المؤلفون: Sun-Mee Lee, Jin Gu Park, Seok-Joo Kim

المصدر: Life Sciences. 90:169-176

مصطلحات موضوعية: Male, medicine.medical_specialty, Liquid diet, Portal venous pressure, Protoporphyrins, General Biochemistry, Genetics and Molecular Biology, Rats, Sprague-Dawley, Lipid peroxidation, chemistry.chemical_compound, Internal medicine, Lactate dehydrogenase, medicine, Animals, Enzyme Inhibitors, Hyaluronic Acid, General Pharmacology, Toxicology and Pharmaceutics, Ethanol, L-Lactate Dehydrogenase, Cold Ischemia, Zinc protoporphyrin, Fatty liver, Organ Preservation, General Medicine, medicine.disease, Glutathione, Portal Pressure, COPP, Liver Transplantation, Rats, Heme oxygenase, Endocrinology, Liver, chemistry, Biochemistry, Enzyme Induction, Reperfusion Injury, Lipid Peroxidation, Heme Oxygenase-1, Fatty Liver, Alcoholic

الوصف: Aims The purpose of this study was to investigate the cytoprotective role of heme oxygenase-1 (HO-1) induction in hepatic injury in alcoholic steatotic liver exposed to cold ischemia/reperfusion (I/R). Main methods Animals were fed an ethanol liquid diet or isocaloric control diet for 5 weeks. Isolated perfused rat livers were preserved in Histidine–Tryptophan–Ketoglutarate at 4 °C. After 24 h of storage, livers were subjected to 120 min of reperfusion with Krebs–Henseleit bicarbonate buffer at 37 °C. Animals were pretreated with cobalt protoporphyrin (CoPP, 5 mg/kg, i.p.) or zinc protoporphyrin (ZnPP, 25 mg/kg, i.p.), HO-1 inducer and antagonist, respectively. Key findings In the model of ischemia/isolated perfusion, endogenous HO-1 was downregulated in the livers fed with ethanol diet (ED I/R). In ED I/R group, portal pressure and lactate dehydrogenase release were significantly increased, while bile output and hyaluronic acid clearance decreased compared to rats fed on control diet (CD I/R). Furthermore, hepatic glutathione content decreased and lipid peroxidation increased in the ED I/R group compared to the CD I/R group. These alterations were attenuated by upregulation of HO-1 with CoPP pretreatment. Significance Our results suggest that chronic ethanol consumption aggravates hepatic injury during cold I/R and it is likely due to downregulation of endogenous HO-1. Prior induction of HO-1 expression may provide a new strategy to protect livers against hepatic I/R injury or to increase the donor transplant pool through modulation of marginal alcoholic steatotic livers.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::638bcdfd22b4ddaacb9db17c66cd5b53Test
https://doi.org/10.1016/j.lfs.2011.10.003Test

المؤلفون: J. Wang, H. Sun, Yue Li, L.G. Miao, M. Li, M. Song, Y.Z. Zhu, Yang Fu

المصدر: Life Sciences. 102:36-40

مصطلحات موضوعية: Male, medicine.medical_specialty, Time Factors, Iron, Administration, Oral, Chloride, General Biochemistry, Genetics and Molecular Biology, chemistry.chemical_compound, Chlorides, hemic and lymphatic diseases, Internal medicine, Lactate dehydrogenase, Testis, Male rats, medicine, Aluminum Chloride, Animals, Rats, Wistar, General Pharmacology, Toxicology and Pharmaceutics, Aluminum Compounds, Spermatogenesis, chemistry.chemical_classification, Dose-Response Relationship, Drug, Sperm Count, biology, Chemistry, Succinate dehydrogenase, Acid phosphatase, General Medicine, Sperm, Rats, Zinc, Endocrinology, Enzyme, biology.protein, Copper, medicine.drug

