المؤلفون: Harinder Singh, Amteshwar Singh Jaggi, Manish Kumar, Nirmal Singh

المصدر: Journal of Cardiovascular Pharmacology. 73:63-69

مصطلحات موضوعية: 0301 basic medicine, Isolated Heart Preparation, Adenosine, Time Factors, Ganglionic Blockers, Myocardial Infarction, Myocardial Reperfusion Injury, Hindlimb, 030204 cardiovascular system & hematology, Pharmacology, Autonomic Nervous System, Hexamethonium, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Lactate dehydrogenase, Animals, Medicine, Rats, Wistar, Ischemic Preconditioning, Creatine Kinase, Cardioprotection, L-Lactate Dehydrogenase, biology, business.industry, Heart, Disease Models, Animal, 030104 developmental biology, chemistry, Regional Blood Flow, biology.protein, Ischemic preconditioning, Creatine kinase, Therapeutic Occlusion, Cardiology and Cardiovascular Medicine, business, medicine.drug

الوصف: Background The role of the neurogenic pathway in early phases of cardioprotection during remote ischemic preconditioning (RIPC) and adenosine preconditioning is reported. Aim This study was designed to explore the involvement of the neurogenic pathway in late phases of cardioprotection during RIPC and adenosine preconditioning. Material and methods Fifty-four Wistar rats were used and divided into 9 experimental groups. RIPC was induced by tying the blood pressure cuff around the hind limb and subjecting to 4 cycles of inflation and deflation of 5 minutes each. In early RIPC, the heart was isolated immediately after the last episode of RIPC, whereas in late RIPC, the heart was isolated 24 hours after the last cycle of RIPC. In a similar way, adenosine preconditioning was instituted in early and late phases by either isolating the heart 40 minutes or 24 hours after adenosine (4 mg/kg, intraperitoneally [i.p.]) administration. Isolated hearts were subjected to ischemia-reperfusion (I/R) injury on the Langendorff's system. Results Both early and late phases of RIPC and adenosine preconditioning significantly abrogated I/R-induced myocardial injury in terms of decrease in the release of lactate dehydrogenase, creatine kinase, and decrease in infarct size. Pretreatment with hexamethonium, a ganglion blocker (20 mg/kg, i.p.), significantly abolished the cardioprotective effects of both early and late phases of RIPC and adenosine preconditioning. Conclusion Apart from the involvement of the neurogenic pathway in the early phases, there is a critical role of the neurogenic pathway in the late phase of cardioprotection during RIPC and adenosine preconditioning.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b16f82e2f31ed18c88566b66e15b99d4Test
https://doi.org/10.1097/fjc.0000000000000634Test

المؤلفون: Ming He, Dan Liu, Dong Yin, Liqing Huang, Huan He, Zhantu Liu

المصدر: Journal of Cardiovascular Pharmacology. 67:526-537

مصطلحات موضوعية: 0301 basic medicine, Cell Survival, Apoptosis, Myocardial Reperfusion Injury, Pharmacology, Rats, Sprague-Dawley, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Sirtuin 1, Lactate dehydrogenase, Animals, Myocyte, Myocytes, Cardiac, Viability assay, chemistry.chemical_classification, Cardioprotection, Reactive oxygen species, L-Lactate Dehydrogenase, biology, Caspase 3, Cytochromes c, Molecular biology, Cell Hypoxia, Rats, 030104 developmental biology, chemistry, Mitochondrial permeability transition pore, 030220 oncology & carcinogenesis, biology.protein, Quercetin, Creatine kinase, Reactive Oxygen Species, Cardiology and Cardiovascular Medicine

