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المصدر: Life sciences. 264
مصطلحات موضوعية: 0301 basic medicine, Male, Cardiotonic Agents, Heart Ventricles, Ischemia, Myocardial Infarction, Blood Pressure, Morin, Pharmacology, 030226 pharmacology & pharmacy, General Biochemistry, Genetics and Molecular Biology, Mitochondria, Heart, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, KATP Channels, Lactate dehydrogenase, Malondialdehyde, medicine, Animals, Myocardial infarction, General Pharmacology, Toxicology and Pharmaceutics, Rats, Wistar, Flavonoids, L-Lactate Dehydrogenase, Chemistry, Hemodynamics, Heart, General Medicine, medicine.disease, Potassium channel, Perfusion, 030104 developmental biology, Mitochondrial permeability transition pore, Tachycardia, Ventricular
الوصف: Aims During heart ischemia, the lack of oxygen in the myocardial cells causes pH and ion disturbances and cell death through opening mitochondrial permeability transition pores (mPTP). Considering the inhibitory effects of mitochondrial ATP-dependent potassium channels (mt-KATP) on these pores and anti-ischemic effects of morin, we hypothesized that it may exert its positive effects via activating mt-KATP as well as its anti-oxidative effects. Main methods Isolated rat hearts were perfused by Krebs-Henseleit solution enriched with the morin (0.25, 0.5 and 1 mg/L) or 5-hydroxydecanoate (5-HD, a mt-KATP blocker;100 μM) or both as needed 5 min before starting regional ischemia till the first 10 min of the reperfusion period. The reperfusion was developed with Krebs-Henseleit solution 60 or 120 min respectively for biochemical evaluations (lactate dehydrogenase and malondialdehyde level) or the assessment of myocardial infarct size. During the experiments, hemodynamic functions were recorded and cardiac arrhythmias were determined. Key findings Our findings demonstrated that morin reduced the infarct size. Also, morin perfusion could remarkably prevent the malondialdehyde over-production during ischemia. Total ventricular ectopic beats had the same significant changes as the malondialdehyde level, in both ischemia and reperfusion phases. Morin could also relatively improve the ischemia-induced hemodynamic dysfunction. All mentioned protective effects of morin were reversed by concomitant perfusion of 5-HD. Significance Morin has protective effects against ischemic hearts through anti-oxidative effects. It also suggests a link between the cardioprotective effects of morin and mt-KATP. However, additional studies are required to prove this preliminary hypothesis.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::10575c6ebd983089076ce24151abd681Test
https://pubmed.ncbi.nlm.nih.gov/33148418Test -
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المؤلفون: Nermeen A. Megahed, Ahmed G. Abd Elhameed, Manar G. Helal
المصدر: Life sciences. 239
مصطلحات موضوعية: 0301 basic medicine, Male, Ovalbumin, H&E stain, Adamantane, Pharmacology, medicine.disease_cause, Nitric Oxide, 030226 pharmacology & pharmacy, General Biochemistry, Genetics and Molecular Biology, Dexamethasone, 03 medical and health sciences, chemistry.chemical_compound, Mice, 0302 clinical medicine, Lactate dehydrogenase, medicine, Animals, General Pharmacology, Toxicology and Pharmaceutics, Lung, Peroxidase, Dipeptidyl-Peptidase IV Inhibitors, medicine.diagnostic_test, biology, L-Lactate Dehydrogenase, business.industry, NF-kappa B, General Medicine, Glutathione, Dipeptides, respiratory system, Asthma, Toll-Like Receptor 4, 030104 developmental biology, Bronchoalveolar lavage, chemistry, Myeloperoxidase, Acute Disease, biology.protein, business, Bronchoalveolar Lavage Fluid, Oxidative stress, medicine.drug