الوصف: Aims The aim of this study was to determine the effects of sub-chronic aluminum chloride (AlCl 3 ) on spermatogenesis and testicular enzymatic activity in male rats. Main methods Forty Wistar male rats were randomly divided into four groups: control group (CG, 0), low-dose group (LG, 64.18 mg/kg BW AlCl 3 ), mid-dose group (MG, 128.36 mg/kg BW AlCl 3 ) and high-dose group (HG, 256.72 mg/kg BW AlCl 3 ). The rats were orally administered with AlCl 3 for 120 days. At the end of the experiment, the contents of Al, Fe, Cu and Zn, the enzyme activities of testicular acid phosphatase (ACP), succinate dehydrogenase (SDH), lactate dehydrogenase (LDH), lactate dehydrogenase isoenzyme (LDH-x), the sperm count and the sperm malformation rate were examined. Key findings The results showed that the Al and Cu contents, sperm count and the enzyme activities of testicular ACP, SDH, LDH and LDH-x decreased, while the Zn and Fe contents and sperm malformation rate increased in AlCl 3 -treated rats. Significance It suggests that sub-chronic AlCl 3 disorders the balance of trace element and decreases the spermatogenesis and the activities of testicular enzymes, indicating that AlCl 3 has adverse effect on the testicular function in male rats.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bb24e17c08f272088a5b09d36409c5adTest
https://doi.org/10.1016/j.lfs.2014.02.035Test

المؤلفون: Ye Zhang, Hai-Juan Zhu, Shufang He, Shiyun Jin, Zhengyi Han, Xiang-Dong Fang, Shijin Xu

المصدر: Life sciences. 170

مصطلحات موضوعية: 0301 basic medicine, Male, Pathology, medicine.medical_specialty, Ischemia, Apoptosis, Myocardial Reperfusion Injury, 030204 cardiovascular system & hematology, Pharmacology, General Biochemistry, Genetics and Molecular Biology, Rats, Sprague-Dawley, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, medicine, Animals, Cluster Analysis, Doxorubicin, Myocytes, Cardiac, fas Receptor, General Pharmacology, Toxicology and Pharmaceutics, Hypoxia, Heart Failure, Ejection fraction, L-Lactate Dehydrogenase, Morphine, Microarray analysis techniques, business.industry, Gene Expression Profiling, General Medicine, Hypoxia (medical), medicine.disease, Rats, Disease Models, Animal, MicroRNAs, 030104 developmental biology, Gene Expression Regulation, Heart failure, medicine.symptom, business, medicine.drug

الوصف: Aims Ischemia reperfusion (I/R) injury is an inevitable event arising during the cardiovascular diseases development and the process of potent surgical treatments. microRNAs (miRNAs) are critical regulators of multiple cell processes including I/R injury. The present study aims to quantify miRNA alterations and regulated genes upon hypoxia-reoxygenation (H/R) injury in a rat heart failure model comparing with normal cardiomyocytes. Main methods Chronic heart failure was established by injecting doxorubicin (2 mg/kg/week) for 6 weeks, then H/R was performed on primary cultured cardiomyocytes isolated from normal and failed heart. Cellular injury was evaluated by detecting LDH release levels, cell variability and apoptotic rate. Dysregulated miRNAs in control, hypoxia preconditioning (HPC) and morphine preconditioning (MPC) groups under two conditions were quantified by microarray analysis. Fas protein expression was analyzed using Western Blotting analysis. Key findings Chronic heart failure was confirmed with lower ejection fraction (EF), and significant cellular injury. HPC could reverse the injury induced by H/R in normal heart rather than failed heart, otherwise, MPC significantly attenuated cellular injury dose dependently in both conditions. There was 12 miRNAs significantly altered after doxorubicin injection, 7 downregulated and 5 upregulated. miR-133b-5p, miR-6216, miR-664-1-5p and let7e-5p were differentially expressed after HPC and MPC treatments. The direct interaction between miR-133b-5p and target gene Fas were established. The Fas protein expression was manipulated by MPC not HPC affording protective effect against H/R injury. Significance We investigated that miR-133b-5p might play a particularly important role in the cardioprotective effect of MPC by regulating the target gene Fas.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::36adae5acb4a54e3b9c6d84f4dd40a33Test
https://pubmed.ncbi.nlm.nih.gov/27919821Test

المؤلفون: Jon J. Ramsey, Robert Soo Hoo, Jose Alberto Lopez-Dominguez, Kevork Hagopian

المصدر: Life sciences, vol 93, iss 24

مصطلحات موضوعية: Male, Mitochondria, Liver, Inbred C57BL, medicine.disease_cause, Protein Carbonylation, Lipid peroxidation, Mice, chemistry.chemical_compound, Malate Dehydrogenase, Pharmacology & Pharmacy, General Pharmacology, Toxicology and Pharmaceutics, Aconitate Hydratase, chemistry.chemical_classification, Pharmacology and Pharmaceutical Sciences, General Medicine, Mitochondria, Succinate Dehydrogenase, Liver, Biochemistry, 1.1 Normal biological development and functioning, Citric Acid Cycle, Calorie restriction, TBARS, Citrate (si)-Synthase, Biology, Thiobarbituric Acid Reactive Substances, Malate dehydrogenase, Article, General Biochemistry, Genetics and Molecular Biology, Underpinning research, medicine, Animals, Caloric Restriction, Nutrition, L-Lactate Dehydrogenase, Mice, Inbred C57BL, Citric acid cycle, Oxidative Stress, Metabolic pathway, Enzyme, Electron Transport Chain Complex Proteins, chemistry, Electron transport chain, Lipid Peroxidation, Protein carbonyls, Biochemistry and Cell Biology, Reactive oxygen species, Krebs cycle, Oxidative stress