الوصف: It has been reported that apoptosis plays a very important role on anoxia/reoxygenation (A/R)-induced injury, and human silent information regulator type 1 (SIRT1) can inhibit the apoptosis of cardiomyocytes. It has been proved that isorhamnetin (IsoRN), 3'-O-methyl-quecetin, can protect the cardiomyocytes, but the mechanism is still not clear. The aim of the study was to explore whether the protective effects of IsoRN on the cardiomyocytes against the A/R-induced injury are mediated by SIRT1. The effects of IsoRN on cardioprotection against A/R injury in neonatal rat cardiomyocytes were monitored by cell viability, the levels of mitochondrial membrane potential (Δψm), apoptosis, and intracellular reactive oxygen species (ROS), the levels of lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and mitochondrial permeability transition pores (mPTP). The effects on protein expression were measured by western blot assay. The results showed that IsoRN can reduce A/R-induced injury by decreasing the level of lactate dehydrogenase and creatine phosphokinase release from the cardiomyocytes, increasing cell viability and expression of SIRT1, reducing the generation of reactive oxygen species, inhibiting opening of mitochondrial permeability transition pores and loss of Δψm and activation of caspase-3, and decreasing the release of cytochrome c, and reducing apoptosis. In addition, sirtinol, a SIRT1 inhibitor, drastically reduced the protective effects of IsoRN on cardioprotective effects in cardiomocytes. In conclusion, we firstly demonstrated that SIRT1 may be involved in the protective effects of IsoRN on cardiomocytes against the A/R-induced injury.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::231ad62b9ace5b0d18d05013b116b777Test
https://doi.org/10.1097/fjc.0000000000000376Test

المؤلفون: Hui-Ting Zhong, Yong-Ping Fu, Li-Hong Wang, Meng-Kai Lu, Xin-Wen Liu

المصدر: Journal of cardiovascular pharmacology. 73(2)

مصطلحات موضوعية: 0301 basic medicine, Male, ATG5, Myocardial Infarction, Panax, Myocardial Reperfusion Injury, 030204 cardiovascular system & hematology, Mitochondrion, Pharmacology, Autophagy-Related Protein 5, Superoxide dismutase, Mitochondrial Proteins, Rats, Sprague-Dawley, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Lactate dehydrogenase, medicine, Autophagy, Animals, Panax notoginseng, Myocytes, Cardiac, chemistry.chemical_classification, Reactive oxygen species, biology, Membrane Proteins, Cardiovascular Agents, Saponins, medicine.disease, biology.organism_classification, Hypoxia-Inducible Factor 1, alpha Subunit, Disease Models, Animal, 030104 developmental biology, chemistry, biology.protein, Beclin-1, Cardiology and Cardiovascular Medicine, Reperfusion injury, Microtubule-Associated Proteins, Signal Transduction

الوصف: Background and objective Panax Notoginseng Saponins (PNS) is a formula of Chinese medicine commonly used for treating ischemia myocardial in China. However, its mechanism of action is yet unclear. This study investigated the effect and the mechanism of PNS on myocardial ischemia-reperfusion injury (MIRI) through the hypoxia-inducible factor 1α (HIF-1α)/bcl-2/adenovirus E1B19kDa-interacting protein3 (BNIP3) pathway of autophagy. Methods We constructed a rat model of myocardial injury and compared among 4 groups (n = 10, each): the sham-operated group (Sham), the ischemia-reperfusion group (IR), the PNS low-dose group, and the PNS high-dose group were pretreated with PNS (30 and 60 mg/kg, respectively). Serum creatine kinase, malonaldehyde (MDA), lactate dehydrogenase, myocardial tissue superoxide dismutase, and reactive oxygen species were detected in rats with myocardial ischemia-reperfusion after the intervention of PNS. The rat myocardial tissue was examined using hematoxylin and eosin (H&E) staining, and the mitochondria of myocardial cells were observed using transmission electron microscopy. The expressions of microtubule-associated protein light chain 3 (LC3), HIF-1α, BNIP3, Beclin-1, and autophagy-related gene-5 (Atg5) in rat myocardial tissue were detected using Western blotting. Results The results showed that PNS was significantly protected against MIRI, as evidenced by the decreasing in the concentration of serum CK, MDA, lactate dehydrogenase, and myocardial tissue superoxide dismutase, reactive oxygen species, the attenuation of myocardial tissue histopathological changes and the mitochondrial damages of myocardial cells, and the increase of mitochondria autophagosome in myocardial cells. In addition, PNS significantly increased the expression of LC3 and the ratio of LC3II/LC3I in rat myocardial tissue. Moreover, PNS significantly increased the expression of HIF-1α, BNIP3, Atg5, and Beclin-1 in rat myocardial tissue. Conclusions The protective effect of PNS on MIRI was mainly due to its ability to enhance the mitochondrial autophagy of myocardial tissue through the HIF-1α/BNIP3 pathway.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::cc450ab4ef87bc63e7484ca9b38cecd8Test
https://pubmed.ncbi.nlm.nih.gov/30531436Test