الوصف: Saxagliptin (Saxa), a dipeptidyl dipeptidase-4 (DPP-4) inhibitor, is widely used for the treatment of type 2 diabetes mellitus. It has been documented to have immunomodulatory and anti-inflammatory actions. Our objective was to delineate the protective effect and the underlying mechanism of Saxa-in comparison with Dexamethasone (Dexa) – in airway inflammation induced by ovalbumin (OVA) in mice. Methods Mice were OVA-sensitized and challenged for the induction of acute asthma. Mice were orally administrated Saxa or Dexa. Total and differential cell counts, lactate dehydrogenase (LDH) and total protein concentrations were assessed in bronchoalveolar lavage fluid (BALF). The toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-kB), reduced glutathione (GSH), and total nitrate/nitrite products (NOx) levels as well as myeloperoxidase (MPO) activity in lung tissues were measured. Histopathological examination of the lung specimens was carried out using the hematoxylin and eosin (H & E) staining. Results Histopathological examination revealed that both Saxa and Dexa ameliorated OVA-induced inflammatory changes and significantly reduced total and differential leukocyte counts, LDH and total protein level in BALF upon comparison with OVA group. In addition, both treatments significantly mitigated OVA-induced oxidative stress as evidenced by diminished lung NOx level and MPO activity and elevated GSH level. The elevation of TLR4 and NF-kB levels in lung tissue were ameliorated by Saxa and Dexa administration. Conclusion Saxa had marked antiasthmatic effect in OVA-induced allergic asthma through modulation of TLR4 and NF-κB signaling. Also, Saxa may represent a promising therapeutic agent for acute allergic asthma.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e2654f3a985ad7c0ce2977ac6cef7faeTest
https://pubmed.ncbi.nlm.nih.gov/31678284Test -
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المؤلفون: Ruisi Xu, Jian Yin, Jun Wei, Siqi Zhang
المصدر: Life Sciences. 223:88-94
مصطلحات موضوعية: 0301 basic medicine, Protein Deglycase DJ-1, Cell Culture Techniques, Down-Regulation, 030226 pharmacology & pharmacy, General Biochemistry, Genetics and Molecular Biology, Cell Line, Superoxide dismutase, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Western blot, Ischemia, Lactate dehydrogenase, medicine, Humans, HSP70 Heat-Shock Proteins, General Pharmacology, Toxicology and Pharmaceutics, Glutaredoxins, chemistry.chemical_classification, Reactive oxygen species, biology, medicine.diagnostic_test, Chemistry, Epithelial Cells, General Medicine, Transfection, Culture Media, Hsp70, Cell biology, Oxygen, Oxidative Stress, Glucose, Kidney Tubules, 030104 developmental biology, Apoptosis, biology.protein, Signal transduction, Signal Transduction
الوصف: Aims Gluaredoxin1 (GRX1) is an important protein of the cellular antioxidant defense system, but its role in renal epithelial cell injury caused by ischemia remains unclear. In this study, we aimed to gain insight into the role of GRX1 in HK-2 cells with oxygen glucose deprivation (OGD) injury, which served as an in vitro cell model of renal epithelial cell ischemic injury. We investigated the underlying regulation of GRX1, DJ-1, and HSP70 as well as the role of the GRX1/DJ-1/HSP70 signaling pathway in this model. Materials and methods The protein and mRNA expressions were measured by Western blot and qRT-PCR assays, respectively. GRX1 was overexpressed by transfection of pcDNA.3.1-GRX1 and DJ-1 was inhibited by transfection with DJ-1 siRNA. Cell apoptosis, caspase-3 activity, lactate dehydrogenase (LDH) leakage, or superoxide dismutase (SOD) content was tested by the related detection kit. Reactive oxygen species (ROS) level was detected via carboxy-H2DCF-DA. Key findings We found that GRX1 was distinctly down-regulated in HK-2 cells after incubation under the OGD condition. GRX1 overexpression markedly constrained cell apoptosis, caspase-3 activity, LDH leakage, and the ROS level, while SOD content was elevated. GRX1 up-regulation increased DJ-1 and HSP70 protein expression, while DJ-1 inhibition significantly offset the effect of GRX1 overexpression on HSP70, indicating that GRX1 could regulate HSP70 via control of DJ-1. Moreover, we observed that HSP70 inhibition removed the constraints imposed by GRX1 overexpression on ROS level, LDH leakage, and caspase-3 activity. Significance Overall, this study showed that GRX1 minimizes cell injury and apoptosis in HK-2 cells under OGD conditions via regulation of DJ-1 and HSP70 expression.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::504041f775ef8c4175a9bf022c41a1b7Test