الوصف: AimsThe purpose of the study was to establish if enzyme activities from key metabolic pathways and levels of markers of oxidative damage to proteins and lipids differed between distinct liver mitochondrial sub-populations, and which specific sub-populations contributed to these differences.Main methodsMale C57BL/6J mice were fed non-purified diet for one month then separated into two groups, control and calorie-restricted (CR). The two groups were fed semi-purified diet (AIN93G), with the CR group receiving 40% less calories than controls. After two months, enzyme activities and markers of oxidative damage in mitochondria were determined.Key findingsIn all mitochondrial sub-populations, enzyme activities and markers of oxidative damage, from control and CR groups, showed a pattern of M1>M3>M10. Higher acyl-CoA dehydrogenase (β-oxidation) and β-hydroxybutyrate dehydrogenase (ketogenesis) activities and lower carbonyl and TBARS levels were observed in M1 and M3 fractions from CR mice. ETC enzyme activities did not show a consistent pattern. In the Krebs cycle, citrate synthase and aconitase activities decreased while succinate dehydrogenase and malate dehydrogenase activities increased in the M1 mitochondria from the CR versus control mice.SignificanceCR does not produce uniform changes in enzyme activities or markers of oxidative damage in mitochondrial sub-populations, with changes occurring primarily in the heavy mitochondrial populations. Centrifugation at 10,000 g to isolate mitochondria likely dilutes the mitochondrial populations which show the greatest response to CR. Use of lower centrifugal force (3000 g or lower) may be beneficial for some studies.

وصف الملف: application/pdf

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::387edec8340fac0f1081f76215ed7bf6Test
https://doi.org/10.1016/j.lfs.2013.10.006Test

المؤلفون: Jun Yamanouchi, Yoji Suzuki, Noriaki Mitsuda, Nobutaka Ohkubo, Mamoru Aoto, Satoshi Hirakawa, Masaki Yasukawa

المصدر: Life Sciences. 93:380-387

مصطلحات موضوعية: STAT3 Transcription Factor, Genetically modified mouse, Erythrocytes, Time Factors, Macrophage, Phagocytosis, Mice, Transgenic, Severity of Illness Index, General Biochemistry, Genetics and Molecular Biology, Body Temperature, Pharmacology, Toxicology and Pharmaceutics(all), Mice, Reticulocyte Count, Conditional gene knockout, Animals, General Pharmacology, Toxicology and Pharmaceutics, Promoter Regions, Genetic, STAT3, Erythropoietin, Mice, Knockout, Stat3, L-Lactate Dehydrogenase, biology, Biochemistry, Genetics and Molecular Biology(all), Macrophages, Anemia, General Medicine, Receptor, TIE-2, Angiopoietin receptor, Cell biology, Ferritins, Splenomegaly, Microscopy, Electron, Scanning, Cancer research, biology.protein, Spleen

الوصف: AimsSTAT3 is a key modulator of activation and differentiation of macrophages. But it is still unknown if deficiency of STAT3 activates macrophages to destroy erythrocytes by phagocytosis. We generated STAT3 conditional knockout mice by crossing floxed STAT3 mice with Tie2 promoter-driven Cre-recombinase transgenic mice and clarified that Stat3 plays a critical role in the formation and activation of macrophages.Main methodsBlood cell count, reticulocyte count, serum lactate dehydrogenase, erythropoietin, iron and ferritin concentration, and life span of the erythrocytes in Tie2 promoter-driven STAT3 conditional knockout mice were analyzed. To explore the erythropoietic function of the mice, we subjected them to brief hemolytic anemia by injecting them intraperitoneally with phenylhydrazine. The fragility of erythrocytes was examined by scanning electron microscopy and osmotic tolerance test.Key findingsThe conditional knockout mice had mild normocytic anemia. They also displayed higher lactate dehydrogenase, ferritin and erythropoietin concentration, higher reticulocyte count, and a shorter lifespan of erythrocytes compared with wild-type controls. These data suggest that destruction of erythrocytes and secondary blood formation were accelerated in the STAT3 conditional knockout mice. It didn't appear due to the fragility of erythrocytes. A few of the conditional knockout mice suddenly developed acute severe anemia, high body temperature and massive splenomegaly, and died within 2weeks after the onset of anemia.SignificanceThis study provided evidence that STAT3 have a critical role in the destruction of erythrocytes by resident macrophages in the spleen.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::66cd69b2f042df5b0f2ee1dfc5d9e2c4Test
https://doi.org/10.1016/j.lfs.2013.07.025Test