المؤلفون: Shou Hu, Jun-Jian Yu, Zi-You Liu, Cheng-Nan Tian, Qin-Wen Zhong, Hou-Mou Ma

المصدر: Journal of Cardiovascular Pharmacology

مصطلحات موضوعية: Male, medicine.medical_specialty, cardiac, ischemic-reperfusion, I/R, Myocardial Reperfusion Injury, cardiomyocyte, 030204 cardiovascular system & hematology, Receptors, N-Methyl-D-Aspartate, Rats, Sprague-Dawley, 03 medical and health sciences, chemistry.chemical_compound, Random Allocation, 0302 clinical medicine, Internal medicine, Lactate dehydrogenase, medicine, Animals, Myocytes, Cardiac, Protein kinase B, Pharmacology, Calcium metabolism, N-methyl-d-aspartate receptor, biology, myocardial, medicine.disease, Rats, NMDAR, Endocrinology, chemistry, nervous system, NMDA, Anesthesia, Ventricular pressure, biology.protein, NMDA receptor, Creatine kinase, Calcium, Original Article, Dizocilpine Maleate, Cardiology and Cardiovascular Medicine, Reperfusion injury, Excitatory Amino Acid Antagonists, 030217 neurology & neurosurgery, Ex vivo

الوصف: Background: Despite the adverse effects of N-methyl-d-aspartate receptor (NMDAR) activity in cardiomyocytes, no study has yet examined the effects of NMDAR activity under ex vivo ischemic-reperfusion (I/R) conditions. Therefore, our aim was to comprehensively evaluate the effects of NMDAR activity through an ex vivo myocardial I/R rat model. Methods: Isolated rat hearts were randomly segregated into 6 groups (n = 20 in each group): (1) an untreated control group; (2) a NMDA-treated control group; (3) an untreated I/R group; (4) an I/R+NMDA group treated with NMDA; (5) an I/R+NMDA+MK-801 group treated with NMDA and the NMDAR inhibitor MK-801; and (6) an I/R+NMDA+[Ca2+]-free group treated with NMDA and [Ca2+]-free buffer. The 4 I/R groups underwent 30 minutes of ischemia followed by 50 minutes of reperfusion. Left ventricular pressure signals were analyzed to assess cardiac performance. Myocardial intracellular calcium levels ([Ca2+]i) were assessed in isolated ventricular cardiomyocytes. Creatine kinase, creatine kinase isoenzyme MB, lactate dehydrogenase, cardiac troponin I, and cardiac troponin T were assayed from coronary effluents. TTC and TUNEL staining were used to measure generalized myocardial necrosis and apoptosis levels, respectively. Western blotting was applied to assess the phosphorylation of PKC-δ, PKC-ε, Akt, and extracellular signal-regulated kinase. Results: Enhanced NMDAR activity under control conditions had no significant effects on the foregoing variables. In contrast, enhanced NMDAR activity under I/R conditions produced significant increases in [Ca2+]i levels (∼1.2% increase), significant losses in left ventricular function (∼5.4% decrease), significant multi-fold increases in creatine kinase, creatine kinase isoenzyme MB, lactate dehydrogenase, cardiac troponin I, and cardiac troponin T, significant increases in generalized myocardial necrosis (∼36% increase) and apoptosis (∼150% increase), and significant multi-fold increases in PKC-δ, PKC-ε, Akt, and extracellular signal-regulated kinase phosphorylation (all P < 0.05). These adverse effects were rescued by the NMDAR inhibitor MK-801 or [Ca2+]-free buffer (all P < 0.05). Conclusions: NMDAR-driven calcium influx potentiates the adverse effects of myocardial I/R injury ex vivo.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::be4702bf6c8cae4278435ff45054efbbTest
https://pubmed.ncbi.nlm.nih.gov/28777252Test