https://doi.org/10.1016/j.lfs.2019.03.015Test -
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المؤلفون: Henrique J. Cardoso, Sílvia Socorro, Cátia V. Vaz, Tiago M.A. Carvalho, Marília I. Figueira
المصدر: Life Sciences. 218:274-283
مصطلحات موضوعية: Male, 0301 basic medicine, medicine.drug_class, Apoptosis, urologic and male genital diseases, 030226 pharmacology & pharmacy, General Biochemistry, Genetics and Molecular Biology, Tyrosine-kinase inhibitor, 03 medical and health sciences, chemistry.chemical_compound, Prostate cancer, 0302 clinical medicine, DU145, Lactate dehydrogenase, Tumor Cells, Cultured, medicine, Humans, Glycolysis, Lactic Acid, Viability assay, General Pharmacology, Toxicology and Pharmaceutics, Protein Kinase Inhibitors, neoplasms, Cell Proliferation, Imatinib, General Medicine, medicine.disease, Prostatic Neoplasms, Castration-Resistant, Glucose, 030104 developmental biology, chemistry, Hyperglycemia, Imatinib Mesylate, Cancer research, medicine.drug
الوصف: Aims The tyrosine kinase inhibitor imatinib has been used in prostate cancer treatment with outcomes that did not follow the in vitro findings. The glycolytic environment has been shown to influence the efficacy of anti-cancer drugs. This study aimed to evaluate the effect of imatinib on cell viability, apoptosis, and metabolism in cell line models of castrate-resistant prostate cancer (CRPC) under hyperglycemic and hypoglycemic conditions. Main methods DU145 and PC3 CRPC cell lines were exposed to 20 μM imatinib under 5 mM (hypoglycemia) or 30 mM glucose (hyperglycemia) for 48–72 h. Cell viability was assessed by the MTS assay. The expression of apoptosis regulators and glycolytic metabolism-related proteins was analysed by Western blot, and the activity of caspase-3 and lactate dehydrogenase (LDH) was determined spectrophotometrically. Glucose consumption and lactate production were determined using biochemical assays. Key findings Imatinib decreased CRPC cells viability, whereas increasing apoptosis; effects only observed in hyperglycemic conditions. Glucose consumption and lactate production were significantly increased in imatinib-treated DU145 and PC3 cells, and independently of glucose availability. Accordingly, LDH expression and activity were significantly increased in response to imatinib. Significance Higher glucose availability improved the effectiveness of imatinib suppressing survival and growth of CRPC cells. It was also shown that imatinib treatment stimulated the glycolytic metabolism of CRPC cells. This study first demonstrated that a glucose-enriched environment intensifies the effect of imatinib, which stimulates the interest for testing this compound into the clinical setting, namely in hyperglycemia conditions (diabetic patients) or in co-administration with inhibitors of glycolytic metabolism.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2ecf6ed8430f90223bd568ae4844263fTest
https://doi.org/10.1016/j.lfs.2018.12.055Test -
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المؤلفون: Ya Guo, Shan Huang, Lijun Jia, Lili Han, Xiaoran Yin, Ying Zan
المصدر: Life Sciences. 208:123-130
مصطلحات موضوعية: 0301 basic medicine, Lactate dehydrogenase A, Cell, Mice, Nude, Apoptosis, Breast Neoplasms, PKM2, Antioxidants, General Biochemistry, Genetics and Molecular Biology, Mice, 03 medical and health sciences, 0302 clinical medicine, Cell Movement, Autophagy, Tumor Cells, Cultured, medicine, Animals, Humans, heterocyclic compounds, General Pharmacology, Toxicology and Pharmaceutics, education, Protein kinase B, PI3K/AKT/mTOR pathway, Cell Proliferation, Mice, Inbred BALB C, education.field_of_study, Tumor microenvironment, Chemistry, TOR Serine-Threonine Kinases, Cell migration, General Medicine, Xenograft Model Antitumor Assays, 030104 developmental biology, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Cancer research, Female, Quercetin, Glycolysis, Proto-Oncogene Proteins c-akt, Signal Transduction
