33 results match your criteria cp-induced myocardial


Cardioprotective effect of fingolimod against calcium paradox-induced myocardial injury in the isolated rat heart.

Can J Physiol Pharmacol 2021 Sep 24. Epub 2021 Sep 24.

University of Cape Town, Human Biology, 5.14 Anatomy Building, Observatory, Cape Town, South Africa, 7925;

Fingolimod (FTY720) inhibits Ca-permeable, Mg-sensitive channels called transient receptor potential melastatin 7 (TRPM7), but its effects on Ca paradox (CP)-induced myocardial damage have not been evaluated. We studied the effect of FTY720 on CP-induced myocardial damage, and used other TRPM7 channel inhibitors nordihydroguaiaretic acid (NDGA) and Mg to test if any effect of FTY720 was via TRPM7 inhibition. Langendorff-perfused Wistar rat hearts were treated with FTY720 or NDGA and subjected to a CP protocol consisting of Ca depletion followed by Ca repletion. Read More

View Article and Full-Text PDF
September 2021

Natural Bioactive as a Potential Therapeutic Approach for the Management of Cyclophosphamide-induced Cardiotoxicity.

Curr Top Med Chem 2021 Aug 13. Epub 2021 Aug 13.

Department of Pharmacology, 3Department of Pharmaceutics, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi. India.

Cyclophosphamide (CP) is an extensively used anticancer drug, but its cardiotoxic manifestation is a major concern for its widespread clinical use. The observed cardiotoxic attributes have been reported at the therapeutic dose and often result into a high mortality rate and poor clinical outcome. Fall in the level of antioxidant enzymes catalase (CAT), reduced glutathione (GSH), superoxide dismutase (SOD) generation of reactive oxygen species (ROS), inflammatory cytokines nuclear factor kappa-light-chain enhancer of activated B cells (NF-kB), tumor necrosis factor-alpha (TNF-α), interleukin 1 beta (IL-1β), apoptotic proteins (caspases) and direct damage to myocardial tissue (histological and ultrastructural damage) are some of the reported manifestations of cardiotoxicity. Read More

View Article and Full-Text PDF

Edaravone and Acetovanillone Upregulate Nrf2 and PI3K/Akt/mTOR Signaling and Prevent Cyclophosphamide Cardiotoxicity in Rats.

Drug Des Devel Ther 2020 30;14:5275-5288. Epub 2020 Nov 30.

Zoology Department Faculty of Science, Beni-Suef University, Beni-Suef, Egypt.

Introduction: Cyclophosphamide (CP) causes redox imbalance and its use is associated with marked cardiotoxicity that limits its clinical applications. The present study investigated the protective effects of acetovanillone (AV) and edaravone (ED) against CP-induced oxidative stress and cardiac damage, emphasizing the role of PI3K/Akt/mTOR and Nrf2 signaling.

Materials And Methods: Rats received either AV (100 mg/kg) or ED (20 mg/kg) orally for 10 days and CP (200 mg/kg) on day 7. Read More

View Article and Full-Text PDF
September 2021

Metformin and/or low dose radiation reduces cardiotoxicity and apoptosis induced by cyclophosphamide through SIRT-1/SOD and BAX/Bcl-2 pathways in rats.

Mol Biol Rep 2020 Jul 14;47(7):5115-5126. Epub 2020 Jun 14.

Radiation Biology Department, National Center for Radiation Research and Technology, Atomic Energy Authority, Cairo, Egypt.

Cyclophosphamide (CP) is a nitrogen mustard alkylating agent with effective antineoplastic, immunomodulatory and immunosuppressive properties. Despite its vast therapeutic uses, it is known to trigger strict cardiac toxicity. The objective of the current study was to examine the protective role of metformin (MET) and/or low dose radiation (LDR) on cardiotoxicity and apoptosis induced by CP in rats. Read More

View Article and Full-Text PDF

Nerolidol attenuates cyclophosphamide-induced cardiac inflammation, apoptosis and fibrosis in Swiss Albino mice.