المؤلفون: Dhanapalan Karthik, Periyasami Viswanathan, Carani Venkatraman Anuradha

المصدر: Journal of Cardiovascular Pharmacology. 58:514-521

مصطلحات موضوعية: Blood Glucose, Male, Antioxidant, medicine.medical_treatment, Gene Expression, Blood Pressure, Protein oxidation, Antioxidants, Lipid peroxidation, chemistry.chemical_compound, Creatine Kinase, MB Form, Insulin, NADPH oxidase, Endothelin-1, biology, Rosmarinic acid, Heart, Organ Size, Lipids, Biochemistry, Hypertension, Kallikreins, Cardiology and Cardiovascular Medicine, Nicotinamide adenine dinucleotide phosphate, medicine.medical_specialty, Nitric Oxide Synthase Type III, Aspartate transaminase, Fructose, Peptidyl-Dipeptidase A, Depsides, Nitric oxide, Hyperinsulinism, Internal medicine, Dietary Carbohydrates, medicine, Animals, Aspartate Aminotransferases, Rats, Wistar, Pharmacology, Nitrates, L-Lactate Dehydrogenase, Myocardium, Body Weight, NADPH Oxidases, Lipid Metabolism, Rats, Oxidative Stress, Endocrinology, chemistry, Cinnamates, biology.protein, Insulin Resistance, Troponin C

الوصف: Rosmarinic acid (RA), a caffeic acid ester, has insulin-sensitizing and antioxidant effects in high fructose-fed model of insulin resistance (IR). This study investigated whether RA supplementation prevents cardiac abnormalities and hypertension in fructose-fed rats (FFR). Rats fed with fructose diet (60 g/100 g) for 60 days exhibited metabolic abnormalities and rise in plasma and cardiac lipids and whole body IR. The levels of cardiac antioxidants and plasma ferric reducing antioxidant power were significantly reduced in FFR concomitant with increased levels of lipid peroxidation and protein oxidation products. A significant rise in troponin T, creatine kinase-MB, aspartate transaminase, and lactate dehydrogenase in plasma of FFR was noted. RA supplementation to FFR (10 mg/kg from the 16th day) significantly improved insulin sensitivity, reduced lipid levels, oxidative damage, and the expression of p22phox subunit of nicotinamide adenine dinucleotide phosphate reduced oxidase, and prevented cardiac hypertrophy. Fructose-induced rise in blood pressure was also lowered by RA through decrease in endothelin-1 and angiotensin-converting enzyme activity and increase in nitric oxide levels. Histology revealed a reduction in myocardial damage in RA-supplemented FFR. These findings suggest that RA acts as a vasoactive substance and a cardioprotector through its antioxidant property. Thus, RA may be useful in reducing the cardiovascular risk associated with IR.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::20c9db9d30342a474ac2967eda0ca67bTest
https://doi.org/10.1097/fjc.0b013e31822c265dTest

المؤلفون: Doaa A. Sourour, Olfat G. Shaker

المصدر: Journal of Cardiovascular Pharmacology. 55:262-268

مصطلحات موضوعية: Male, medicine.medical_specialty, Cardiotonic Agents, Cardiomyopathy, Nitric Oxide Synthase Type II, Matrix metalloproteinase, Gene Expression Regulation, Enzymologic, chemistry.chemical_compound, Lisinopril, Lactate dehydrogenase, Internal medicine, Animals, Medicine, Doxorubicin, RNA, Messenger, Rats, Wistar, Pharmacology, Antibiotics, Antineoplastic, Tissue Inhibitor of Metalloproteinase-1, biology, Human Growth Hormone, business.industry, Cumulative dose, medicine.disease, Rats, Nitric oxide synthase, Endocrinology, chemistry, biology.protein, Matrix Metalloproteinase 2, Drug Therapy, Combination, Creatine kinase, Cardiomyopathies, Cardiology and Cardiovascular Medicine, business, medicine.drug