الوصف: Tumor metastasis is the primary factor causing death of cancer patients and it is a study emphasis in cancer treatment to suppress tumor metastasis by inhibiting glycolysis, which is the main way of energy supply for cell mobility in tumor. In the present study, we aimed to explore the effect of quercetin, a bioactive flavonoid, on tumor metastasis and cell glycolysis and its related functionary mechanism in breast cancer progression. Firstly, trans-well invasion assay and wound healing assay indicated that quercetin effectively suppressed cell mobility. The corresponding western blot revealed that quercetin treatment down-regulated the expression of cell migration marker proteins, such as matrix metalloproteinase 2 (MMP-2), MMP-9 and vascular endothelial growth factor (VEGF). The further experiments exhibited that quercetin successfully blocked cell glycolysis by inhibiting the level of glucose uptake and the production of lactic acid, and also decreased the level of glycolysis-related proteins Pyruvate kinase M2 (PKM2), Glucose transporter1(GLUT1) and Lactate dehydrogenase A (LDHA). The above results revealed that quercetin might inhibit glycolysis to limit the migration of tumor cells by reducing the acidity of the tumor microenvironment. Moreover, our further investigation showed that quercetin induced obvious autophagy via inactivating the Akt-mTOR pathway. At the same time, the application of autophagy inhibitor 3-MA and Akt-mTOR pathway inducer IGF-1 further demonstrated that quercetin exerted inhibiting effect on cell mobility and glycolysis through Akt-mTOR pathway mediated autophagy induction. At last, the in vivo experiments also showed that quercetin treatment could suppress tumor growth and metastasis, inhibit glycolysis and induce autophagy through the inhibition of p-AKT/AKT. Taken together, we firstly revealed that quercetin suppressed the progression of breast cancer by inhibiting cell mobility and glycolysis through Akt-mTOR pathway mediated autophagy induction and may provide a potential therapeutic target for breast cancer treatment.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::271b005cbeb5ca1e68921589eaac381bTest
https://doi.org/10.1016/j.lfs.2018.07.027Test -
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المؤلفون: Lingyu Chang, Wei Wang, Jingbo Zhu, Honglin Yu, Xiaohu Li, Chaozhao Liang
المصدر: Life sciences. 272
مصطلحات موضوعية: 0301 basic medicine, Male, China, Lactate dehydrogenase A, Kidney, 030226 pharmacology & pharmacy, General Biochemistry, Genetics and Molecular Biology, Cell Line, Transforming Growth Factor beta1, 03 medical and health sciences, Mice, 0302 clinical medicine, Western blot, medicine, Animals, Glycolysis, General Pharmacology, Toxicology and Pharmaceutics, Fibroblast, education, Myofibroblasts, Pyruvates, Urinary Tract, Cell Proliferation, education.field_of_study, medicine.diagnostic_test, Chemistry, Kinase, General Medicine, Fibroblasts, Molecular biology, Fibrosis, Rats, Blot, Mice, Inbred C57BL, Molecular Docking Simulation, Disease Models, Animal, 030104 developmental biology, medicine.anatomical_structure, Anaerobic glycolysis, Kidney Diseases, Pyruvate kinase, Signal Transduction, Ureteral Obstruction
الوصف: AIMs Enhanced aerobic glycolysis is a motivation of fibroblast–myofibroblast transdifferentiation (FMT), leading to kidney fibrosis. 3-Bromopyruvate (3-BrPA) is a glycolysis inhibitor and has fibrosis-protected effect in liver. This study aims to explore the effects of 3-BrPA on aerobic glycolysis and kidney fibrosis in a unilateral ureteral obstruction (UUO) mice model and transforming growth factor-β1(TGF-β1)-stimulated normal rat kidney fibroblast (NRK 49F) cell model in vitro. Main methods In vivo UUO mouse model and in vitro TGF-β1 stimulated cell model were built. Immunohistochemical staining, Western blots, Real-time PCR and fluorescence microscopy were employed to detect extra cellular matrix (ECM) synthesis, fibroblast activation, aerobic glycolysis switch and related signaling pathways. Key findings HE and Masson's Trichrome staining showed that 3-BrPA substantially suppressed kidney injury and interstitial collagen production. 