المؤلفون: Montserrat Feijóo, Francisco Franco, Pedro Montilla, Maria C. Muñoz, Juan A. Collado, Isaac Túnez, José Peña, Ignacio Rueda, Ignacio Jimena, Francisco J. Medina, Jordi Muntané

المصدر: Life Sciences. 80:1221-1227

مصطلحات موضوعية: medicine.medical_specialty, Injections, Subcutaneous, Ovariectomy, Neurotoxins, Oxidative phosphorylation, Striatum, medicine.disease_cause, General Biochemistry, Genetics and Molecular Biology, chemistry.chemical_compound, Huntington's disease, Internal medicine, Lactate dehydrogenase, medicine, Animals, Testosterone, Rats, Wistar, General Pharmacology, Toxicology and Pharmaceutics, Cell damage, Cell Death, L-Lactate Dehydrogenase, Chemistry, General Medicine, Nitro Compounds, medicine.disease, Corpus Striatum, Rats, Disease Models, Animal, Oxidative Stress, Huntington Disease, Endocrinology, Androgens, Ovariectomized rat, Female, Lipid Peroxidation, Propionates, Drug Antagonism, Injections, Intraperitoneal, Oxidative stress

الوصف: This paper evaluates the effects of testosterone (0.5 mg/kg subcutaneously (s.c.) for 8 days) on oxidative stress and cell damage induced by 3-nitropropionic acid (20 mg/kg intraperitoneally (i.p.) for 4 days) in ovariectomized rats. Gonadectomy triggered oxidative damage and cell loss, evaluated by the detection of caspase-3, whereas 3-nitropropionic acid increased the levels of oxidative stress induced by ovariectomy and prompted cell damage characterized by enhanced levels of lactate dehydrogenase. These changes were blocked by testosterone administration. Our results support the following conclusions: i) ovariectomy triggers oxidative and cell damage via caspase-3 in the striatum; ii) 3-nitropropionic acid exacerbates oxidative stress induced by ovariectomy and leads to cell damage characterized by increased levels of lactate dehydrogenase; iii) testosterone administration decreases oxidative stress and cell damage. Additionally, these data support the hypothesis that testosterone might play an important role in the onset and development of neurodegenerative diseases.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1d06e7eeda98e468142e155890559e30Test
https://doi.org/10.1016/j.lfs.2006.12.013Test

المؤلفون: Liqun Liu, Wenjuan Wang, Huanhuan Ren, Mingjie Zhou, Dong Wang, Qiusheng Zheng, Jichun Han

المصدر: Life sciences. 132

مصطلحات موضوعية: Anti-Inflammatory Agents, Apoptosis, Pharmacology, Cell morphology, General Biochemistry, Genetics and Molecular Biology, Antioxidants, Superoxide dismutase, chemistry.chemical_compound, Chalcones, Lactate dehydrogenase, Malondialdehyde, medicine, In Situ Nick-End Labeling, Animals, General Pharmacology, Toxicology and Pharmaceutics, Creatine Kinase, Analysis of Variance, TUNEL assay, biology, L-Lactate Dehydrogenase, Chemistry, Superoxide Dismutase, Tumor Necrosis Factor-alpha, General Medicine, Glutathione, medicine.disease, Rats, Biochemistry, Reperfusion Injury, biology.protein, Glutathione disulfide, Creatine kinase, Reperfusion injury