Eur J Pharmacol 2019 Nov 18;863:172666. Epub 2019 Sep 18.

Department of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, 110062, India. Electronic address:

Incidence and prevalence of cancer is an alarming situation globally. For the treatment of cancer many anticancer drugs have been developed but, unfortunately, their potential cardiotoxic side effects raised serious concerns about their use among clinicians. Cyclophosphamide is a potent anticancer and immunosuppressant drug but its use is limited due to cardiotoxic side effect. Read More

View Article and Full-Text PDF
November 2019

Evaluating the protective potency of Acacia hydaspica R. Parker on histological and biochemical changes induced by Cisplatin in the cardiac tissue of rats.

BMC Complement Altern Med 2019 Jul 23;19(1):182. Epub 2019 Jul 23.

Department of Biochemistry, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan.

Background: Increase oxidative trauma is the main cause behind Cisplatin (CP) induced cardiotoxicity which restricts its clinical application as anti-neoplastic prescription. Acacia hydaspica is a natural shrub with diverse bioactivities. Acacia hydaspica ethyl acetate extract (AHE) ameliorated drug-induced cardiotoxicity in animals with anti-oxidative mechanisms. Read More

View Article and Full-Text PDF

Role of ATP-Sensitive Potassium Channel (K) and eNOS in Mediating the Protective Effect of Nicorandil in Cyclophosphamide-Induced Cardiotoxicity.

Cardiovasc Toxicol 2020 02;20(1):71-81

Department of Biochemistry, Faculty of Pharmacy, Minia University, El-Minia, 61511, Egypt.

Cyclophosphamide (CP) is a widely used chemotherapeutic agent but its clinical usefulness is challenged with different forms of toxicities. No studies have evaluated the possible protective effect of nicorandil (NIC) in CP-induced cardiotoxicity. Our study aimed to investigate this effect by using NIC (3 mg/kg/day) orally for 5 days, in the presence or absence of cardiotoxicity induced by intraperitoneal (i. Read More

View Article and Full-Text PDF
February 2020

Cardioprotective effect of green tea extract and vitamin E on Cisplatin-induced cardiotoxicity in mice: Toxicological, histological and immunohistochemical studies.

Biomed Pharmacother 2019 May 6;113:108731. Epub 2019 Mar 6.

Zoology Department, Faculty of Science, Tanta University, Tanta, Egypt. Electronic address:

Background: Cisplatin (CP) has been used in wide range for cancer treatment. Although nephrotoxicity of CP was the main complication, cardiotoxicity has been reported.

Objectives: This study investigates the protective role of green tea extract (GTE) and vitamin E (Vit-E) against CP-induced cardiotoxicity, and assesses their impact on CP antitumor efficacy. Read More

View Article and Full-Text PDF

Molecular mechanism involved in cyclophosphamide-induced cardiotoxicity: Old drug with a new vision.

Life Sci 2019 Feb 12;218:112-131. Epub 2018 Dec 12.

Department of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi 110062, India. Electronic address:

Cyclophosphamide (CP) is an important anticancer drug which belongs to the class of alkylating agent. Cyclophosphamide is mostly used in bone marrow transplantation, rheumatoid arthritis, lupus erythematosus, multiple sclerosis, neuroblastoma and other types of cancer. Dose-related cardiotoxicity is a limiting factor for its use. Read More

View Article and Full-Text PDF
February 2019

Characterization of L. root extract and its evaluation of cardioprotective effect in Wistar rat model.

Indian J Pharmacol 2018 Jan-Feb;50(1):12-21

Department of Molecular Medicine, Central Research Laboratory, RajaRajeswari Medical College and Hospital, Bangalore, Karnataka, India.

Objectives: L. (RC) is a well-known and highly valuable medicinal plant in the Ayurvedic system. The present study involves evaluating antioxidant and cardioprotective property of RC root extract. Read More

View Article and Full-Text PDF
October 2018

Protective Effect of Kolaviron on Cyclophosphamide-Induced Cardiac Toxicity in Rats.