3-BrPA also attenuated ECM accumulation in a dose-dependent manner, as shown by immunohistochemistry staining, RT-PCR and western blot. Furthermore, 3-BrPA inhibited FMT, as indicated by α-SMA and PCNA immunofluorescence double staining. Additionally, the results of MTT assay indicated 3-BrPA prevented TGF-β1 induced fibroblasts proliferation in a time- and dose-dependent manner. Mechanistically, molecular docking results showed that 3-BrPA effectively decreased the aerobic glycolysis related enzymes Hexokinase-2 (HK-2), Lactate dehydrogenase A (LDHA) and Pyruvate kinase isozymes M2 (PKM-2), as well as inhibited IL-1 receptor–associated kinase 4 (IRAK4)/MYC protein levels. Significance Our study highlighted that 3-BrPA is a potential reno-protective agent in kidney fibrosis through the inhibition of fibroblasts aerobic glycolysis might via IRAK4/MYC signal pathways.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ce21ca9407b81756f4eb0af6be207decTest
https://pubmed.ncbi.nlm.nih.gov/33577854Test -
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المؤلفون: Ke Zhang, Zhouyu Ning, Jie Sheng, Yongqiang Hua, Ye Li, Luming Liu, Weidong Shi
المصدر: Life sciences. 287
مصطلحات موضوعية: 0301 basic medicine, Male, endocrine system diseases, Carcinogenesis, Lactate dehydrogenase A, Mice, Nude, Cell Cycle Proteins, Adenocarcinoma, medicine.disease_cause, 030226 pharmacology & pharmacy, Deoxycytidine, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, Mice, 0302 clinical medicine, Pancreatic cancer, medicine, Animals, Humans, General Pharmacology, Toxicology and Pharmaceutics, education, Wnt Signaling Pathway, Aged, education.field_of_study, Gene knockdown, Chemistry, Wnt signaling pathway, General Medicine, Middle Aged, medicine.disease, Xenograft Model Antitumor Assays, Gemcitabine, digestive system diseases, Pancreatic Neoplasms, 030104 developmental biology, Anaerobic glycolysis, Drug Resistance, Neoplasm, Catenin, Cancer research, Female, Microtubule-Associated Proteins
الوصف: Background Elevated expression of family with sequence similarity 83 member D (Fam83D) has been found in various cancers; however, its role in pancreatic adenocarcinoma (PDAC) remains unclear. The current study was designed to elucidate the roles of Fam83D in pancreatic cancer. Method The level of Fam83D was detected in PDAC tissues and adjacent no-tumorous tissues. Effects of Fam83D on proliferation, glycolysis and gemcitabine (GEM) sensitivity of pancreatic cancer cells were examined. Results Fam83D was overexpressed in PDAC and associated with clinical stage, metastatic status and survival rates of PDAC patients. Function study showed that Fam83D knockdown (KD) caused inhibited proliferation, suppressed mitochondrial respiration capacity, reduced aerobic glycolysis, and down-regulation of nuclear β-catenin, proto-oncogene C-Myc, and lactate dehydrogenase A (LDHA). Fam83D KD enhanced the sensitivity of PDAC cells to GEM in vitro and in vivo. On the contrary, Fam83D overexpression displayed reverse effects on PDAC cells. Moreover, the Wnt/β-catenin inhibitor abolished the effects of Fam83D overexpression in PDAC cells. Conclusions the current data suggest that enhanced Fam83D expression contributes to PDAC progression and the development of chemoresistance through the Wnt/β-catenin signaling.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::374ff2a7b6e2b394a3661dbe2029e371Test
https://pubmed.ncbi.nlm.nih.gov/33571515Test -
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المؤلفون: Noha A. Salem, Omayma M. Mahmoud, Basma S. Mansour, Gamal Abdel-Alrahman, Ghada Abdel Kader
المصدر: Life Sciences