الوصف: Aims This study aimed to evaluate the protective effect of licochalcone C against myocardial ischemia/reperfusion injury in rats. Main methods Left ventricular developed pressure (LVDP) and its maximum up/down rate (± dp / dt max ) were recorded as myocardial function. Levels of creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione/glutathione disulfide (GSH/GSSG) ratio, and tumor necrosis factor-alpha (TNF-α) were determined by using enzyme-linked immunosorbent assay. Cell morphology was observed and mitochondrial damage was assessed by HE coloration and transmission electron microscopy, respectively. Cardiomyocyte apoptosis was determined by using terminal deoxynucleotidyl transferased UTP nick-end labeling (TUNEL). Key findings Pretreatment with licochalcone C significantly improved the recovery of LVDP and ± dp / dt max , and increased the levels of SOD and GSH/GSSG ratio. However, pretreatment with licochalcone C not only decreased the TUNEL-positive cell ratio and morphological changes, but also weaken the mitochondrial injury and the levels of CK, LDH, MDA, and TNF-α. Significance These results suggested an important function of licochalcone C extracted from traditional Chinese medicine in the cardioprotection via antioxidant, anti-inflammatory, and anti-apoptotic activities.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fac7c72392a396ba92abfa2f0254d4e8Test
https://pubmed.ncbi.nlm.nih.gov/25921769Test

المؤلفون: Göksel Şener, Nursal Gedik, Levent Kabasakal, Meral Keyer-Uysal, Feriha Ercan, Özer Şehirli, Serap Sirvanci

المصدر: Life Sciences. 76:2593-2606

مصطلحات موضوعية: Male, medicine.medical_specialty, Antioxidant, medicine.medical_treatment, Liver Cirrhosis, Experimental, digestive system, General Biochemistry, Genetics and Molecular Biology, Lipid peroxidation, chemistry.chemical_compound, Fibrosis, Malondialdehyde, Lactate dehydrogenase, Internal medicine, medicine, Animals, Rats, Wistar, General Pharmacology, Toxicology and Pharmaceutics, Garlic, Ligation, Saline, Peroxidase, L-Lactate Dehydrogenase, biology, Plant Extracts, Tumor Necrosis Factor-alpha, Alanine Transaminase, General Medicine, Glutathione, medicine.disease, digestive system diseases, Rats, Endocrinology, Liver, chemistry, Myeloperoxidase, biology.protein, Bile Ducts, Collagen, Lipid Peroxidation, Oxidation-Reduction

الوصف: The aim of this study was to assess the antioxidant and antifibrotic effects of chronic administration of aqueous garlic extract on liver fibrosis induced by biliary obstruction in rats. Liver fibrosis was induced in male Wistar albino rats by bile duct ligation and scission (BDL). Aqueous garlic extract (AGE, 1 ml/kg, i.p., corresponding to 250 mg/kg) or saline was administered for 28 days. At the end of the experiment, rats were killed by decapitation. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) levels were determined to assess liver functions and tissue damage, respectively. Tumor necrosis factor-alpha (TNF-α) was also assayed in serum samples. Liver tissues were taken for determination of the free radicals, renal malondialdehyde (MDA) levels, an end product of lipid peroxidation; glutathione (GSH) levels, a key antioxidant; and myeloperoxidase (MPO) activity, as an indirect index of neutrophil infiltration. Hepatic collagen content, as a fibrosis marker was also determined. Serum AST, ALT, LDH, and TNF- α levels were elevated in the BDL group as compared to control group, while this increase was significantly decreased by AGE treatment. Hepatic GSH levels, significantly depressed by BDL, were elevated back to control levels in AGE-treated BDL group. Increases in tissue free radical and MDA levels and MPO activity due to BDL were reduced back to control levels by AGE treatment. Similarly, increased hepatic collagen content in the BDL rats was reduced to the level of the control group with AGE treatment. Since AGE administration alleviated the BDL-induced oxidative injury of the liver and improved the hepatic structure and function, it seems likely that AGE with its antioxidant and antifibrotic properties, may be of potential therapeutic value in protecting the liver fibrosis and oxidative injury due to biliary obstruction.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0dcf53f5df9c1121bc5d2d90217b790eTest
https://doi.org/10.1016/j.lfs.2004.11.021Test

المؤلفون: Yan Xie, Le Chen, Huang-Tian Yang, Yi Zhu, Zhao-Nian Zhou, Wei-Zhong Zhu

المصدر: Life Sciences. 76:559-572

مصطلحات موضوعية: Male, medicine.medical_specialty, Potassium Channels, Time Factors, Myocardial Reperfusion Injury, Ventricular Function, Left, General Biochemistry, Genetics and Molecular Biology, Rats, Sprague-Dawley, Contractility, chemistry.chemical_compound, Lactate dehydrogenase, Internal medicine, Ca2+/calmodulin-dependent protein kinase, parasitic diseases, medicine, Animals, Myocyte, General Pharmacology, Toxicology and Pharmaceutics, Hypoxia, Cardioprotection, L-Lactate Dehydrogenase, business.industry, Altitude, Myocardium, Body Weight, Intermittent hypoxia, Organ Size, General Medicine, Hypoxia (medical), Adaptation, Physiological, Potassium channel, Rats, Endocrinology, chemistry, Anesthesia, Calcium-Calmodulin-Dependent Protein Kinases, Calcium, medicine.symptom, Calcium-Calmodulin-Dependent Protein Kinase Type 2, business