الوصف: The present study was designed to compare the cardioprotective effects of the combination of lisinopril with growth hormone over lisinopril alone in doxorubicin (Dox)-induced cardiomyopathy in rats. Forty male Wister albino rats were divided into 4 groups: group 1, control group; group 2, received Dox; group 3, received lisinopril + Dox; and group 4, received lisinopril + Dox + growth hormone. Dox (cumulative dose) was administered to rats in 6 equal intraperitoneal injections over a period of 2 weeks. Histopathological changes and plasma aspartate aminotransferase, lactate dehydrogenase, and creatine kinase and plasma levels of matrix metalloproteinase (MMP)-2, tissue inhibitor matrix metalloproteinase (TIMP)-1, and cardiac inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) expression were determined 9 weeks after the first dose of Dox. Dox produced cardiac structural injury and significant elevation in plasma levels of cardiac enzymes, MMP-2, and cardiac iNOS mRNA expression together with significant reduction in plasma TIMP-1 level. Lisinopril significantly decreases plasma MMP-2 level and cardiac iNOS mRNA expression by 13% and 15%, respectively, in group 3 compared with 36% and 47%, respectively, in group 4 as compared with group 2. In addition, compared with Dox group, lisinopril significantly increases plasma TIMP-1 level by 23% compared with 49% in group 4. We can conclude that the combination of lisinopril and growth hormone produced better cardioprotective effect against Dox-induced cardiomyopathy. This effect may be attributed on their antiremodeling actions by regulating plasma MMP-2/TIMP-1 levels and to the reduction of cardiac iNOS mRNA expression.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0a2e7481f7f3cc65c131d95cac69d04cTest
https://doi.org/10.1097/fjc.0b013e3181cf91acTest

المؤلفون: Rajarsi Mandal, Damodar Kumbala, Vandana Potaraju, Vijay Kumar Kutala, Mahmood Khan, Giuseppe Colantuono, Periannan Kuppusamy

المصدر: Journal of Cardiovascular Pharmacology. 48:79-87

مصطلحات موضوعية: Myocardial Ischemia, Ischemia, Myocardial Reperfusion Injury, Pharmacology, Nitric Oxide, medicine.disease_cause, Nitric oxide, Cyclic N-Oxides, Rats, Sprague-Dawley, Superoxide dismutase, chemistry.chemical_compound, Superoxides, Peroxynitrous Acid, medicine, Animals, Creatine Kinase, chemistry.chemical_classification, Cardioprotection, Reactive oxygen species, Aspirin, L-Lactate Dehydrogenase, biology, Superoxide Dismutase, Superoxide, medicine.disease, Rats, Uric Acid, chemistry, Anesthesia, biology.protein, Spin Labels, Cardiology and Cardiovascular Medicine, Peroxynitrite, Oxidative stress

الوصف: Nitric oxide (NO) plays a protective role in myocardial ischemia-reperfusion (I/R) injury. However, the concomitant production of superoxide and other reactive oxygen species (ROS) during I/R may diminish the bioavailability of NO and hence compromise the beneficial effects. The objective of this study was to investigate the protective effect of the coadministration of NCX-4016 [2-(acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester] (an NO donor) with antioxidants Tempol, superoxide dismutase (SOD), or urate on I/R injury. Isolated rat hearts, perfused with Krebs-Henseleit buffer, were subjected to 30 minutes of global ischemia, followed by 45 minutes of reperfusion. Before the induction of ischemia, the hearts were infused for 1 minute with NCX-4016 (100 microM) either alone or in combination with Tempol (100 microM), SOD (200 U/mL), or urate (100 microM). Hearts pretreated with NCX-4016 showed a significantly enhanced recovery of function and decreased infarct size and LDH/CK release compared with the controls. However, treatment of hearts with NCX-4016 + Tempol, SOD, or urate showed a significantly enhanced recovery of heart function compared with NCX-4016 alone. The treatment of hearts with NCX-4016 + Tempol showed significantly enhanced NO generation and decreased ROS and dityrosine (a marker of peroxynitrite) formation. In conclusion, NCX-4016 in combination with Tempol demonstrated significant cardioprotection and, thus, may offer a novel therapeutic strategy to prevent I/R-mediated myocardial injury.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d1d2575bd271bb262c71139ed270ef07Test
https://doi.org/10.1097/01.fjc.0000242050.16790.65Test