مصطلحات موضوعية: 0301 basic medicine, Male, Statin, medicine.drug_class, Apoptosis, Pharmacology, Azithromycin, medicine.disease_cause, 030226 pharmacology & pharmacy, Article, General Biochemistry, Genetics and Molecular Biology, Antioxidants, Rosuvastatin, Rats, Sprague-Dawley, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Lactate dehydrogenase, Malondialdehyde, Medicine, Animals, General Pharmacology, Toxicology and Pharmaceutics, Rosuvastatin Calcium, Inflammation, Cardiotoxicity, biology, business.industry, nutritional and metabolic diseases, Heart, General Medicine, Glutathione, Anti-Bacterial Agents, Rats, COVID-19 Drug Treatment, Disease Models, Animal, Oxidative Stress, 030104 developmental biology, chemistry, biology.protein, Rat, Creatine kinase, Hydroxymethylglutaryl-CoA Reductase Inhibitors, business, Oxidative stress, medicine.drug
الوصف: Aims Azithromycin is widely used broad spectrum antibiotic recently used in treatment protocol of COVID-19 for its antiviral and immunomodulatory effects combined with Hydroxychloroquine or alone. Rat models showed that Azithromycin produces oxidative stress, inflammation, and apoptosis of myocardial tissue. Rosuvastatin, a synthetic statin, can attenuate myocardial ischemia with antioxidant and antiapoptotic effects. This study aims to evaluate the probable protective effect of Rosuvastatin against Azithromycin induced cardiotoxicity. Main method Twenty adult male albino rats were divided randomly into four groups, five rats each control, Azithromycin, Rosuvastatin, and Azithromycin +Rosuvastatin groups. Azithromycin 30 mg/kg/day and Rosuvastatin 2 mg/kg/day were administrated for two weeks by an intragastric tube. Twenty-four hours after the last dose, rats were anesthetized and the following measures were carried out; Electrocardiogram, Blood samples for Biochemical analysis of lactate dehydrogenase (LDH), and creatine phosphokinase (CPK). The animals sacrificed, hearts excised, apical part processed for H&E, immunohistochemical staining, and examined by light microscope. The remaining parts of the heart were collected for assessment of Malondialdehyde (MDA) and Reduced Glutathione (GSH). Key findings The results revealed that Rosuvastatin significantly ameliorates ECG changes, biochemical, and Oxidative stress markers alterations of Azithromycin. Histological evaluation from Azithromycin group showed marked areas of degeneration, myofibers disorganization, inflammatory infiltrate, and hemorrhage. Immunohistochemical evaluation showed significant increase in both Caspase 3 and Tumor necrosis factor (TNF) immune stain. Rosuvastatin treated group showed restoration of the cardiac muscle fibers in H&E and Immunohistochemical results. Significance We concluded that Rosuvastatin significantly ameliorates the toxic changes of Azithromycin on the heart.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::14b28e4f093bfe3578ef77bd7e6ad7a7Test
https://pubmed.ncbi.nlm.nih.gov/33476632Test -
9
المؤلفون: Dan Li, Menglong Wang, Zhen Wang, Jun Wan, Yao Xu, Mengmeng Zhao, Di Ye, Jishou Zhang, Jing Ye
المصدر: Life sciences. 277
مصطلحات موضوعية: 0301 basic medicine, Cardiac function curve, Lipopolysaccharides, China, Docosahexaenoic Acids, Inflammation, Apoptosis, Pharmacology, medicine.disease_cause, Protective Agents, 030226 pharmacology & pharmacy, General Biochemistry, Genetics and Molecular Biology, Superoxide dismutase, 03 medical and health sciences, chemistry.chemical_compound, Mice, 0302 clinical medicine, Sepsis, Medicine, Animals, General Pharmacology, Toxicology and Pharmaceutics, biology, L-Lactate Dehydrogenase, business.industry, Macrophages, Cell Differentiation, General Medicine, M2 Macrophage, Malondialdehyde, Heme oxygenase, Mice, Inbred C57BL, Oxidative Stress, 030104 developmental biology, chemistry, Heart Injuries, biology.protein, Cytokine secretion, medicine.symptom, business, Oxidative stress