J Evid Based Integr Med 2018 Jan-Dec;23:2156587218757649

1 Obafemi Awolowo University, Ile-Ife, Osun State, Nigeria.

Background: Cyclophosphamide (CP) is a nitrogen mustard alkylating drug used for the treatment of chronic and acute malignant lymphomas, myeloma, leukemia, neuroblastoma, adenocarcinoma, retinoblastoma, breast carcinoma, and immunosuppressive therapy. Despite its vast therapeutic uses, it is known to cause severe cardiac toxicity. Kolaviron (KV), a Garcinia kola seed extract containing a mixture of flavonoids, is reputed for its antioxidant and membrane stabilizing properties. Read More

View Article and Full-Text PDF

Modulation of cyclophosphamide-induced cardiotoxicity by methyl palmitate.

Cancer Chemother Pharmacol 2017 02 27;79(2):399-409. Epub 2017 Jan 27.

Cardiology Unit, Department of Pediatrics, College of Medicine, Taibah University, Al-Madinah Al-Munawwarah, 30001, Saudi Arabia.

Purpose: Cyclophosphamide (CP) is a frequently used anticancer and immunosuppressant although its use has been associated with severe cardiotoxicity. The present study examined the ability of methyl palmitate (MP) to counteract CP-induced cardiotoxicity.

Methods: Adult male Wistar rats were divided into four groups. Read More

View Article and Full-Text PDF
February 2017

Effects of thymoquinone against cisplatin-induced cardiac injury in rats.

Acta Cir Bras 2016 Apr;31(4):271-7

Faculty of Medicine, Afyon Kocatepe University, Afyon, Turkey.

Purpose: T o investigate the possible protective effect of thymoquinone (TQ) in cisplatin (CP) induced myocardial injury.

Methods: A total of 28 adult male Wistar-Albino rats were randomly and equally divided into four groups as follows: Group 1 (control), Group 2 (CP at 15 mg/kg dose), Group 3 (TQ 40 mg/kg/day for two days prior to CP injection and on third day, CP at 15 mg/kg dose was intraperitoneally administered and TQ treatment continued until fifth day) and Group 4 (TQ at 40mg/kg/day dose for five days).

Results: There was a significant increment in CP group in terms of congestion, edema and pycnotic nuclei in myocardial fibers, comparing with other groups. Read More

View Article and Full-Text PDF

CT-1-CP-induced ventricular electrical remodeling in mice.

J Huazhong Univ Sci Technolog Med Sci 2015 Feb 12;35(1):21-27. Epub 2015 Feb 12.

Department of Physiology, Hainan Medical University, Haikou, 571101, China.

The chronic effects of carboxyl-terminal polypeptide of Cardiotrophin-1 (CT-1-CP) on ventricular electrical remodeling were investigated. CT-1-CP, which contains 16 amino acids in sequence of the C-terminal of Cardiotrophin-1, was selected and synthesized, and then administered to Kunming mice (aged 5 weeks) by intraperitoneal injection (500 ng·g⁻¹·day⁻¹) (4 groups, n=10 and female: male=1:1 in each group) for 1, 2, 3 and 4 weeks, respectively. The control group (n=10, female: male=1:1) was injected by physiological saline for 4 weeks. Read More

View Article and Full-Text PDF
February 2015

Rottlerin increases cardiac contractile performance and coronary perfusion through BKCa++ channel activation after cold cardioplegic arrest in isolated hearts.

Circulation 2011 Sep;124(11 Suppl):S55-61

Cardiovascular Research Center, Department of Surgery, Rhode Island Hospital and Alpert Medical School, Brown University, Coro 5.230, 1 Hoppin St, Providence, RI 02903, USA.

