensin-Converting Enzyme Activity in Human Endothelial Cells
2009 (English)In: Journal of Agricultural and Food Chemistry, ISSN 0021-8561, E-ISSN 1520-5118, Vol. 57, no 11, p. 4626-4629Article in journal (Refereed) Published
Abstract [en]

This study investigates if the connection between Vaccinium myrtillus and angiotensin-converting enzyme (ACE) might be an explanation of the pharmacological effects on circulation. Cultured endothelial cells from human umbilical veins were incubated with bilberry 25E extract. The main anthocyanidins combined in myrtillin chloride and separately in cyanidin, delphinidin, and malvidin, respectively, were examined concerning their effects on ACE. After 10 min of incubation with bilberry 25E, a significant, dose-dependent inhibition of ACE activity was seen, and after incubation with myrtillin chloride a significant inhibition was seen. No effect was seen with the anthocyanidins. The effect seems to be dependent on this specific mixture of anthocyanins in the bilberry. V. myrtillus may thus have the potential to prevent and protect against cardiovascular diseases.

Keywords
Angiotensin-converting enzyme; Vaccinium myrtillus; anthocyanidins
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-18654 (URN)10.1021/jf900128s (DOI)
Note

On the day of the defence date the status of this article was Submitted.

Available from: 2009-06-03 Created: 2009-06-03 Last updated: 2018-03-27Bibliographically approved
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