الوصف: Background Maresin 1 (MaR1) is a pro-resolving lipid mediator that has been reported to have strong regulatory effects on oxidative stress and inflammation. This study aimed to determine the effect of MaR1 on lipopolysaccharide (LPS)-induced sepsis-related cardiac injury and explore its possible mechanisms. Methods Mice were administered MaR1 or PBS and then treated with LPS or saline for 6 h. Then, cardiac function, cardiac injury markers, cardiac macrophage differentiation, oxidative stress and myocardial cell apoptosis in each group were measured. Results MaR1 treatment significantly decreased the serum levels of lactate dehydrogenase (LDH) and kinase isoenzyme (CK-MB) and improved cardiac function in LPS-induced mice. Treatment with MaR1 also inhibited LPS-induced M1 macrophage differentiation and reduced M1 macrophage-related cytokine secretion while promoting M2 macrophage differentiation and increasing M2 macrophage-related inflammatory mediator expression. In addition, MaR1 decreased serum malondialdehyde (MDA) levels and increased serum levels of superoxide dismutase (SOD) and glutathione (GSH), as well as cardiac expression of nuclear factor erythroid-2 related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1), in LPS-induced mice. Furthermore, fewer TUNEL-positive cells were observed in the LPS + MaR1 group than in the LPS group. Conclusions Our experimental results show that MaR1 alleviates cardiac injury and protects against cardiac dysfunction and may be beneficial in reducing sepsis-induced cardiac injury.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f4405b6b24daeeffd45b7f148b0d32caTest
https://pubmed.ncbi.nlm.nih.gov/33811894Test -
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المؤلفون: Mehdi Shahrouzian, Sara Banihashemi, Majid Ghanavat, Seyedeh Maryam Kazemi, Zeinab Deris Zayeri, Najmaldin Saki
المصدر: Life sciences. 264
مصطلحات موضوعية: 0301 basic medicine, Carbohydrate metabolism, 030226 pharmacology & pharmacy, General Biochemistry, Genetics and Molecular Biology, Metastasis, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Lactate dehydrogenase, Neoplasms, medicine, Biomarkers, Tumor, Animals, Humans, Glycolysis, Lactic Acid, General Pharmacology, Toxicology and Pharmaceutics, Neoplasm Metastasis, business.industry, Glucose transporter, Cancer, General Medicine, Oncogenes, medicine.disease, Oxidative Stress, 030104 developmental biology, Glucose, chemistry, Anaerobic glycolysis, Cancer cell, Cancer research, Carbohydrate Metabolism, business
الوصف: Glucose metabolism enzymes and transporters play major role in cancer development and metastasis. In this study, we discuss glucose metabolism, transporters, receptors, hormones, oncogenes and tumor suppressors which interact with glucose metabolism and we try to discuss their major role in cancer development and cancer metabolism. We try to highlight the. Metabolic changes in cancer and metastasis upregulation of glycolysis is observed in many primary and metastatic cancers and aerobic glycolysis is the most favorable mechanism for glucose metabolism in cancer cells, and it is a kind of evolutionary change. The question that is posed at this juncture is: Can we use aerobic glycolysis phenotype and enzymes beyond this mechanism in estimating cancer prognosis and metastasis? Lactate is a metabolite of glucose metabolism and it is a key player in cancer and metastasis in both normoxic and hypoxic condition so lactate dehydrogenase can be a good prognostic biomarker. Furthermore, monocarboxylic transporter which is the main lactate transporter can be good target in therapeutic studies. Glycolysis enzymes are valuable enzymes in cancer and metastasis diagnosis and can be used as therapeutic targets in cancer treatment. Designing a diagnostic and prognostic profile for cancer metastasis seems to be possible base on glycolysis enzymes and glucose transporters. Also, glucose metabolism enzymes and agents can give us a clear vision in estimating cancer metastasis. We can promote a panel of genes that detect genetic changes in glucose metabolism agents to diagnose cancer metastasis.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::770056a653390b3bd0b2cae1d7928888Test
https://pubmed.ncbi.nlm.nih.gov/33091446Test