Background: Cardioplegia and cardiopulmonary bypass (CP/CPB) subjects myocardium to complex injurious stimuli that can result in cardiomyocyte and vascular contractile abnormalities. Rottlerin, originally identified as a delta-protein kinase C inhibitor, has a number of known additional effects that may be beneficial in the setting of CP/CPB. We tested the hypothesis that rottlerin mitigates deleterious effects associated with CP/CPB. Read More

View Article and Full-Text PDF
September 2011

p38 MAPK-dependent small HSP27 and αB-crystallin phosphorylation in regulation of myocardial function following cardioplegic arrest.

Am J Physiol Heart Circ Physiol 2011 May 25;300(5):H1669-77. Epub 2011 Feb 25.

Cardiovascular Research Center, Rhode Island Hospital and Alpert Medical School, Brown University, Providence, Rhode Island, USA.

We previously demonstrated that myocardial p38 mitogen-activated protein kinase (MAPK) and heat shock protein 27 (HSP27) are phosphorylated following cardioplegic arrest in patients undergoing cardiac surgery and correlate with reduced cardiac function. The following studies were performed to determine whether inhibition of p38 MAPK and/or overexpression of nonphosphorylatable HSP27 improves cardiac function following cardioplegic arrest. Langendorff-perfused isolated rat hearts were subjected to 2 h of intermittent cold cardioplegia followed by 30 min of reperfusion. Read More

View Article and Full-Text PDF

Viscum album L. extract and quercetin reduce cyclophosphamide-induced cardiotoxicity, urotoxicity and genotoxicity in mice.

Asian Pac J Cancer Prev 2011 ;12(11):2925-31

Department of Biology, Faculty of Science, Ordu University, Ordu, Turkey.

Possible protective effects of a methanolic extract of Viscum album (VA) and quercetin (QE) against cyclophosphamide (CP) induced cardiotoxicity, urotoxicity and genotoxicity in mice were evaluated. Mice were administered orally VA (250 mg/kg/day) and QE (50 mg/kg/day) for 10 days alone or in combination with CP. After the same doses of VA and QE given for 7 days, rats were intraperitoneally administered CP (40 mg/kg) on days 8 and 9 of the experiment. Read More

View Article and Full-Text PDF

Probucol attenuates cyclophosphamide-induced oxidative apoptosis, p53 and Bax signal expression in rat cardiac tissues.

Authors:
Yosef A Asiri

Oxid Med Cell Longev 2010 Sep-Oct;3(5):308-16. Epub 2010 Sep 1.

Department of Clinical Pharmacy, College of Pharmacy, King Saud University, Riyadh, Kingdom of Saudi Arabia.

Cyclophosphamide (CP) is a widely used in cancer chemotherapy and immunosuppression, which could cause toxicity of the normal cells due to its toxic metabolites. Probucol, cholesterol-lowering drug, acts as potential inhibitor of DNA damage and shows to protect against doxorubicin-induced cardiomyopathy by enhancing the endogenous antioxidant system including glutathione peroxidase, catalase and superoxide dismutase. This study examined the possible protective effects of probucol, a lipid-lowering compound with strong antioxidant properties, against CP-induced cardiotoxicity. Read More

View Article and Full-Text PDF

Thymoquinone supplementation attenuates cyclophosphamide-induced cardiotoxicity in rats.

J Biochem Mol Toxicol 2011 May-Jun;25(3):135-42. Epub 2010 Oct 18.

Department of Pharmacology, College of Pharmacy, King Saud University, Riyadh, Kingdom of Saudi Arabia.

This study examined the possible protective effects of thymoquinone (TQ), the main constituent of the volatile oil of black seed (Nigella sativa), against cyclophosphamide (CP)-induced cardiotoxicity. Adult male Wistar albino rats were divided into four treatment groups. Rats in the first group were served as control. Read More

View Article and Full-Text PDF
February 2012

Cytoprotective effects of DL-alpha-lipoic acid or squalene on cyclophosphamide-induced oxidative injury: an experimental study on rat myocardium, testicles and urinary bladder.

Food Chem Toxicol 2010 Aug-Sep;48(8-9):2326-36. Epub 2010 May 31.

Biochemistry Department, Faculty of Pharmacy, Cairo University, Cairo, Egypt.