المؤلفون: Giuseppina Basta, Claudia Kusmic, Nicoletta Vesentini, Renata Barsacchi, Guido Lazzerini

المصدر: Journal of Cardiovascular Pharmacology. 44:356-362

مصطلحات موضوعية: Male, medicine.medical_treatment, Myocardial Ischemia, Ischemia, Electrophoretic Mobility Shift Assay, Myocardial Reperfusion Injury, 6-Ketoprostaglandin F1 alpha, Pharmacology, medicine.disease_cause, Phospholipase A2, Animals, Vitamin E, Medicine, Rats, Wistar, Cell Nucleus, L-Lactate Dehydrogenase, biology, Plant Extracts, business.industry, Ginkgo biloba, Myocardium, NF-kappa B, biology.organism_classification, medicine.disease, Free radical scavenger, NFKB1, Rats, Perfusion, Oxidative Stress, Freeze Drying, Anesthesia, biology.protein, Female, Cardiology and Cardiovascular Medicine, business, Oxidative stress, Transcription Factors

الوصف: The effect of Ginkgo biloba extract (EGb 761) was studied in rat hearts submitted to ischemia/reperfusion. Isolated hearts perfused in Langendorff mode were subjected to 60 minutes of global ischemia and 15 minutes of reperfusion. EGb 761 was administered by chronic or acute treatment: intra-peritoneal injections of 5 mg/Kg extract for 5 days, or 100 mg /L extract addition to the perfusion buffer, respectively. In hearts not treated with EGb 761, ischemia induced a 20% decrease in the concentration of membrane alpha-tocopherol. This effect was not worsened by reperfusion. alpha-tocopherol consumption was accompanied by about 650% increase in 6-ketoPGF1alpha release within 3 minutes of reperfusion. Moreover, ischemia induced activation of transcription factor NF-kappaB, as compared with the untreated group. In both chronic and acute treatment with EGb 761, heart concentration of alpha-tocopherol was completely spared during ischemia as much as after reperfusion, and a significant decrease of 6-ketoPGF1alpha release was observed at 3 minutes of reperfusion. Nuclear translocation of NF-kappaB was lowered during ischemia. EGb 761 might act as direct free radical scavenger or as tocopheryl radical recycler; in both cases sparing membrane vitamin E should affect phospholipase A2 activity. Finally, EGb 761, by lowering ROS produced during ischemia, challenges nuclear translocation of NF-kappaB.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::664bfa3e6abcacf798843a9e41cafd77Test
https://doi.org/10.1097/01.fjc.0000137164.99487.42Test

المؤلفون: Mahaveer Golechha, Santosh Kumari, Jaspreet Sachdeva, Dharamvir Singh Arya, Vineeta Tanwar

المصدر: Journal of cardiovascular pharmacology. 55(4)

مصطلحات موضوعية: Cardiac function curve, Male, Curcumin, Thiobarbituric acid, HSP27 Heat-Shock Proteins, Myocardial Ischemia, Blood Pressure, Pharmacology, Creatine, medicine.disease_cause, Thiobarbituric Acid Reactive Substances, Antioxidants, Superoxide dismutase, chemistry.chemical_compound, Ventricular Dysfunction, Left, Heart Rate, Isoprenaline, Lactate dehydrogenase, medicine, Animals, Creatine Kinase, MB Form, Rats, Wistar, biology, L-Lactate Dehydrogenase, Superoxide Dismutase, Myocardium, Isoproterenol, Heart, Catalase, Glutathione, Rats, chemistry, Biochemistry, biology.protein, Lipid Peroxidation, Cardiology and Cardiovascular Medicine, Oxidative stress, medicine.drug