الوصف: Adaptation to intermittent high altitude (IHA) hypoxia can protect the heart against ischemia-reperfusion injury. In view of the fact that both Ca2+ paradox and ischemia-reperfusion injury are associated with the intracellular Ca2+ overload, we tested the hypothesis that IHA hypoxia may protect hearts against Ca2+ paradox-induced lethal injury if its cardioprotection bases on preventing the development of intracellular Ca2+ overload. Langendorff-perfused hearts from normoxic and IHA hypoxic rats were subjected to Ca2+ paradox (5 min of Ca2+ depletion followed by 30 min of Ca2+ repletion) and the functional, biochemical and pathological changes were investigated. The Ca2+ paradox incapacitated the contractility of the normoxic hearts, whereas the IHA hypoxic hearts significantly preserved contractile activity. Furthermore, the normoxic hearts subjected to Ca2+ paradox exhibited a marked reduction in coronary flow, increase in lactate dehydrogenase release, and severe myocyte damage. In contrast, these changes were significantly prevented in IHA hypoxic hearts. We, then, tested and confirmed our hypothesis that the protective mechanisms are mediated by mitochondria ATP-sensitive potassium channels (mitoKATP) and Ca2+/calmodulin-dependent protein kinase II (CaMKII), as the protective effect of IHA hypoxia was abolished by 5-hydroxydecanoate, a selective mitoKATP blocker, and significantly attenuated by KN-93, a CaMKII inhibitor. In conclusion, our studies offer for the first time that IHA hypoxia confers cardioprotection against the lethal injury of Ca2+ paradox and give biochemical evidence for the protective mechanism of IHA hypoxia. We propose that researches in this area may lead a preventive regimen against myocardial injury associated with Ca2+ overload.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ea9df347c4257f1b55beccfbef831e22Test
https://doi.org/10.1016/j.lfs.2004.09.017Test

المؤلفون: Roberto Ventura Santos, R. A. Bassit, L. F. B. P. Costa Rosa, Erico Chagas Caperuto

المصدر: Life Sciences. 75:1917-1924

مصطلحات موضوعية: Adult, Male, medicine.medical_specialty, Inflammation, Creatine, Dinoprostone, General Biochemistry, Genetics and Molecular Biology, Running, chemistry.chemical_compound, Internal medicine, Lactate dehydrogenase, medicine, Humans, General Pharmacology, Toxicology and Pharmaceutics, Prostaglandin E2, Muscle, Skeletal, Creatine Kinase, Cell damage, Analysis of Variance, L-Lactate Dehydrogenase, Myositis, biology, Tumor Necrosis Factor-alpha, business.industry, General Medicine, medicine.disease, Endocrinology, chemistry, Biochemistry, Dietary Supplements, Muscle Fatigue, biology.protein, Tumor necrosis factor alpha, Creatine kinase, Analysis of variance, medicine.symptom, business, medicine.drug

الوصف: We have evaluated the effect of a creatine supplementation protocol upon inflammatory and muscle soreness markers: creatine kinase (CK), lactate dehydrogenase (LDH), prostaglandin E2) (PGE2) and tumor necrosis factor-alpha (TNF-alpha) after running 30km. Runners with previously experience in running marathons, with their personal best between 2.5-3h were supplemented for 5 days prior to the 30km race with 4 doses of 5g of creatine and 15g of maltodextrine per day while the control group received the same amount of maltodextrine. Pre-race blood samples were collected immediately before running the 30km, and 24h after the end of the test (the post-race samples). After the test, athletes from the control group presented an increase in plasma CK (4.4-fold), LDH (43%), PGE2 6.6-fold) and TNF-alpha (2.34-fold) concentrations, indicating a high level of cell injury and inflammation. Creatine supplementation attenuated the changes observed for CK (by 19%), PGE2 and TNF-alpha (by 60.9% and 33.7%, respectively, p

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0eae3459cbac8a3a7ffe8f9afad5d326Test
https://doi.org/10.1016/j.lfs.2003.11.036Test