The present study aimed to evaluate the role of DL-alpha-lipoic acid (LA) and squalene (SQ) on oxidative cardiac, testicular and urotoxic damage induced by cyclophosphamide (CP). Male Wistar rats were divided into four groups; three groups received a single intraperitoneal injection of CP (200mg/kg BW) to induce toxicity, and two of these groups received either LA (35 mg/kg BW) or SQ (0.4 ml/rat) orally 7 days before and 7 days after CP injection. Read More

View Article and Full-Text PDF
November 2010

Increased expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in rat cardiac allografts.

Transplant Proc 2008 Oct;40(8):2720-3

Department of Cardiovascular Surgery, Shandong University Qi Lu Hospital, Jinan, Shandong, P.R. China.

This study was designed to investigate the role of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) during chronic cardiac allograft rejection. Wistar rats were used as donors, and SD rats as recipients heterotopic cardiac transplants. Recipients pretreated with inoculation of donor splenocytes (SPC) followed by cyclophosphamide (CP) were divided into 4 groups: (A) untreated group (n = 18) without immunosuppression; (B) SPC plus CP-treated group (n = 18) that were euthanized at 15-120 days posttransplantation; (C) CsA-treated group (n = 18) euthanized at 2-3 months posttransplantation; and (D) tolerance group (n = 18) treated with SPC plus CP and monitored for at least 1 year posttransplantation. Read More

View Article and Full-Text PDF
October 2008

The experimental study of cardiac allograft vasculopathy and myocardial fibrosis in rats.

Transplant Proc 2008 Oct;40(8):2712-5

Department of Cardiovascular Surgery, Shandong University Qi Lu Hospital, Jinan, Shandong, P.R. China.

We sought to analyze the development of myocardial fibrosis and cardiac allograft vasculopathy (CAV) as a theoretical basis for the prevention and treatment of rejection. Heterotopic cardiac transplantation was performed from Wistar rats to Sprague-Dawley rats. The recipients pretreated with donor splenocyte (SPC) infusion followed by cyclophosphamide (CP) were divided into 3 groups: Control animals without immunosuppression (Group 1; n = 10); Group 2, CsA treatment (n = 10) with euthanasia 2-3 months posttransplantation; and Group 3 (n = 20), CP plus SPC treatment with 10 recipients euthanized at 2 weeks posttransplantation and 10 animals monitored for at least 1 year posttransplantation. Read More

View Article and Full-Text PDF
October 2008

Effect of DL-alpha-lipoic acid on cyclophosphamide induced lysosomal changes in oxidative cardiotoxicity.

Life Sci 2007 May 12;80(21):1993-8. Epub 2007 Mar 12.

Department of Medical Biochemistry, Dr. ALM. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai - 600 113, India.

Cyclophosphamide (CP), one of the widely prescribed antineoplastic drugs can cause fatal cardiotoxicity. The present study is aimed at evaluating the cardioprotective role of lipoic acid in CP induced toxicity. Male albino rats of Wistar strain were divided into four groups and treated as follows: Group I served as control, Group II received a single dose of CP (200 mg/kg b. Read More

View Article and Full-Text PDF

Lupeol and its ester inhibit alteration of myocardial permeability in cyclophosphamide administered rats.

Mol Cell Biochem 2006 Nov 29;292(1-2):39-44. Epub 2006 Sep 29.

Department of Medical Biochemistry, Dr. ALM. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600113, India.

Cyclophosphamide (CP), an alkylating agent widely used in cancer chemotherapy causes cardiac membrane damage. Lupeol, a pentacyclic triterpene, isolated from Crataeva nurvala stem bark and its ester, lupeol linoleate possess a wide range of medicinal properties. The effect of lupeol and its ester was evaluated in CP induced alterations in cardiac electrolytes in rats. Read More

View Article and Full-Text PDF
November 2006

Lupeol and its ester exhibit protective role against cyclophosphamide-induced cardiac mitochondrial toxicity.