الوصف: This investigation examines the role of heat shock protein (Hsp) 27 and its modulation by curcumin in isoproterenol-induced myocardial ischemic injury in rats. Evidence from hemodynamic functions and oxidative stress parameters were also included in the study. The animals were divided into control, isoproterenol, and curcumin 100, 200, and 400 mg/kg treatment groups. Curcumin was administered orally for 15 days to all the treated groups. On 13th and 14th day, isoproterenol (85 mg/kg, s.c.) was injected to curcumin-treated and isoproterenol group. On day 15, hemodynamic parameters were recorded. Thereafter, animals were sacrificed and hearts were kept for biochemical and Western blot analysis. We found dose-dependent increase in the expression of Hsp27 with drastic fall at highest dose. Hemodynamically, the lower 2 doses also restored the cardiac function as evident by improved contractile functions, decreased left ventricular end-diastolic pressure, restored arterial pressures, and heart rate. In addition, there was an increase in then level of superoxide dismutase, catalase, reduced glutathione, and decreased production of thiobarbituric acid reactive substances and leakage of cardiac necroenzyme creatine kinase-MB isoenzyme and lactate dehydrogenase in curcumin 100 and 200 mg/kg group as compared with isoproterenol. However, at a dose of 400 mg/kg, there was ineffectual protection against isoproterenol-induced myocardial damage. Our results suggested 200 mg/mg as the most optimum therapeutic dose showing improved cardiac function due to stabilization of cytoskeleton structure which in turn is attributed to Hsp27 expression along with fortified antioxidant defense system.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::622e35e3baacdaf4db62ce6fe5faf227Test
https://pubmed.ncbi.nlm.nih.gov/20125031Test

المؤلفون: Yin-Tie Jin, Shinsuke Kido, Kenjiro Kikuchi, Takafumi Ohta, Naoyuki Hasebe, Motohiko Sato, Shiro Tsuji, Shunsuke Natori

المصدر: Journal of Cardiovascular Pharmacology. 38:S63-S67

مصطلحات موضوعية: Male, Lipid Peroxides, medicine.medical_specialty, Heart Diseases, Angiotensin-Converting Enzyme Inhibitors, urologic and male genital diseases, Receptor, Angiotensin, Type 1, Quinaprilat, Angiotensin Receptor Antagonists, Ventricular Dysfunction, Left, Dogs, Isoprenaline, Internal medicine, medicine, Animals, Creatine Kinase, MB Form, cardiovascular diseases, Creatine Kinase, Pharmacology, L-Lactate Dehydrogenase, biology, Lipid peroxide, Chemistry, Angiotensin II, Hemodynamics, Isoproterenol, Angiotensin-converting enzyme, Adrenergic beta-Agonists, medicine.disease, female genital diseases and pregnancy complications, Isoenzymes, Candesartan, Endocrinology, Heart failure, ACE inhibitor, biology.protein, Female, Cardiology and Cardiovascular Medicine, medicine.drug

الوصف: We examined whether angiotensin converting enzyme (ACE) inhibitors and angiotensin II type 1 receptor blockers (ARB) prevent isoproterenol (ISO)-induced left ventricular (LV) dysfunction in dogs. The effects of a large dose of ISO, 1 microg/kg/min, 3 h infusion, were investigated in three groups with simultaneous infusion of an ACE inhibitor (quinaprilat), ARB (candesartan) or saline. ISO infusion significantly decreased LV dP/dt, LV ejection fraction and LV fractional shortening, and significantly increased tau, the time constant of isovolume relaxation of LV, and LV end diastolic pressure. All of these changes were significantly attenuated in both the ACE inhibitor and ARB groups, especially in the ARB group. Serum levels of creatinin kinase isoform MB, lactate dehydrogenase and lipid peroxide were significantly increased by ISO. However, the increases in these markers of myocardial damage were significantly diminished by simultaneous infusion of an ACE inhibitor or ARB, especially by ARB. In conclusion, an ACE inhibitor and ARB prevent LV systolic and diastolic dysfunction as well as myocardial damage induced by excess beta-adrenergic stimulation.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::00949c08aa72838f397678d5b5f0a16fTest
https://doi.org/10.1097/00005344-200110001-00014Test