J Cardiovasc Pharmacol 2006 Feb;47(2):205-10

Department of Medical Biochemistry, Dr. ALM. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, India.

Cyclophosphamide (CP), an anti-cancer and immunosuppressant drug, causes fatal cardiotoxicity during high dose chemotherapy. Lupeol, a pentacyclic triterpene, isolated from Crataeva nurvala stem bark and its ester, lupeol linoleate, possess wide range of medicinal properties. The objective of this study was to establish the pharmacological efficacy of lupeol and its ester against CP-induced mitochondrial-cardiomyopathy. Read More

View Article and Full-Text PDF
February 2006

Lupeol and its ester ameliorate the cyclophosphamide provoked cardiac lysosomal damage studied in rat.

Mol Cell Biochem 2006 Jan;282(1-2):23-9

Department of Medical Biochemistry, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, India.

Cyclophosphamide (CP), an alkylating agent widely used in cancer chemotherapy causes fatal cardiotoxicity. Lupeol, a pentacyclic triterpene, isolated from Crataeva nurvala stem bark and its ester, lupeol linoleate possess a wide range of medicinal properties. The effect of lupeol and its ester was evaluated in CP-induced myocardial toxicity in rats. Read More

View Article and Full-Text PDF
January 2006

Cytoprotective role of DL-alpha-lipoic acid in cyclophosphamide induced myocardial toxicity.

Mol Cell Biochem 2005 Aug;276(1-2):39-44

Department of Medical Biochemistry, Dr. ALM. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, 600 113, India, .

Cyclophosphamide (CP), a potent antitumor drug is known to cause severe cardiotoxicity. The present study is aimed at evaluating the cardioprotective role of lipoic acid in CP induced toxicity. Male albino rats of Wistar strain were divided into four groups and treated as follows: Group I served as control, Group II received a single dose of CP (200 mg/kg b. Read More

View Article and Full-Text PDF

dl-alpha-lipoic acid ameliorates cyclophosphamide induced cardiac mitochondrial injury.

Toxicology 2005 Nov 8;215(1-2):108-14. Epub 2005 Aug 8.

Department of Medical Biochemistry, Dr. ALM. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600113, India.

Mitochondria play a central role in heart metabolism and function. Administration of antineoplastic drug cyclophosphamide (CP) adversely affects the heart mitochondria which may result in cardiotoxicity. The present study is aimed at evaluating the role of lipoic acid (LA) in CP induced myocardial injury. Read More

View Article and Full-Text PDF
November 2005

Cardioprotective effect of pentacyclic triterpene, lupeol and its ester on cyclophosphamide-induced oxidative stress.

Hum Exp Toxicol 2005 Jun;24(6):313-8

Department of Medical Biochemistry, Dr. ALM. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, India.

Cyclophosphamide (CP), an alkylating agent widely used in cancer chemotherapy, causes fatal cardiotoxicity. In the present study, lupeol, a pentacyclic triterpene, isolated from Crataeva nurvala stem bark and its ester, lupeol linoleate were investigated for their possible cardioprotective effects against CP-induced toxicity. Male albino rats of Wistar strain were injected with a single dose of CP (200 mg/kg body weight, ip). Read More

View Article and Full-Text PDF

Preconditioning prevents alterations in cardiac SR gene expression due to ischemia-reperfusion.

Am J Physiol Heart Circ Physiol 2002 Apr;282(4):H1461-6

Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre and Department of Physiology, University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6.

We have previously shown that ischemic preconditioning (IP) improves cardiac performance and sarcoplasmic reticulum (SR) function in hearts subjected to ischemia-reperfusion (I/R). In this study, we examined the effect of IP on I/R-induced changes in gene expression for SR proteins such as the Ca(2+) release channel, Ca(2+) pump ATPase, phospholamban, and calsequestrin in the isolated rat heart. Normal isolated rat hearts exposed to three brief cycles of IP (5-min ischemia and 5-min reperfusion) exhibited a significant decrease in the transcript levels of SR genes. Read More

View Article and Full-Text PDF